'DNA editing' enzyme could fuel breast cancer

Friday 8 February 2013

Genetic errors driving the majority of breast cancers may be caused by a hyperactive enzyme called APOBEC3B, according to US researchers.

The finding could lead to new ways to diagnose and treat breast cancer, exploiting the root cause of genetic damage - 'DNA editing' by the enzyme - rather than the damage itself.

Under normal circumstances, APOBEC enzymes help repair damaged DNA and protect against viruses like HIV.

But the University of Minnesota researchers showed in a research paper published in Nature that one particular form of APOBEC was found in high levels in breast cancer cells.

Lead researcher Dr Reuben Harris and his team measured the activity of seven related enzymes known collectively as the APOBEC3 family, in breast cancer cells grown in the lab and breast tumour samples.

They found that only one, known as APOBEC3B, was present in high levels inside cancer cells.

But APOBEC3B appears to be a biological "double-edged sword", as it protects some cells from viruses such as HIV, yet can produce changes giving rise to cancer in others.

Last year, researchers at the Wellcome Trust Sanger Institute in Cambridge published a detailed analysis of the DNA damage in breast cancer, and spotted signs that looked like the activity of APOBEC enzymes.

"Our next steps will focus on the connections between high levels of APOBEC3B, age and other genetic risk factors that are known breast cancer markers," said Dr Harris, who stressed the need for additional research.

"Ultimately, we hope our discovery leads to better therapeutic outcomes for patients."

In 2010, about 50,000 women and 400 men in the UK were diagnosed with breast cancer, and there were nearly 12,000 deaths from the disease.

If future studies confirm that high APOBEC3B levels indicate the early presence of breast cancer, a simple blood test could be a strategy for early detection.

Cancer Research UK's Professor Charlie Swanton, who studies the genetic complexity inside tumours, said it was a "fascinating and important study" which showed how researchers are beginning to understand the precise mechanisms that drive the genetic chaos found in cancer cells.

"Pinpointing these mechanisms give us new avenues to try to limit this chaos, or maybe even exploit it to tip cancers over the edge.

"There's a long way to go before we get a handle on the cancer's true genetic complexity, let alone turn this into treatments to help patients," he added.

"But studies like this show that important and tangible progress is being made in understanding this disease."

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More evidence that beta blockers help stop cancers from spreading

Wednesday 30 January 2013

US researchers have taken a step forward in understanding how beta blockers may slow the spread of cancer.

The study is the latest in a series of findings that suggest the drugs, commonly used to treat conditions such as heart disease, high blood pressure, glaucoma and migraines, might also have a role to play in cancer treatment.

Previous studies have shown lower rates of death from various cancers among people who take beta blockers for long periods for other conditions, leading researchers to speculate that the drugs could help treat patients.

The new research, published in Nature Communications and led by Professor Anil Sood at the MD Anderson Cancer Center in Texas, focused on a molecule on the surface of cells, known as the beta-adrenergic receptor, or ADRB - the target of beta blocker drugs.

Working in a mouse model of ovarian cancer, the researchers showed that signals sent from ADRB into the cell’s interior activated a key cancer protein called Src.

This in turn switched on a variety of processes linked to the spread of the disease.

The effect was counteracted by giving the mice propanolol, a commonly used beta blocker, and this also appeared to slow the growth of the cancers.

“This is a major step forward in understanding [beta blockers’] biology and impact,” said Professor Sood. “It opens the door to study drugs that could inhibit this unique signalling pathway".

To add further weight to their findings, the researchers looked at medical records from a large database called the Adverse Event Reporting System. They found that patients’ chances of dying from cancer were reduced by 17 per cent if they were also taking beta blockers for other conditions.  

This echoed the findings of recent studies into lung cancer and ovarian cancer.

Dr Des Powe, a Nottingham-based researcher running a Cancer Research UK-funded study into beta blockers and breast cancer, agreed the evidence was becoming more and more compelling.

“Evidence has been building for several years that beta blockers could be used to help treat certain cancers – notably some forms of breast, bowel, lung, melanoma and ovarian cancer, and possibly prostate cancer.

“These cancers seem to have a more favourable prognosis in people who regularly take beta blockers, and trials are underway to find out more. On top of this, labs around the world have begun to work out exactly why and how this may be happening.”

But he cautioned that there was still a way to go before beta blockers – prescription drugs with known side effects – were proven safe and suitable for patients undergoing cancer treatment.

“This is an idea that needs to be fully tested in the clinic to be sure,” he warned.

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Israeli researchers developing BRCA 'radiation' test

Tuesday 22 January 2013

A new blood test that measures cells’ response to radiation could detect inherited faults in a person’s BRCA genes, according to Israeli researchers.

Rather than directly analysing an individual’s DNA, the scientists propose the new test could identify at-risk people with mutations that current methods find hard to spot.

But others cautioned that the method, while promising, would need significant development and testing before it could replace existing methods, which rely on DNA sequencing.

Discovered in the 1980s, the BRCA1 and BRCA2 genes are found in all human cells, and normally make proteins that are involved in cell division and DNA repair - two processes that go wrong in cancer.

As a result, people who inherit faulty copies of either gene have a significantly increased risk of breast, ovarian and prostate cancers, and these cancers often run in their families. About five in every hundred breast cancers are thought to be caused by an inherited BRCA gene.

At the moment, DNA samples from members of affected families can be tested, and carriers offered extra monitoring or treatment.

But the test relies on being able to predict whether a fault is likely to be harmful, by comparing the DNA analysis against previously known mutations.

This has disadvantages, says study author Dr Asher Salmon, from the the Hadassah Hebrew University Medical Center in Jerusalem.

"The current tool for mutation detection is gene sequencing, which is expensive, time-consuming and, in many cases, lacking clear and decisive clinical decision making information," he said.

"In many cases, [it] identifies a mutation, but we do not know if the mutation is neutral or harmful."

Since they are unable to repair damaged DNA, cells that contain faulty BRCA genes are more sensitive to radiation. So Salmon's team tested whether this response could be used as a marker for faulty BRCA genes.

Initially analysing blood samples from nine healthy women with a mutated BRCA1 gene and eight healthy women with a mutated BRCA2 gene, they developed a 'signature' of the cells' response to radiation, made up of a number of genes that were switched on or off in response to radiation.

They then confirmed this signature's presence in radiation-treated blood samples from an independent group of 40 women who were carriers of mutated BRCA1 and/or BRCA2, but absent from 17 non-carrier women.

The test correctly identified 95 percent of BRCA carriers, and 88 percent of non-carriers.

According to Salmon, the test can show whether an individual carries a cancer-linked fault, regardless of the specific mutation they carry. In addition, it could be extremely useful across the developing world, where expensive gene-sequencing equipment may not be accessible.

However, Cancer Research UK’s Dr Julie Sharp urged caution.

"This is a very preliminary finding. The current test - DNA sequencing - is easy to standardise across different labs, whereas this new method would require substantial expertise and training to make sure its results were as consistent between labs.

"And we don't currently know whether there are indeed significant numbers of families out there who are unidentified carriers of BRCA mutations, who would not be picked up by existing methods."  

"That said, if further development goes as planned, this could be a useful technique to spot BRCA mutation carriers under certain circumstances."

The research is published in the journal Cancer Prevention Research

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Blood cell gene fault linked to breast and ovarian cancer

Monday 17 December 2012

Scientists have linked a rare genetic fault in the immune system to an increased risk of breast and ovarian cancers.

The research from a team at The Institute of Cancer Research suggests an entirely new way tumours develop.

The lead researcher on the study, Professor Nazneen Rahman, said it was one of her lab's "most interesting and exciting discoveries".

According to the study, published in the journal Nature, women with faults in a gene called PPM1D in their blood cells were 20 per cent more likely to develop breast or ovarian cancer.

That is twice the average breast cancer risk and more than 10 times the ovarian cancer risk of women in the general population.

The discovery could have implications for future genetic testing and targeted prevention, especially in the case of ovarian cancer.

Dr Emma Smith, Cancer Research UK's senior science information officer said: "This exciting discovery could help doctors identify women at higher risk of developing breast and ovarian cancer in the future.

"This may have a particular impact on ovarian cancer, which is often diagnosed at a late stage.

"Understanding the genetic mistakes that drive these cancers may also lead to new ways to treat these diseases."

The researchers speculate that they have uncovered a new cancer-causing process, since the PPM1D gene appears to operate differently to other genes known to increase the risk of breast and ovarian cancer, such as BRCA1 and BRCA2.

The team found that changes in PPM1D were not inherited and rather than being present in every cell - as in most inherited cancer-causing genes - they were only present in immune cells known as lymphocytes.

Even more surprisingly, the PPM1D gene was not altered in women's cancer cells, nor in their normal breast or ovarian cells, the study discovered.

The changes make the PPM1D gene overactive, reducing the action of a gene called TP53, one of the most frequently altered genes in cancer cells.

The ICR's Professor Nazneen Rahman, who led the study, said: "This is one of our most interesting and exciting discoveries. At every stage the results were different from the accepted theories.

"We don't yet know exactly how PPM1D mutations are linked to breast and ovarian cancer, but this finding is stimulating radical new thoughts about the way genes and cancer can be related."

Professor Rahman said the findings could also help inform women's decisions about future medical treatments.

A woman might, for example, consider keyhole surgery to remove her ovaries after completing her family if she knew she had PPM1D changes and had a one in five chance of developing ovarian cancer.

The study was funded by Cancer Research UK, the ICR, the Wellcome Trust and Breakthrough Breast Cancer.

Researchers analysed 507 genes involved in DNA repair in 1,150 women with breast or ovarian cancer, identifying PPM1D gene changes in five women.

They then sequenced the PPM1D gene in 7,781 women with breast or ovarian cancer and 5,861 people from the general population.

25 of the women with cancer had faults in PPM1D, compared with only one in the general population, a highly statistically significant difference, the researchers said.

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Inherited gene fault influences breast cancer survival

Tuesday 11 December 2012

Cancer Research UK Press Release

Researchers have shown that an inherited gene fault influences the chances of some women surviving breast cancer. It also increases the risk of women developing a second breast cancer. The research is published in this week’s Journal of Clinical Oncology1.

The scientists, funded by Cancer Research UK, found that women with the fault, and who had the oestrogen-receptor-positive form of breast cancer, were more likely to die from the disease - 62 out of 100 women who carry the fault will be alive ten years after being diagnosed compared with 73 of 100 who do not carry the fault.

The research also found that women with the fault were more likely to develop a second cancer. In the study, 24 per cent of women with the fault developed a second breast cancer compared to seven per cent without the fault2.

The gene fault, called CHEK2*1100delC, creates a faulty protein that interrupts a cell’s ability to repair damaged DNA, so increasing the number of DNA mistakes that can lead to cancer.

The fault is carried by about one per cent of all women and it is already known that women with it are more likely to develop breast cancer.

Dr Paul Pharoah, lead researcher based at the University of Cambridge, said: “This is the first time we’ve shown how CHEK2 faults influence the long-term prognosis of breast cancer. We need further studies to see if we can find other similar faults that affect how the disease develops so that one day we can test and predict how each individual woman’s breast cancer will behave.”

The researchers also predict that women with this genetic mistake are more susceptible to other forms of cancer, contributing to the increased risk of early death after a breast cancer diagnosis.

Dr Julie Sharp, senior science information manager at Cancer Research UK, said: “We’ve made huge progress improving the diagnosis and treatment of breast cancer - in the 1970s around five out of 10 women with breast cancer survived beyond five years but now it's more than eight out of 10. But, we still need better ways to predict how the cancer will behave to help doctors treat the disease more effectively.

“These results suggest that more widespread testing for the CHEK2 fault could help identify women with oestrogen-positive breast cancers who are at a greater risk of developing a second breast cancer. Further research needs to be done to see if these women would benefit from long-term treatment with anti-oestrogen drugs, such as tamoxifen, to try and reduce this risk.”

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Study confirms fewer, bigger doses of radiotherapy benefit breast cancer patients

Thursday 6 December 2012

Cancer Research UK Press Release

A lower total dose of radiotherapy, delivered in fewer, larger treatments, is as safe and effective at treating early breast cancer as the international standard dose, according to the 10-year follow-up results of a major Cancer Research UK trial presented at the 2012 CTRC-AACR San Antonio Breast Cancer Symposium today (Thursday).

Nearly 4,500 women across the UK have taken part in the START trials, which were co-ordinated by the Clinical Trials and Statistics Unit at The Institute of Cancer Research, London, and funded by Cancer Research UK, the Medical Research Council and the Department of Health.

The initial five-year results showed it was just as effective and safe to give women a lower total dose of radiotherapy in fewer, larger treatments than the 25-dose international standard. The new treatment routine also offered important benefits for women, including fewer trips to hospital, as well as cost savings for the health service.

As a result, the shorter treatment course of 15 treatments was adopted in the UK in 2008, but the longer course is still used in many other countries.

This latest 10-year follow-up, funded by Cancer Research UK, confirms these benefits and shows that very few women (around six per cent) experience a relapse of cancer within the same breast, regardless of whether or not they have a shorter course of radiotherapy after surgery.

Chief investigator Professor John Yarnold, professor of clinical oncology at The Institute of Cancer Research (ICR) and honorary consultant at The Royal Marsden NHS Foundation Trust, said: “We have shown conclusively that less can be more in breast cancer radiotherapy. Three weeks of radiotherapy is as good as five weeks – as well as being more convenient and less tiring for patients and cheaper for the health service.

“The risk of breast cancer recurring continues beyond five years, and side-effects of radiotherapy can often develop many years after treatment, so these long-term results provide a very important reassurance that the shorter treatment course is definitely the best option for patients. Some doctors may have been hesitant to change their practice on the basis of five-year results, but these long-term findings should convert those sceptics.”

The same team is now setting out to investigate whether even fewer doses of radiotherapy could be just as effective, as part of a new Phase III randomised controlled trial of 4,000 women called FAST-FORWARD. The trial will compare the new standard 15-dose course of radiotherapy treatment, delivered over three weeks, with an even shorter five-dose course, delivered over one week.

Jo Haviland, a senior statistician at the ICR, added: “The START trial has had a huge impact on changing the standard of care for women with breast cancer in the UK, and increasingly around the world. Recruitment is already underway for the new FAST-FORWARD trial we are co-ordinating, to see if we can further improve treatment and spare both women and the health system the burden of extra treatments.”

Kate Law, Cancer Research UK’s director of clinical research, said: “What’s really exciting is that, as a result of this trial, women are already benefiting from the added physical and emotional wellbeing of needing fewer hospital visits for their treatment. Minimising the long-term side effects of treatment is becoming increasingly important as cancer patients live longer. We hope that women around the world will now be able to benefit from this improved standard of care.”

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Trial reveals 10 years of tamoxifen halves later deaths from commonest kind of cancer

Wednesday 5 December 2012

Cancer Research UK Press Release

Ten years of tamoxifen treatment can approximately halve the number of deaths from  the most common form of breast cancer during the second decade after diagnosis,  according to the results of the Cancer Research UK- funded ATLAS trial published in the Lancet today (Wednesday).

Around three-quarters of women with breast cancer in the UK are diagnosed with oestrogen-receptor positive (ER+) disease, which is driven by the female hormone, oestrogen.  After any surgery, radiotherapy or chemotherapy, many women receive some years of endocrine treatment with a drug like tamoxifen or with an aromatase inhibitor, to prevent any remaining cancer cells being ‘re-fuelled’ by oestrogen.

Tamoxifen taken daily for five years – the current standard duration of treatment – is already known to reduce death rates by around a third throughout the first 15 years after diagnosis, as the protective effects continue for at least a decade after the five years of treatment has ended.

The new trial investigated whether continuing to take tamoxifen for a total of 10 years would reduce the breast cancer death rate still further.

The international ATLAS study, also co-funded by the Medical Research Council, recruited nearly 7,000 women with ER+ breast cancer who were completing five years of tamoxifen treatment. They were randomly allocated, half to stop treatment immediately and half to continue for five more years.  All were followed for an average of another eight years.

Initially there was little difference in outcome from the two groups, because throughout the first decade both groups were protected by the first five years of treatment. But, after year 10 the additional benefits of longer treatment emerged in the group that continued taking tamoxifen. Among them, the risk of dying during the second decade from breast cancer was further reduced by about a quarter – on top of the substantial benefits due to the first five years of treatment.

Most of the extra protection from taking the drug for longer occurred after the end of the 10-year treatment period.

Dr Christina Davies, a Cancer Research UK scientist at Oxford University and leader of the ATLAS study, said: “Around three-quarters of all UK women with breast cancer have hormone sensitive disease, and ATLAS shows that 10 years of tamoxifen helps save lives not just during the decade women are taking the drug, but also during the second decade after diagnosis.”

In post-menopausal women tamoxifen increases the risk of endometrial – or womb – cancer. The ATLAS results showed that the extra risk of dying from this disease was two per thousand women who took tamoxifen for five years, and four per thousand women who took tamoxifen for 10 years. The reduction in the numbers of deaths from breast cancer after 10 years of tamoxifen was about 30 times as great as this increase in the numbers of endometrial cancer deaths.

Cancer Research UK is a major funder of breast cancer research in the UK. Our research has contributed to developing treatments that mean that eight out of 10 women now survive their breast cancer for more than five years, compared with five out of 10 women in the 1970s. And 64 per cent of women now survive their breast cancer for at least 20 years.

Martin Ledwick, Cancer Research UK’s head information nurse, said: “This important study adds further clarity to the question about the length of time women should take tamoxifen.  Although treatment for hormone receptor positive breast cancer has become more complex in recent years with some women receiving aromatese inhibitors, these results will help in deciding the length of treatment for women who are prescribed tamoxifen alone.”

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Smokers leave a history of their addiction in DNA

Tuesday 6 November 2012

Cancer Research UK Press Release

Smokers are leaving a history of addiction in their DNA that may help to measure their risk of cancer, according to research presented at the NCRI Cancer Conference today.

Researchers at Imperial College London and the Human Genetics Foundation (HuGeF) in Italy have identified a number of sites in the DNA of blood that have been chemically tagged as a result of smoking. These tags are also detectable in lung tissue and could be used to measure the increased risk of certain cancers such as breast and bowel, as well as lung.

Smoking leaves a footprint on the surface of the DNA but the sequence of genetic code remains the same. This is known as an “epigenetic” modification. Once you give up smoking, these tags start to disappear although they never quite match the unmarked DNA of a non-smoker.

In this initial study, measuring DNA tagging in blood samples from smokers and non-smokers allowed the researchers to investigate the link between smoking and these tags. The study also looked at the risk of developing breast and bowel cancer in relation to these DNA tags, with plans to expand the work into other areas such as lung cancer*.

While smoking is associated with bowel cancer risk, a link between smoking and breast cancer has not been proven but the researchers believe that previous studies haven’t had the same genetic or epigenetic measures of smoke exposure available. This research will make that information available to scientists so they can spot any DNA tags that might be attributable to any risk that might exist.

Dr James Flanagan, Breast Cancer Campaign scientific fellow at Imperial College London and co-author of the research, said: “This research may help to build a test that will be able to look at a person’s epigenetic information at the molecular level and measure in great detail the added risk of cancer from exposures such as smoking.

“Previous research into smoking has often asked people to fill out questionnaires, which have their obvious drawbacks and inaccuracies. Using this approach, we will be able to read the fingerprint on a person’s DNA to tell us a story of how their habit may have changed over the course of their life.”

Professor Paolo Vineis, chair in environmental epidemiology at Imperial College London’s School of Public Health and head of the HuGeF laboratory in Italy, said: “This research will help us to build a molecular profile of cancer risk, where we can screen people and quantify the exposure they’ve had to a number of risk factors over their lifetime, just by examining a blood sample.

“We hope that smoking is just the start – further work will look into other factors like alcohol and start to measure the risk an individual has built up over a lifetime of exposure to these contributors to cancer.”

Dr Jane Cope, director of the NCRI, said: “This is a very interesting piece of research that applies basic biology to everyday life to reveal just how much damage smoking can do to the fundamental biology of a person. If these early results hold true in more detailed studies, this finding could play an important role in understanding smokers’ cancer risk in the future.”

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Three-in-one 'supermolecule' could detect cancer early, help destroy tumours and monitor treatment

Tuesday 6 November 2012

Cancer Research UK Press Release

The same protein could potentially be targeted to detect precancerous breast cells; deliver radiotherapy to destroy tumours; and monitor the effectiveness of treatment, according to a Cancer Research UK study presented at the NCRI Cancer Conference in Liverpool today (Tuesday).
 
Oxford University scientists at the Cancer Research UK/MRC Gray Institute for Radiation Oncology and Biology showed in the laboratory that a technique monitoring high levels of a protein called Gamma H2AX, found in many pre-cancerous cell types including breast, lung and skin cancer, could be used to detect cancer early.

The team took microscopic images of fluorescent ‘flag’ molecules attached to an antibody which ‘homes in’ on and attaches to Gamma H2AX, to identify areas of DNA damage*. The fluorescent ‘snap shots’ of Gamma H2AX revealed the location of pre-cancerous breast cancer cells at a very early stage.

Professor Katherine Vallis, who led the study at the Cancer Research UK/MRC Gray Institute for Radiation Oncology and Biology at Oxford University, said: “This early research reveals that tracking this important molecule could allow us to detect DNA damage throughout the body. If larger studies confirm this, the protein could provide a new route to detect cancer at its very earliest stage – when it is easier to treat successfully.”

Previously the team modified an antibody to target Gamma H2AX and deliver radiotherapy to breast cancer cells which contained high levels of the protein. This form of radiotherapy works by boosting DNA damage until cells can no longer repair mistakes – and die.

The results confirmed that the radioactive antibody killed breast cancer cells and slowed tumour growth.

Prof Vallis added: “We need to confirm these findings in larger studies before we know if this approach could benefit patients. But these initial results show that it may be possible to track down cells with high levels of DNA damage, and destroy them before they became cancerous.

“One day we may be able to scan the body to map out the radioactive antibodies that have attached to the Gamma H2AX molecule. This could also allow doctors to paint a useful picture of how effective a treatment is.”

Dr Julie Sharp, Cancer Research UK’s senior science information manager, said: “This important study reveals that targeting this  key molecule could provide an exciting route for new ways to detect cancer at an earlier stage – and help to deliver radiotherapy and monitor its effect on tumours.

“Thousands of cancer patients in the UK, and millions worldwide, benefit from radiotherapy every year. Cancer Research UK has invested heavily in research such as this to explore new ways to improve this vital treatment.”

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Experimental combination therapy trial for breast cancer patients no longer responding to treatment

Friday 2 November 2012

Cancer Research UK Press Release

Cancer Research UK’s Drug Development Office (DDO) has joined forces with academia and industry to trial an experimental drug from AstraZeneca called AZD4547 in combination with existing therapies, to treat post-menopausal women whose breast cancer has spread and is no longer responding to standard treatment.

The Phase IIa clinical trial will be run through the Cancer Research UK and NIHR Experimental Cancer Medicine Centre (ECMC) in conjunction with the Imperial Clinical Trials Unit Section on cancer (ICTU-Ca), Imperial College London. It will recruit post-menopausal women with oestrogen positive breast cancer* who are no longer responding to either anastrozole or letrozole – standard treatments for this patient group.

The trial will be divided into two groups. In one group, patients will receive AstraZeneca’s experimental treatment AZD4547 alongside either anastrozole or letrozole. In the second group, patients will be treated with exemestane alone. The trial will evaluate whether the combination of this experimental drug with an existing therapy that has begun to fail may halt the progression of the disease, and make the tumour respond again to the original therapy.

AstraZeneca is the first pharmaceutical industry partner to join the ECMC Combinations Alliance, which launched in 2011. The alliance aims to increase patient access to trials of potential new cancer treatments by combining molecularly-targeted experimental drugs developed and owned by the company – with standard chemotherapy, radiotherapy and other new drugs.

This study is the third launched by the Alliance, and AstraZeneca is providing both supply of AZD4547 and additional funding, with Cancer Research UK’s DDO also providing support.  Imperial College London is sponsoring the trial.

Chief investigator, Professor Michael Seckl, at Imperial College London, said: “The opening of this trial is great news. It’s an incredibly tough part of my job telling breast cancer patients that they are no longer responding to the drugs they are taking. We hope that this trial will be a step forward in finding new and better ways to treat advanced breast cancer, to increase survival from this disease.

“More women are surviving breast cancer than ever before. But while we’re making great progress in developing new targeted treatments there’s still an urgent need for medicine that will treat the disease once it has spread.”

Andrew Foxley, clinical programme director for AZD4547 at AstraZeneca, said: “AstraZeneca has a long-standing commitment to cancer research and has developed medicines that are making a meaningful difference for people with breast cancer. We believe that collaboration is crucial to finding solutions in the fight against cancer and are pleased to partner with others in the UK who share our dedication to bringing new medicines to patients.”

Dr Ian Walker, head of alliance management at Cancer Research UK’s DDO, said: “This is the third trial we’ve launched through collaboration with AstraZeneca – with others in the pipeline. This unique alliance is powering UK research to bring together combinations of new and existing drugs in early clinical trials to find better ways to treat patients and increase survival from a range of cancers.

“Without this important alliance these trials might not be possible. We want to build on the foundations established with AstraZeneca to add additional partners to collaborate with us in the future. Our aim is to set up cross-company agreements to provide access to a larger number of potential treatment combinations.”

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Cancer Research UK's response to the breast screening review

Tuesday 30 October 2012

Cancer Research UK Press Release

Dr Harpal Kumar, chief executive of Cancer Research UK, said: “The independent review shows screening saves lives.

“Screening remains one of the best ways to spot the very early signs of breast cancer, at a stage when treatment is most likely to be successful.

“Yet, as the review shows, some cancers will be diagnosed and treated that would never have caused any harm. Clearly, everyone wants to minimise this.

“But because we can’t yet tell which cancers are harmful and which are not, we cannot predict what will happen in an individual woman’s case.
 

“We think it’s vitally important for women to have access to clear information about breast screening, the balance of benefits and harms and the fact that they could be diagnosed with and treated for a cancer that might not cause them harm.

“So, on balance, taking all the evidence into account, Cancer Research UK recommends that women go for breast screening when invited.
“Research is advancing at pace and we hope that in the future there will be a number of new techniques that we can use alongside the screening programme to make it more sophisticated and reduce the numbers of women having unnecessary treatment.

“Until this is possible, we’d recommend women who have had something unusual picked up through screening to seek full advice and discuss all possible options with their breast cancer specialist team.

“We urge the screening programme to update the breast screening information leaflet in the light of the findings of the independent review.”

More information:

• A press release from the Independent Breast Screening Review panel (PDF) 
• More information about the Independent Breast Screening Review and its findings
• A Q&A for women considering breast screening
• A detailed infographic summarising the findings
• Blog post: How can we improve breast screening?

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Scientists discover potential new ‘roots’ of breast cancer

Friday 26 October 2012

Cancer Research UK Press Release

Scientists have discovered new types of early cells in mammary glands, uncovering clues to the origins of different breast cancers - and potential new drug targets, according to findings published in Breast Cancer Research.

The team at Cancer Research UK’s Cambridge Research Institute identified at least two types of early cells, called progenitor cells. Unlike stem cells, which can develop into any type of cell and keep on dividing, progenitor cells can only divide a limited number of times. Previously scientists only knew of one type of progenitor cells in mammary glands.

Cancer is thought to begin in cells that can produce many daughter cells, which form the tumour mass. So different progenitor cells may explain why there are different types of breast cancer.

The team discovered that one group of progenitor cells, called oestrogen positive progenitors, had oestrogen receptors. This protein receives signals from the sex hormone, oestrogen. The other group - oestrogen negative cells - lacked this receptor.

Oestrogen positive progenitor cells survive better in a low oestrogen and progesterone environment - similar to the breast tissue of post-menopausal women. This suggests that tumours in post-menopausal women may develop from these cells, but further experiments are needed to confirm this.

The oestrogen negative progenitor cells have a genetic fingerprint resembling an aggressive type of breast cancer called basal-like breast cancer, more likely to affect younger women. This suggests the disease may develop from the oestrogen negative progenitors.

Study author, Dr John Stingl, at Cancer Research UK’s Cambridge Research Institute, said: “This exciting discovery reveals that mammary glands are much more complicated than scientists initially thought. Uncovering new types of ‘mother’ cells may explain why there are different types of breast cancer, and why young and older women tend to get different types. It could also provide new starting points for ways to diagnose and treat the disease in the future.”

Dr Julie Sharp, Cancer Research UK’s senior science information manager, said: “This research takes us right to the root of how breast cells develop. This fresh understanding could reveal new ways to block the development of cancer and tell us more about what happens when tumours become resistant to treatment.

“Cancer Research UK is a major funder of breast cancer research in the UK. Our research has contributed to progress that means eight out of 10 women now survive breast cancer for more than five years, compared with five out of 10 women in the 1970s. But there’s much more to do. Research like this will build on our understanding of breast cancer to bring forward the day when we can beat this disease.”
 

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Combining imaging and gene analysis could transform breast cancer diagnosis

Wednesday 24 October 2012

Cancer Research UK Press Release

COMBINING two approaches - one that digitally scans images of tumour samples and another that analyses genetic information - gives a more accurate prediction of how breast cancer will behave. The research is published today in Science Translational Medicine1.

Researchers at the Cancer Research UK Cambridge Research Institute have built a computer system that automatically analyses microscopy images of hundreds of breast cancer samples. The new approach looks at the makeup of the cells within a tumour, normally undertaken by a pathologist looking down a microscope, and combines these images with the key genetic changes that are crucial for the development of breast cancer.

Compared to carrying out these tests individually, the new system was more accurate and could give researchers more detailed information about a woman’s breast cancer.

Survival from a type of breast cancer called oestrogen receptor negative can be predicted by the number of white blood immune cells that have entered the tumour. The new test increased the accuracy of predictions based on this from 67 to 86 per cent.

The researchers also found a new way to predict survival based on the arrangement of supporting cells within the cancer. Known as the stroma, these cells play a role in encouraging the growth of breast cancers and are not detected in current tests.

Dr Florian Markowetz, the lead researcher at Cancer Research UK’s Cambridge Research Institute, said: “Cancers are a mix of different cells – not just cancer cells – they also include those from the immune system and others that support the structure of the tumour. These cells play an important role in how cancers behave, but this information is not currently detected in tests that focus on the genetic makeup of the cancer.

“By bridging the gap between the ‘two cultures’ of pathology and genomics our research has a huge potential for better understanding breast cancer.”

Professor Carlos Caldas, also based at Cancer Research UK’s Cambridge Research Institute, said: “This research complements our study earlier this year that found breast cancer was in fact at least ten different diseases. This now takes us a step closer to being able to use this knowledge in the clinic and directly benefit women with breast cancer.”

Dr Julie Sharp, senior science information manager at Cancer Research UK, said: “Combining the visual information from a breast tumour with knowledge of its genetic makeup using computer systems could have a profound impact on how cancer clinics of the future work, enabling doctors to offer women treatments that are tailored to their individual breast cancer.”

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Breast cancer cells spread by digging their escape route

Monday 22 October 2012

Cancer Research UK Press Release

Breast cancer cells puncture  holes into neighbouring tissues and crawl though the spaces they create to spread around the body, according to research published in the Journal of Cell Biology.

Scientists at Cancer Research UK’s Beatson Institute in Glasgow discovered that there are high levels of a protein called N-WASP in breast cancer cells.

The protein helps form branches with sharp points on the cell surface by rearranging the cell’s internal ‘skeleton’, made of a protein called actin. Actin is essential in all cells for structural support, movement and shape changes.

The branches with sharp points – called pseudopodia – can grab onto and poke holes into the extracellular matrix, the supporting tissue in-between cells. And the team showed that enzymes attach to the protrusions and dig into the extracellular matrix, creating larger spaces.
 
Cancer cells invade their surrounding environment by a combination of pushing and pulling into the newly created spaces – movement which is captured for the first time in 3D on video.

The scientists showed that removing N-WASP from cells resulted in much blunter protrusions, to which fewer enzymes became attached. This reduced the ability of the cells to puncture their surrounding extracellular matrix and spread.

Lead author, Dr Laura Machesky, at Cancer Research UK’s Beatson Institute in Glasgow, said: “Our exciting results reveal a completely new process by which cells can break away from a tumour to invade surrounding spaces and spread around the body. We found that cells assemble specialised structures, with the ability to hold onto the surrounding tissue matrix and dig tunnels into it, which they can then crawl through.

“Our research suggests that N-WASP is a promising target for the development of drugs to combat cancer spread.  We were particularly intrigued because blocking N-WASP activity didn’t affect healthy cells, so we think that N-WASP could be specifically targeted to prevent cancer spread.”

Dr Julie Sharp, Cancer Research UK’s senior science information manager, said: “This important research reveals fresh understanding of how cancer spreads, which will help scientists to translate discoveries into effective treatments to beat cancer.

“Most cancer deaths are caused when cancer cells travel to new sites within the body and grow as secondary tumours so there’s an urgent need to find a way to stop this happening.
“We’re funding groundbreaking lab research into how cancer cells move around the body as well as important clinical trials which aim to combat the advanced disease. Finding the best ways to tackle cancer spread will save thousands more lives every year.”

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Starting periods younger and finishing earlier signals a greater risk of specific types of breast cancer

Wednesday 17 October 2012

Cancer Research UK Press Release

The younger a women starts her periods, and the later she finishes, the more at risk she is from developing breast cancer but new research* published in the Lancet Oncology today (Wednesday) shows that these risk factors are particularly relevant for specific types of breast cancer.

Researchers from the University of Oxford found that increases in the risk of breast cancer associated with both earlier periods and later menopause were greater for lobular than for ductal cancers, and that that the increased risk associated with a later menopause was also more marked for oestrogen-sensitive (ER-positive) cancers .  

In the most comprehensive study of its kind, funded by Cancer Research UK, the researchers reanalysed original data from 117 studies worldwide, including 118, 964 women with breast cancer and over 300, 000 women without the disease.  

They also discovered that starting periods earlier had a greater impact on breast cancer risk than did finishing periods later – suggesting that the effects of these factors may not simply reflect the number of reproductive cycles in a woman’s lifetime.

Dr Gillian Reeves, from The University of Oxford, said: “Our new research should helps us towards a better understanding of the way in which female sex hormones affect breast cancer risk.”

“We already knew that hormones associated with reproduction have a big impact on breast cancer risk and that starting periods early and having a late menopause increase risk but these findings suggest that sex hormone levels may be more relevant for specific types of breast cancer – ER positive tumours, and lobular, rather than ductal tumours.”

The average age in the UK for women to start their period is around 12 years old and most women start the menopause between the ages of 45 and 54.

Dr Julie Sharp, senior science information manager at Cancer Research UK, said: “This study adds some key details to our understanding of how breast cancer develops and the role that hormones play.

“The ovaries begin producing steroid hormones around the time a women starts her periods and stop rapidly around the time she begins the menopause. It’s very interesting to see that these hormones play a bigger part in the development of certain types of breast cancer and this will be important for future work in this area.”

Hazel Nunn, head of health information at Cancer Research UK, said: “Even though women can’t control the age they start their period there’s many things they can do to reduce their breast cancer risk. Keeping a healthy weight, cutting back on alcohol and having a more active lifestyle will all help to prevent the disease developing.”

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First trial of whole-genome scans to select breast cancer treatment

Wednesday 3 October 2012

The first clinical trial in which the entire DNA 'genome' of breast cancer patients' tumours was scanned to help select the best treatment has been carried out in France.

The study shows that it could soon be possible to replace commonly used single-gene tests with more comprehensive whole-genome scans. The researchers say that such scans could be more likely to pick up both common and more unusual genetic faults that could be targeted by treatments.

Several drugs have been developed to target specific genetic alterations that cause cancer. For some tumours such as breast cancer, doctors already use genetic tests to work out which treatment a patient will respond to best. But in most cases only a limited number of genes are examined.

A study at the Institute Gustave Roussy in Villejuif, scanned the entire genome of breast cancer patients to find genetic faults that could be targeted by existing treatments.

In the trial, doctors took biopsies from secondary tumours in patients - those that had spread from the breast to other parts of the body.

They then analysed the genetic code of the tumour samples using a technique called array CGH, which scans the genome for gains, losses or changes in the genetic material, and gives information about genes likely to be driving the disease.

They used this information to choose treatments for the patients that were targeted at the specific cancers they had.

Biopsies were taken from 402 patients. Of these, the researchers were able to map the full genome in 248 samples. The process resulted in 172 patients being given drugs that were designed to target a specific genetic change.

The research showed that 20 per cent of the patients were found to have extremely uncommon genetic changes. The tumours shrank in 18 out of 48 patients whose treatment was selected based on the results of a genome scan.

Dr Fabrice Andre who led the research, said: "This study suggests that the time has come to bring personalised medicine to the cancer field."

Kate Law, Cancer Research UK's director of clinical research, said: "Routine whole-genome sequencing of tumours is on the horizon for cancer patients, but we're not there yet."

She said that the research shows that whole-genome tumour testing can be used to help select the most appropriate treatment for breast cancer patients, but that there are several hurdles to overcome before such tests become routine.

"The fact that genetic results weren't generated for all patients highlights the need to improve technical aspects of the tests. And before such genome tests are available in the clinic, we absolutely need further good-quality clinical trials to show they help to improve treatment for cancer patients," she added.

She also said that Cancer Research UK's Stratified Medicine Programme is working towards "standardised, high quality, cost-effective and timely genetic testing of tumours within the NHS".

The work was presented at the ESMO 2012 Congress of the European Society for Medical Oncology in Vienna.

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A simple blood test could be used to detect breast cancer

Tuesday 2 October 2012

Cancer Research UK Press Release

A simple blood test could one day be a more accurate way to test for the early signs of breast cancer than using mammograms to spot a lump say researchers today (Tuesday), as Breast Cancer Awareness Month gets underway.

They also hope the blood test could improve treatment by detecting whether breast cancer patients are likely to relapse and what drugs their particular type of tumour will respond to.

This pioneering new clinical study – funded by Cancer Research UK in collaboration with the University of Leicester and Imperial College London – is about to start in the UK’s largest breast screening clinic at Charing Cross Hospital, London.

Researchers will take blood samples from women attending the breast screening clinic and compare the DNA in the blood of women who are diagnosed with breast cancer with those that do not have cancer to see what DNA markers are consistent.

Dr Jacqui Shaw, principal investigator from the University of Leicester, said: “This exciting research means we could one day have a blood test that detects the very early signs of cancer meaning women could have an annual blood test rather than breast screening. This would remove any worry and anxiety for women who are called for further investigations after a mammogram only to find they don’t have cancer.

"As things stand we aren't able to monitor breast cancer patients after they’ve had surgery and treatment - which is like treating diabetes but not measuring blood sugar levels. The new blood test could change that."

Professor Charles Coombes, co-investigator and Cancer Research UK’s breast cancer expert from Imperial College, said: “This type of translational science is extremely promising and the international scientific community is collaborating on its development. When a woman has breast cancer we can tell by the DNA in their blood. But what we’re trying to find out in our study is how early the signs of breast cancer show up in a blood test. So by looking at blood samples of women who have breast cancer diagnosed through screening we can see if the cancer is already showing in their blood.

“Our research team is only looking at breast cancer, but there are a number of other projects that are looking at using a blood test to detect other cancers such as bowel and lung.”

Kate Law, director of clinical research at Cancer Research UK, said: “We really do hope that in the not too distant future a simple blood test for breast cancer, which could not only detect cancer but help with treatment options, will become standard practice on the NHS.

“Cancer Research UK has invested over a million pounds into this project as this fascinating area of science could prove to be a huge step forward in the way certain types of cancer are diagnosed and treated.”

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Gene variant linked to male breast cancer

Monday 24 September 2012

An inherited gene variant that increases a man's chance of developing breast cancer by up to 50 per cent has been identified by an international team of scientists.

The finding suggests that the causes of the disease may differ between women and men.

The result comes as part of the worlds largest ever study of male breast cancer, in which researchers analysed the genetic code of 823 male breast cancer patients for genetic variants called 'single nucleotide polymorphisms' (SNPs). They wanted to find SNPs that are more common in men with the disease.

While male breast cancer has a much lower public profile than its female counterpart, around 350 men are diagnosed with the disease in the UK each year

Scientists have previously shown that mutations in the BRCA2 gene are involved in around one in 10 male breast cancers. But one of the strongest risk factors for the disease is having a male family member with the disease. So researchers have long suspected that other inherited genetic factors may be involved.

The researchers found that a specific variation in the RAD51B gene could be even more significant than BRCA2, increasing a man's chances of developing breast cancer by up to half.

RAD51B, like BRCA2, helps repair damaged DNA inside cells. Changes RAD51B have been previously linked to women's risk of breast cancer, but the new variant is in a different part of the gene to the 'female' version.

Dr Nick Orr, from the Breakthrough Breast Cancer Research Centre at The Institute of Cancer Research in London, who led the research, said it was a "leap forward" in the understanding of male breast cancer.

"[This] shows that while there are similarities with female breast cancer, the causes of the disease can work differently in men. This raises the possibility of different ways to treat the disease specifically for men," he added.

Henry Scowcroft, science information manager at Cancer Research UK, said: "It's starting to emerge that the genetic triggers of breast cancer vary between men and women. For example, men who inherit a damaged BRCA2 breast cancer gene have a higher risk of developing breast cancer than women with similar faulty genes, and those with a male family member who had breast cancer are also at much higher risk. This suggests there are probably differences between the sexes in how the disease develops, and how best to treat it.

"Researchers have been hunting for genes involved in male breast cancer and this new study identifies several regions in our genetic material that can influence a man's risk. This research should spur further efforts to understand how breast cancer arises in men, and ultimately more effective treatments for them."

The study is published in the journal Nature Genetics.

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Study gives better picture of genetic causes of breast cancer

Sunday 23 September 2012

Research from the US has given scientists a better understanding of the genetic and molecular defects inside breast cancer cells.

International researchers working as part of the Cancer Genome Atlas (TCGA) project have completed the genetic mapping of 800 breast tumours, giving researchers a clearer view into the defects behind each sub-type of breast cancer, as well as providing pointers towards new treatments.

The study, published in Nature, also identified a molecular similarity between one sub-type of breast cancer - known as 'Basal-like' - and a hard-to-treat form of ovarian cancer.

The researchers looked at the 800 tumours in vast detail, examining their genetic defects, and other aspects of their biology, such as the degree to which different genes and pathways were switched on, and whether their DNA was chemically modified ('epigenetics').

They compared these analyses to four previously known sub-types of breast cancer: HER2-enriched, Luminal A, Luminal B and Basal-like.

"This comprehensive new analysis of 800 breast tumours is a welcome addition to the wealth of new information about the underlying biology of breast cancer, and will be a precious and valuable resource for cancer researchers," said Professor Carlos Caldas, a breast cancer expert for Cancer Research UK, who was not involved in the study.

"This will allow us to further refine understanding of the disease, with the ultimate aim of improving things for those who matter most - people diagnosed with breast cancer."

Professor Caldas added that the study corroborated the findings of the Cancer Research UK-funded METABRIC study, which revealed breast cancer to be ten separate diseases.

Dr Charles Perou, from the University of North Carolina, and one of the paper's authors, said the study represented "a near complete framework for the genetic causes of breast cancer, which will significantly impact clinical medicine in the coming years."

The mapping project gave scientists a better picture of the genetic causes behind the most common form of breast cancer, known as Estrogen-Receptor positive/Luminal A disease.

The researchers found that this sub-type had the widest range of genetic alterations, some of which could be targeted by drugs currently in clinical development.

The striking similarity between basal-like breast tumours, which are often hard-to-treat 'triple-negative' breast cancers, and ovarian tumours suggests a common origin and the future possibility of treatments that would be effective for both diseases, the researchers said.

"The molecular similarity of one of the principal subtypes of breast cancer to that found in ovarian cancer gives us additional leverage to compare treatments and outcomes across these two cancers," said Professor Harold Varmus, director of the US's National Cancer Institute, which funded the study.

"This treasure trove of genetic information will need to be examined in great detail to identify how we can use it functionally and clinically."

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Post-menopausal women with diabetes at greater risk of breast cancer

Friday 14 September 2012

Cancer Research UK Press Release

Women with type II diabetes are nearly 30 per cent more likely to get breast cancer, according to results of a comprehensive review published in the British Journal of Cancer today (Friday).

The study, by researchers at the International Prevention Research Institute (i-PRI), Lyon, analysed the results of 40 separate studies examining the potential link between breast cancer and diabetes.

These studies involved over 56,000 cases of breast cancer across four continents and found that post-menopausal women with type II diabetes had a 27 per cent increased risk of breast cancer.

The increase in breast cancer risk seems to be restricted to post menopausal women with type II diabetes, as the research found no link between women of pre-menopausal age or those with type I diabetes.

The authors have also suggested that a high Body Mass Index (BMI), which is often associated with diabetes, may be an underlying contributing factor.

Professor Peter Boyle, President of i-PRI and lead author of the study, said: “Our study found a significantly increased risk of breast cancer in women who had diabetes, which was restricted to those of post-menopausal age.

“We don’t yet know the mechanisms behind why type II diabetes might increase the risk of breast cancer. On the one hand, it’s thought that being overweight, often associated with type II diabetes, and the effect this has on hormone activity may be partly responsible for the processes that lead to cancer growth. But it’s also impossible to rule out that some factors related to diabetes may be involved in the process.”

Being obese increases the risk of postmenopausal breast cancer by up to 30 per cent and more than 4,000 cases of breast cancer each year in the UK are linked to excess bodyweight.

Martin Ledwick, head information nurse at Cancer Research UK, said: “From this study, it’s not clear whether there’s a causal link between diabetes and the risk of breast cancer in post menopausal women.

“But as we know that having a high BMI can contribute to an increased risk of both type II diabetes and breast cancer, it makes sense for women to try and maintain a healthy weight.

“Anyone who is concerned should consult their GP for advice and consider changes to their lifestyle, such as increasing their level of physical activity and changes to their diet, to keep the risks as low as possible.”

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Study highlights potential drug target for one in ten breast cancers

Tuesday 11 September 2012

Cancer Research UK Press Release

CANCER RESEARCH UK scientists have discovered how a key protein fuels breast cancer growth by boosting numbers of cancer stem cells in tumours that have low levels of a protein called claudin, accounting for up to 10 per cent of all breast cancers.

This raises the prospect that treatments currently being developed to inhibit this key protein – called Transforming Growth Factor Beta (TGF-beta) – could be used to treat this group of women, who tend to have poorer survival and for whom there are currently no targeted treatments.

The study is published in Nature Communications today (Tuesday).*

Earlier this year the same team, from Cancer Research UK’s Cambridge Research Institute, published a groundbreaking study showing that breast cancer was not one disease, but ten, each defined by its own unique ‘genetic fingerprint’.

In this study they used this knowledge to explore, for the first time, how the network of genes activated by TGF-beta differs among different types of breast cancer.

This revealed that, in cancers with low levels of the protein claudin, TGF-beta activates a specific network of genes that boosts the number of breast cancer stem cells – which promote cancer spread and are associated with poor survival.

TGF-beta does this through the regulation of two other proteins – Smad and SRF – and with the help of a third – NEDD9 – which helps to assemble the three into their active form.

Dr Alejandra Bruna, senior author on the study, said: “For years scientists have been puzzling how TGF-beta can be seen to both fuel and suppress the growth of cancer. And now, thanks to the improved understanding we are building of the different genetic types of breast cancer, we can pinpoint one of the specific pathways that account for these differences.”

Study leader Professor Carlos Caldas, added: “Crucially this study highlights the role of TGF-beta in one particular subtype that accounts for up to 10 per cent of all breast cancers. A number of promising treatments are already in early phase trials to target TGF-beta, meaning there is genuine hope of improved treatment options for this group of women in the near future. The next step will be to design the appropriate clinical trials.”

Dr Julie Sharp, senior science information manager at Cancer Research UK, said: “This study provides us with important insights into TGF-beta’s ‘split personality’ and how it can both prevent and fuel the growth of cancer cells. Our scientists have been at the forefront of research into the role of growth factors in cancer and it’s immensely heartening to see this now paving the way for powerful new treatments with the potential to benefit patients.”

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Exposure to X-rays raises risk of breast cancer in young women with BRCA faults

Thursday 6 September 2012

Cancer Research UK Press Release

Women with faults in BRCA genes are more likely to develop breast cancer if they are exposed to chest X-rays before they are 30, according to a study published in the BMJ online today (Friday)1.

The international study2, part-funded by Cancer Research UK,  looked at almost 2,000 women with BRCA faults in the Netherlands, France and the UK between 2006 and 2009 to see if variations in their DNA increased the risk of breast cancer after exposure to low doses of radiation.

It found that women under 30 with BRCA faults who were exposed to chest X-rays and other radiation procedures3 were 43 per cent more likely to develop breast cancer, compared with women with the same faults who were not exposed. But, this increased risk did not apply to procedures carried out in women over 30.

Around two per cent of breast cancers are caused by BRCA faults, and women with these faults have a 45 to 65 per cent chance of developing the disease.

In the UK, women with BRCA faults are only screened for breast cancer after they are 30, and with a procedure called MRI that does not expose them to radiation.

Study author, Professor Douglas Easton, a Cancer Research UK scientist at the University of Cambridge, said: “BRCA genes help repair DNA damage – damage which can be caused by exposure to radiation like X-rays. Women with faults in these genes are less able to repair damage caused by radiation, so they are at a greater risk of developing breast cancer. It’s important that these women and their doctors are aware of this.”

The study was led by the University of Cambridge in the UK, in association with The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust, St Mary’s Hospital and Addenbrookes Hospital.

Dr Julie Sharp, senior science information manager at Cancer Research UK, said: “This research highlights that young women with a faulty BRCA gene are potentially more sensitive to low doses of radiation and doctors need to be aware of these risks when considering procedures using X-rays. In the UK younger women are already screened using MRI scans rather than mammograms to avoid these risks – but this isn’t the case in all countries yet.”  

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Study uncovers simple way of predicting severe pain following breast cancer surgery

Wednesday 5 September 2012

Cancer Research UK Press Release

WOMEN having surgery for breast cancer are up to three times more likely to have severe pain in the first week after surgery if they suffer from other painful conditions, such as arthritis, low back pain and migraine, according to a Cancer Research UK study published today (Wednesday) in the British Journal of Cancer.

Of the women surveyed, 41 per cent reported moderate to severe pain at rest, and 50 per cent on movement, one week after their surgery. Most patients having breast cancer surgery are discharged home by this time.  

Psychological state was also important, with women who felt more optimistic before their surgery found to suffer lower intensity pain in the week afterwards. While those who had more extensive surgery to remove their lymph nodes were prone to more severe pain in the week after surgery.

The findings could be used as a simple way of identifying before surgery which breast cancer patients might benefit from extra pain relief or support, according to the researchers, based at the Universities of Warwick, Aberdeen and Dundee.

Study leader Dr Julie Bruce, from the University of Warwick, said: “Women generally receive the same advice and treatment for pain relief following breast cancer surgery, but this study shows how factors such as a patient’s psychological state and whether they have a prior history of chronic pain can really affect their recovery.

“Importantly, doctors may be able to use this as a way of identifying women who need more intensive pain relief immediately after surgery. These results are particularly important because research shows that severe pain in the first week after surgery can significantly delay recovery.”

Three hundred and thirty-eight patients from across North Scotland took part in the study. Each patient was asked to fill out detailed questionnaires before surgery, asking about their general health, how they were feeling and whether they had any existing pain. A week after surgery, patients were contacted by a member of the research team and asked specific questions about the amount and type of any pain they were experiencing and whether they had taken pain killers.

Catherine Harkin, a GP from Edinburgh, was diagnosed with breast cancer six years ago, aged 49. Her cancer was discovered by chance after she had a mammogram to investigate a large benign cyst in her left breast, revealing a small 1cm tumour in the opposite breast. After several attempts at removing the tumour surgically, she opted to have a mastectomy with full breast reconstruction.

She remembers what it was like afterwards: “I’d been very against having a mastectomy, but in some ways it was a relief because it meant an end to the rollercoaster of having lumps removed and then waiting for the results. In total I spent five days in hospital, after which I was given anti-inflammatory drugs and sent home. The drugs really helped with the pain, but it was a long time before I felt myself again and that’s something that no one can really prepare you for.”

“For me the worst part was not feeling in control of my pain, so it’s really interesting to hear about research into ways of finding out in advance which women are likely to need extra help to recover from their surgery. I think this could really improve people’s quality of life in the long term.

“I still suffer some after-effects from my surgery, but one of the real turning points for me was earlier this year, when I decided to join a local Dragon Boat paddling team set up especially for breast cancer survivors and their friends and family. It’s great exercise and really helped me get my body confidence back and realise that, while I may not be as strong as I was, there are still lots of activities I can get involved in.”

Liz Woolf, head of Cancer Research UK’s information website, CancerHelp UK, said: “As well as being extremely important for a patient’s comfort, post operative pain levels can have a significant impact on their treatment – for example it can increase risk of complications because they are unable to move as much as they should.  It may also lead to them missing appointments, or being unable to carry out important postoperative exercises which aid their recovery. This is why it’s so important to be able to identify in advance those who may be in need of extra pain relief or support.

“Earlier studies suggest that up to half of women who undergo surgery for breast cancer may continue to suffer from pain for up to a year afterwards. This study is ongoing and it will be helpful to see what impact things like having a history of chronic pain and psychological state may have on longer term pain after surgery.”

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NICE says 'no' to Avastin for advanced breast cancer

Wednesday 22 August 2012

The National Institute for Health and Clinical Excellence (NICE) has published new guidance on the use of bevacizumab, better known as Avastin, as a treatment for breast cancer that has spread.

It recommends that bevacizumab - when used in conjunction with chemotherapy drug capecitabine - should not be used as an initial treatment for breast cancer that has already spread, in people for whom other chemotherapy options are not considered appropriate.

They say this is because there is little evidence that the combination works better than existing, cheaper drugs.

The development of the final guidelines included a review of all available evidence as well as a public consultation.

It marks the sixth time NICE has assessed bevacizumab as a treatment for cancer, having previously looked at its use for advanced bowel cancer (in combination with oxaliplatin, cetuximab or other drugs), advanced breast cancer with taxane chemotherapy, lung cancer, and kidney cancer.

On each occasion it has not recommended that the drug be routinely used.

Peter Johnson, Cancer Research UK's chief clinician, pointed out that bevacizumab "is an expensive treatment", and there was little evidence that the benefits outweigh the risks of taking the drug for the majority of patients - a situation he described as "disappointing".

"Doctors can apply for their patients to receive the drug if they believe it will benefit them, through the cancer drugs fund in England, and through individual patient treatment requests in the rest of the UK," he added.

Sir Andrew Dillon, NICE's chief executive, said the organisation couldn't recommend a drug that hasn't been shown to work as well as, or better than, current treatments and costs much more.

"Evidence presented to the independent Appraisal Committee did not conclusively show that bevacizumab, in combination with capecitabine, could improve overall survival or improve a patient's quality of life more than current treatment. These uncertainties, combined with the high cost of bevacizumab, mean the drug simply isn't cost-effective."

He added that while he understood the news would be disappointing to people, especially those with breast cancer that has spread elsewhere in their body, NICE does recommend a range of treatments that the NHS can use to treat metastatic disease and these are outlined in its clinical guideline on the diagnosis and treatment of advanced breast cancer.

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One in five women who opt for breast-conserving surgery 'need second operation'

Friday 13 July 2012

One in five women with breast cancer who undergo breast conserving surgery rather than a mastectomy will need a second operation, according to a major UK study.

The results, published in BMJ, confirm the findings of previous, smaller studies. It is standard for women who opt for breast conserving surgery to be informed about the risks involved in removing only part of the breast.

Around 45,000 women are diagnosed with breast cancer each year in the UK. Of these, 58 per cent chose to have only part of their breast removed rather than a mastectomy, which sees the whole breast removed.

When combined with radiotherapy, breast conserving surgery produces similar survival rates to those achieved with mastectomy alone.

But because some tumours prove hard to fully define with imaging techniques, breast conserving surgery may occasionally result in cancer cells being left behind and require a second operation.

The study examined the reoperation rates of 55,297 women who had primary breast conserving surgery in 156 NHS trusts in England between April 2005 and March 2008.

Of these women, 11,032 needed a second operation within three months. Around 40 per cent of women who had a reoperation underwent a mastectomy. And among the women who needed a second operation, and chose to have breast conserving surgery again, just one in seven needed a third operation.

Commenting on the research, Mr Ramsey Cutress, Cancer Research UK breast cancer surgeon at University of Southampton, said: "This is a very interesting and important study on a large group of UK women, and previous studies, in the UK and elsewhere, have shown similar results.

"It's standard practice to discuss the possibility of further surgery and it's important for patients to fully understand the pros and cons of this.

He said the aim of repeat operations after breast conserving surgery is to cut the chances that breast cancer will return - increasing survival.

"Rates of breast cancer recurrence are also reduced by other treatments such as radiotherapy, hormone therapy and chemotherapy where appropriate," he added.

"There's an ongoing need to better identify those at high risk of breast cancer recurrence, and to carefully select those who would benefit the most from further surgery."

Reoperation rates also varied between NHS trusts - in some Trusts reoperation rates were below 10 per cent while in others they were above 30 per cent - but the authors stress that further research is required to understand why this may be the case.

"Just over half of women diagnosed as having breast cancer in England now select breast conserving surgery as their primary treatment," the authors write.

"Cosmetic outcomes after surgery for breast cancer are an important consideration, and women should be made aware of the local rates of reoperation after primary breast conserving surgery, along with the likelihood of proceeding to mastectomy.

"In addition, breast cancer teams should do a local review of surgical technique, the definition of an adequate excision margin, imaging methods, and criteria for selecting patients.

"This may lead to an overall reduction in the reoperation rate after breast conserving surgery."

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‘Post-it note’ on breast cancer gene signals risk of disease spreading

Wednesday 11 July 2012

Cancer Research UK Press Release

A molecular 'post-it note' added to a breast cancer gene could flag up the risk that the disease will spread in patients, according to research published in the BJC today.

Cancer Research UK scientists at Imperial College London showed that high levels of a molecular modification called methylation on a gene called CACNA2D3, were linked to the spread of the disease in breast cancer patients.  

Methylation is a common cell process that adds methyl groups onto DNA to prevent the gene’s instructions from being given – acting like a post-it note on the DNA telling the cell when to switch genes off.  

The gene CACNA2D3 is a known tumour suppressor gene which prevents cancer. It is not methlyated in healthy breast cells and highly methlyated in breast cancer cells.

The research revealed that the addition of methyl groups to the gene stops it from protecting against cancer development.

The gene is known to be faulty or missing in a range of cancers including lung, renal cell, neuroblastoma and osteosarcoma but this is the first time it has been linked to breast cancer.

Lead author, Dr Carlo Palmieri, Cancer Research UK scientist at Imperial College London, said: “Our research suggests that methyl groups can muffle the messages given by the CACNA2D3 gene - blocking its potential protective effect against breast cancer. Methylation of the gene could be used to flag up breast cancer patients who have a greater chance of the disease spreading – helping doctors decide what treatment plan would be most effective.

“The next stage is to repeat these findings in larger studies with patients to confirm whether analysing methylation of the gene could be a useful test.”

Epigenetics is the study of DNA modifications - such as methylation –which change the way genes behave, rather than faults in the genes themselves.

Dr Julie Sharp, Cancer Research UK’s cancer information manager, said: “These results show the exciting potential of our research into epigenetics. It’s an emerging and very promising area of research that looks at how changes made to DNA can control whether genes are switched on or off, and to different amounts.

“Understanding the effect of epigenetics in cancer cells has enormous untapped potential – it could provide powerful clues about how to treat the disease in new ways and save more lives in the future.”

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‘Master switch’ experimental drug could treat different cancers

Tuesday 10 July 2012

Cancer Research UK Press Release

A unique multi-target experimental drug could treat a range of cancer types, according to research published in Clinical Cancer Research today.

Cancer Research UK-funded work at The Institute of Cancer Research in London shows that AT13148 – a type of drug called a kinase inhibitor – operates like a master switch to simultaneously block several different enzymes that control cancer cell growth and cell death.

Many kinase inhibitors have been developed that block only a single enzyme, but so far these drugs have shown only limited effectiveness. Scientists hope that switching off cell signals at multiple points could make the drug more likely to benefit patients and also delay drug resistance.

Laboratory tests showed that AT13148 was able to kill a range of cancer cell types including sarcoma, breast and prostate.

Lead author Dr Michelle Garrett, team leader in the Cancer Research UK Cancer Therapeutics Unit at The Institute of Cancer Research, said: “Our study shows that this drug is effective against a range of tumour types, and operates by blocking multiple targets. These promising results have led to the decision to take the drug into patient trials.”

The molecule was originally discovered by scientists on the PKB drug discovery programme, a collaboration between Astex Pharmaceuticals, Cancer Research Technology and The Institute of Cancer Research, which ran from 2003 through to 2006. The collaboration generated a series of compounds, of which a preferred candidate was then selected.

Dr Julie Sharp, Cancer Research UK’s senior science information manager, said: “This is exciting research showing that this experimental drug does the job of several drugs all at once, by targeting numerous weak spots in cancer cells.

“Using one master switch to turn off the different faulty messages forcing cancer cells to keep growing could be an effective way to destroy tumours. It could also reduce the chance of patients becoming resistant to treatment."

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Asbestos and shift work boost work-related cancer deaths to over 8,000 a year

Wednesday 20 June 2012

Cancer Research UK Press Release

Around 8,000 cancer deaths in Britain each year are linked to occupations - especially those where asbestos, diesel engine fumes or shift work is involved - a new study shows today. This equates to around 5 per cent of all cancer deaths in Britain.

The study1, funded by the Health and Safety Executive and published in the British Journal of Cancer, also found that just under half of these deaths were among male construction workers who are most likely to come into contact with asbestos as well as other important carcinogens such as silica and diesel engine exhaust.2

Researchers used a list of work-related cancer causing substances identified by the International Agency for Research on Cancer (IARC) to calculate the impact of work on cancer cases and deaths. And they found that around 13,600 new cancer cases are caused by risk factors related to work each year.

After asbestos, the main work-related risk factors were night shift-work – linked to around 1,960 female breast cancer cases, mineral oil from metal and printing industries – linked to around 1730 cases of bladder, lung and non-melanoma skin cancers, sun exposure – linked to around 1540 skin cancer cases, silica exposure – linked to 910 cancer cases and diesel engine exhaust – linked to 800 cases.3

And researchers warned that these estimates of cancer cases and deaths linked to occupation are likely to be conservative and could be even higher as new work-related risk factors are identified or the understanding of potential risk factors becomes more definite.4

In addition there are now more cases of cancer than there were back in 2004.

Lead author Dr Lesley Rushton, an occupational epidemiologist based at Imperial College London, said: “This study gives us a clear insight into how the jobs people do affect their risk of cancer.

“We hope these findings will help develop ways of reducing health risks caused by exposure to carcinogens in the workplace.

“The cancer with the greatest number of cases and deaths linked to work is lung – a disease which is hard to detect early and has poor survival. Over 30 occupational exposures have been identified by IARC as definite or probable lung cancer causing substances.

“One of the best ways we can beat the disease is by preventing it in the first place. Smoking has the single biggest impact on lung cancer risk, but work-place risks are also having a significant effect.”

Asbestos remains the most important occupational risk factor. Even though it is no longer used in construction, maintenance on old buildings can still be a risk for workers today. And the number of asbestos-related cancers will continue to rise as they can take a long time to develop.

Researchers said that some of the risk factors had an effect on cancer beyond the workplace – for example, asbestos can be found in some households and diesel engine exhaust contributes to air pollution.

Sara Hiom, director of information at Cancer Research UK, said: “It’s very worrying to see so many people developing and dying from occupation-related cancers. A large proportion of the deaths are a result of exposure to asbestos in past decades and improved safety measures should mean that in the next generation or so we will see this number tail off dramatically.

“The Health and Safety Executive has commissioned a review of the evidence on shift work and cancer – at the moment it’s still only classified as a probable cause of cancer. Once the review is complete in 2015, we will have a more definite understanding of the role it may play in influencing cancer risk.

“At this point, we expect the government and employers to take fast and appropriate action to minimise the risks faced by workers and Cancer Research UK will be watching this closely.

“Not smoking is the single most important thing that can reduce the likelihood of developing cancer - to put this in perspective, there are around 43,000 cancer deaths due to smoking in the UK each year. Maintaining a healthy weight, cutting back on alcohol and taking plenty of exercise can also have a big impact on reducing the risk of cancer.”

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Multidisciplinary teams improve survival rates

Monday 18 June 2012

Survival rates for women who have undergone surgery for breast cancer are improved if decisions are made as part of a healthcare team rather an individual doctor, according to a new study.

The research from NHS Greater Glasgow and Clyde, published in the BMJ, shows decision-making by teams made up of surgeons, cancer physicians and nurses is likely to improve survival following surgery for breast cancer.

The health board said that before the introduction of multi-disciplinary care in 1995, breast cancer mortality was 11 per cent higher than in the surrounding west of Scotland health board areas.

Eileen Kesso, project manager, carried out the study and found survival was 18 per cent higher in patients managed in Glasgow when decisions about their care were made by a group rather than an individual doctor.

She said: "Multidisciplinary teams (MDTs) were introduced in Greater Glasgow Health Board in the mid-1990s, several years before the rest of the UK.

"They marked a new development in the delivery of cancer services but until now there has not been any strong evidence that they made any difference to patients' survival."

The study, carried out at the West of Scotland Cancer Surveillance Unit, compared breast cancer survival in the greater Glasgow area to the rest of the west of Scotland.

It found survival was poorer in Glasgow in the early 1990s but after team decision-making through MDTs were introduced in 1995, survival was nearly 20 per cent higher in Glasgow compared with other areas.

The teams, comprising a range of specialists, use evidence-based guidelines, audit their performance and meet regularly to discuss how patients should be treated.

The study found survival from breast cancer improved in all areas throughout the 1990s but it improved even more in Glasgow after team decision-making was introduced.

Chief Medical Officer Sir Harry Burns is co-author of the report and as director of public health in Glasgow in the 1990s he was involved in establishing MDTs.

Sir Harry said: "We looked at the way the surgeon with the best survival in Glasgow worked in a team with his clinical and nursing colleagues, and modelled care for the whole health board on his approach.

"We are pleased these findings confirm our belief that this is the best way to deliver breast cancer care.

"I'm also pleased to report that this is the way in which all breast cancer care is now delivered in Scotland and other parts of the UK."

But Sarah Woolnough, Cancer Research UK's director of policy, said the Government needed to make sure all patients received the best possible care.

"This study highlights how properly delivered cancer care can really improve things for patients. Multidisciplinary teams were brought in as the 'gold standard' of cancer care in the 1990s and have helped the UK begin to catch up with the best in Europe in terms of cancer outcomes," she said.

"But we know that not all hospitals are offering the same standard of multidisciplinary care to all patients, so we need to make sure best practice is shared around the NHS."

She also highlighted the impact of the forthcoming changes to the NHS in England.

"We need to keep monitoring things, to ensure that the imminent NHS restructure is seen as an opportunity to reinforce this way of caring for patients in all regions," she added.

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Cancer Research UK initiative attracts innovative targeted cancer trials to the UK

Thursday 31 May 2012

Cancer Research UK Press Release

A Cancer Research UK initiative to improve cancer gene testing has prompted two pharmaceutical companies to plan pioneering international trials into targeted cancer treatments in the UK.

Cancer Research UK’s Stratified Medicine Programme launched last year in a bid to test tumour samples from 9,000 UK patients across six different tumour types to help further research into new targeted therapies.

Each tumour sample is being tested for a range of gene faults linked to cancer, and the information entered into a database that will allow researchers to compare the results of treatment to specific faults within cancer cells.

As a result of the programme, Roche and Bristol-Myers Squibb are working with Cancer Research UK to run trials in the UK that rely on this testing. The Roche trial will look at whether patients with a range of cancers could benefit from the targeted skin cancer drug vemurafenib. The Bristol-Myers Squibb trial is seeking health authority and ethics approval.

Doctors will be able to use the Stratified Medicine testing to see if any of their patients have the specific faults in their tumour, which would make them suitable to join these trials.

Michelle Rashford, medical director, Roche UK said: “The stratified medicines programme run by Cancer Research UK is an exciting initiative, as the opportunity to test tumour samples for a range of biomarkers is an important step in the continued development of personalised medicines.  Our VE-Basket study of vemurafenib in patients with V600 mutation positive cancers across different disease areas will allow us to identify patients that may benefit from treatment, and get closer to the goal of truly targeted medicines that provide better patient outcomes, reduce unnecessary side effects and ultimately deliver life-saving and life-prolonging treatments.”  

Oracle has also signed an agreement with Cancer Research UK to provide Oracle Health Sciences Translational Research Center software that will allow such information to be integrated and analysed much more efficiently, helping drive forward research into targeted cancer treatments.

Neil de Crescenzo, senior vice president and general manager at Oracle Health Sciences, said: “As we move toward the next generation of care, the ability to integrate and meaningfully analyse data will be a critical component in the ability to deliver more targeted, personalised therapies.

“We are delighted to work with Cancer Research UK to provide the analytical foundation needed to unlock real value from their data to support new insights at the molecular level, as they seek to expand on the genetic testing of tumours to enable more advanced, targeted and effective treatments for cancer patients.”

Cancer Research UK’s programme is a partnership with AstraZeneca, Pfizer, the Technology Strategy Board (TSB), and a range of other universities, hospitals and companies in six collaborations funded by the TSB: a total investment of £18 million. More than 2600 patients have so far enrolled, putting the programme on target to finish recruiting at the end of next summer.

David Willetts, Minister for Universities and Science, said: “This is an excellent example of collaboration between the research base and industry. It shows how Cancer Research UK is driving forward the delivery of significant benefits for patients. Two further pharmaceutical companies have got onboard and decided to carry out clinical trials - this is evidence of the attractiveness of the UK as a location for science and innovation."

James Peach, director of Cancer Research UK’s stratified medicine programme, said: “We’re delighted that our programme has helped bring these two highly innovative cancer trials to the UK, where we hope they will be of benefit to patients.

“Being able to quickly and efficiently identify patients on the basis of the faults within their tumour is a key step in developing targeted cancer treatments. This will be particularly important in relation to rare cancer types, where the target gene faults may only be present in a relatively small number of patients making it more difficult to do research.

“Patients are the heart of this work, so I’d like to thank the thousands of them who have volunteered, as well as the donors who enable this vital work to take place, and the dedicated teams in the 21 hospitals and three genetics labs across the UK that make it happen every day.”

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Study uncovers genetic diversity of breast cancer

Wednesday 16 May 2012

Nine new genes involved in the development of breast cancer have been uncovered, bringing the total number to at least 40.

Scientists led by a team at the Wellcome Trust Sanger Institute examined genetic changes in the breast tumours of 100 women.

The authors say their research, published in the journal Nature, gives a "sobering perspective on the complexity and diversity" of breast cancer, as no two breast cancers shared the same combination of faulty cancer genes.

Many cancers develop when non-inherited faults in genes accumulate during a person's lifetime.

Some faults are relatively harmless, but, so-called 'driver' mutations occur in cancer genes and contribute to the development of cancer.

Dr Patrick Tarpey from the Wellcome Trust Sanger Institute said: "To identify new cancer genes that lead to the development of breast cancer, we searched for driver mutations in over 21,000 genes, and found evidence for nine new cancer genes involved in the development of this cancer."

Most individual cancers contained different combinations of mutated genes.

The Institute's director, Professor Mike Stratton, said: "We found that breast cancer can be caused by more than 70 different combinations of mutations.

"If we consider three breast cancers, each with four driver mutations: they might share none of those driver mutations - so each is a different genetic 'animal'. They are different cancers driven by different genes. We need to classify them as carefully as we can. This study is a step towards that goal," he added.

Breast cancer is the most common cancer among women in the UK, with more than 48,000 women diagnosed with the disease every year.

The researchers hope that understanding genetic diversity in breast cancer will be an important step towards more rational treatment for the disease.

Professor Andy Futreal, also from the Wellcome Trust Sanger Institute, said: "One of the most striking things about breast cancer is how it progresses differently in each patient and how each patient responds differently to therapy. Our results can help us to understand these differences.

Professor Stratton added: "The picture is certainly more complicated than we would have wanted, but as with many other things knowledge is our strongest weapon.

Professor Carlos Caldas, a Cancer Research UK-funded breast cancer expert who was involved in the work, agreed.

"This is a very important and rigorous analysis," he said.

"When taken together with other recent results, these new genes contribute to a detailed and ever-more complex catalogue of the genetic faults in breast cancer.

"And this knowledge will doubtless drive further research that will, when replicated in larger numbers of cancer samples, lead to better ways to diagnose and treat breast cancer patients in the future."

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Scientists re-write rule book on breast cancer in landmark global study

Wednesday 18 April 2012

Cancer Research UK Press Release

A major study carried out by Cancer Research UK scientists could revolutionise the way women with breast cancer will be diagnosed and treated in the future, by reclassifying the disease into 10 completely new categories based on the genetic fingerprint of a tumour.

Doctors should one day be able to predict survival more accurately in women with breast cancer based on these new subtypes, and better tailor treatment to the individual patient.

The research – published in Nature1 today (Wednesday) – is the largest global gene study of breast cancer tissue ever performed – the culmination of decades of research into the disease.


The team at Cancer Research UK’s Cambridge Research Institute, in collaboration with the BC Cancer Agency Vancouver Canada, analysed the DNA and RNA2 of 2,000 tumour samples taken from women diagnosed with breast cancer between five and 10 years ago.

The scientists:

• Classified breast cancer into at least 10 subtypes3 grouped by common genetic features that correlate with survival. This new classification could change the way drugs are tailored to treat women with breast cancer.
  
• Discovered several completely new breast cancer genes that drive the disease. They are all potential targets for the development of new types of drugs. This information will be available to scientists worldwide to boost drug discovery and development.
  
• Revealed the relationship between these genes and known cell signalling pathways – networks that control cell growth and division. This could pinpoint how these gene faults cause cancer, by disrupting important cell processes.

Study co-lead author, Professor Carlos Caldas, senior group leader at Cancer Research UK’s Cambridge Research Institute and the Department of Oncology, University of Cambridge, said: “Our results will pave the way for doctors in the future to diagnose the type of breast cancer a woman has, the types of drugs that will work, and those that won’t, in a much more precise way than is currently possible.

“This research won’t affect women diagnosed with breast cancer today. But in the future, breast cancer patients will receive treatment targeted to the genetic fingerprint of their tumour.

“We’ve drilled down into the fundamental detail of the biological causes of breast cancer in a comprehensive genetic study. Based on our results we’ve reclassified breast cancer into 10 types – making breast cancer an umbrella term for an even greater number of diseases.
“Essentially we’ve moved from knowing what a breast tumour looks like under a microscope to pinpointing its molecular anatomy – and eventually we’ll know which drugs it will respond to.

“The next stage is to discover how tumours in each subgroup behave – for example do they grow or spread quickly? And we need to carry out more research in the laboratory and in patients to confirm the most effective treatment plan for each of the 10 types of breast cancer.”

Professor Samuel Aparicio, co-lead author of the study based at the BC Cancer Agency in Vancouver, Canada, said: “Breast cancer is a global problem and it’s exciting to see a new framework for the understanding of breast cancer emerge from our partnership with colleagues in the UK.

“The new molecular map of breast cancer points us to new drug targets for treating breast cancer and also defines the groups of patients who would benefit most.”

He added: “The size of this study is unprecedented and provides insights into the disease such as the role of immune response, which will stimulate other avenues of research.”

Dr Harpal Kumar, chief executive of Cancer Research UK, said: “This landmark study will completely change the way we look at breast cancer. It’s the result of decades of research by our scientists to identify the causes and drivers of the disease, which included a pivotal role in decoding the well-known BRCA genes.

“We’re entirely funded by the generosity of the public and this incredible support has put us at the heart of progress that’s underpinned the dramatic increase in the number of women surviving from breast cancer in the UK. This new study will enable us to make a further step-change for patients with breast cancer.  

“Our research has underpinned important drugs, such as tamoxifen and herceptin, which have saved the lives of many thousands of women with breast cancer. And we’ve helped to improve and refine radiotherapy for breast cancer - a vital part of treatment for this disease.

“These latest results demonstrate again how solid scientific research is the foundation for translation into patient benefit and ultimately improving breast cancer survival.”

Cancer Research UK is a major funder of breast cancer research in the UK. Eight out of 10 women now survive breast cancer for more than five years, compared with five out of 10 women in the 1970s.

Dr Kumar added: “More women than ever before are surviving breast cancer thanks to our work. But there is much more to be done. We’ve a clear view of the questions- ahead and now we must focus on finding the answers.”

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International consortium releases cancer gene data

Thursday 15 March 2012

The International Cancer Genome Consortium (ICGC) has released genetic data from a series of studies into different types of cancer.

The data can now be used by researchers worldwide, to help drive forward their own research projects.

The data were released on the same day that the ICGC announced a new project in South Korea to pin down the genetic faults that cause breast cancer in East Asian women.

The consortium says it is ahead of schedule in its plan to deliver genomic data on more than 50 types of cancer over a period of 10 years.

The ICGC involves various research organisations around the world, including Cancer Research UK, which is working on prostate and oesophageal cancers.

The Consortium's eighth major data release includes the first findings from the UK's myelodysplastic syndrome study, alongside liver cancer research in France and a childhood brain cancer project in Germany.

Other findings include updates from the UK's breast cancer (triple negative) project, pancreatic research projects in Australia and Canada, and liver cancer research in Japan.

Cancer Research UK's Professor David Scott, welcomed the new data, saying it would drive forward cancer research.

"It's good to see that the International Cancer Genome Consortium is continuing to make progress and is ahead of schedule," he said.

"The release of data announced today should help researchers worldwide - including those funded by Cancer Research UK - gain new insights into how these cancers develop, and open up new avenues in the search for targets for treatments," he added.

For its latest study in South Korea, the ICGC will collaborate with the National Centre for Cancer Genomics in Seoul.

Because there are significant genetic and lifestyle differences between Caucasian and East Asian patients, data from the study will be compared with ICGC breast cancer projects in the UK, France and the US.

The study will be led by Dr Gu Kong from Hanyang University, alongside teams from Seoul National University, the Asian Medical Centre, and Gachon University of Medicine and Science.

Dr Hyung-Lae Kim, director of the national project for personalised genomic medicine at Korea&aposs Ministry of Health, said: "It is our great pleasure to join the ICGC.

"We believe that genomic data from Asian cancer patients will contribute to the current ICGC breast cancer project both scientifically and clinically."

Henry Scowcroft, Cancer Research UK's science information manager, said the research would ultimately improve the way genetic knowledge was applied to people of different ethnicities.

"Most of the research into the gene faults that cause cancer has predominantly looked at Caucasian populations, so it's great to hear South Korea is joining the ICGC.

"It's extremely important to make sure that our knowledge of cancer's inner workings applies to as many people from as broad a range of ethnicities as possible," he said.

ICGC has already received funding commitments from groups in Asia, Australia, Europe and North America for 47 project teams to study the genomes of more than 18,000 tumours. Information on more than 3,493 tumours is available through its website.

Previous data released by ICGC include its Chinese gastric cancer project and the Spanish chronic lymphocytic leukaemia project.

Meanwhile, submissions from the US Cancer Genome Atlas have contributed information on 10 types of cancer affecting the blood, brain, colon, kidney, lung, ovaries, rectum, and uterus.

Cancer Research UK's oesophageal and prostate cancer projects have recently successfully completed pilot phases, with the full projects now starting.

These projects are funded by the Dallaglio Foundation (prostate) and the Catalyst Club (oesophageal).

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Oestrogen-only HRT after hysterectomy 'may protect against breast cancer'

Wednesday 7 March 2012

Women who use oestrogen-only hormone replacement therapy (HRT) to relieve menopausal symptoms after a hysterectomy have a reduced risk of developing or dying from breast cancer.

This is the conclusion of a US study of around 7,500 women who took oestrogen-only HRT or a placebo for about six years then stopped.

Previous research indicates that the more common form of HRT, which contains both oestrogen and the hormone progesterone, increases the risk of developing breast cancer.

In this new study, around five years after stopping treatment, 151 women in the oestrogen-only HRT group developed breast cancer, versus 199 women in the placebo group, a difference of 23 per cent.

Women in the HRT group who did develop breast cancer were also 63 per cent less likely to die from the disease.

Oestrogen-only HRT is known to be linked to cancer of the womb and for this reason is only given to women who have undergone a hysterectomy.

The new results, published in The Lancet Oncology journal, come from the Women's Health Initiative (WHI), a major US study of post-menopausal women launched in 1993.

The study showed that women who had oestrogen-only HRT had long-lasting protection against breast cancer.

But this potential benefit needs to be balanced against an increased risk of blood clots and strokes associated with HRT, say the researchers, who were led by Professor Garnet Anderson, from the Fred Hutchinson Cancer Research Centre in Seattle.

And women with a family history of breast cancer do not seem to benefit from the protective effects of oestrogen-only HRT.

The researchers said that the study does not support the use of oestrogen solely to reduce breast cancer risk.

Professor Jack Cuzick, a Cancer Research UK epidemiologist based at Queen Mary, University of London, said the results were important: "This is the first randomised controlled trial of oestrogen-only HRT and breast cancer risk, and is well designed. So although this study contradicts some research showing that oestrogen-only HRT moderately increases the risk of breast cancer, it shouldn't be ignored. We need further research to clarify exactly how oestrogen-only HRT affects breast cancer risk in women of different ages and family histories.

"If a woman is considering starting or stopping HRT, or using it for a long time, she should discuss it with her doctor who can help weigh up the benefits and risks of different types of HRT and make the right choice based on her own circumstances.

"There are different types of HRT, and it's clear that combined types increase the risk of breast cancer and other health problems. For women who've had a hysterectomy, oestrogen-only HRT is an effective short-term treatment for menopausal symptoms. But women taking it should use the lowest dose possible for as short a time as they need it."

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CRT unveils 'screen test' for potential drugs to treat oestrogen positive breast cancer

Monday 5 March 2012

Cancer Research UK Press Release

Cancer Research UK and its commercial arm, Cancer Research Technology have developed a unique test to discover molecules that could lead to potential new treatments for oestrogen receptor (ER)-positive breast cancer.

The team at Cancer Research UK’s Cambridge Research Institute has unveiled a cell-based test that allows scientists to screen a library of 150,000 small drug-like molecules and identify those that switch off a cell signalling system called the FOXA1 pathway.

The team has previously shown that blocking the main protein in the pathway, FOXA1, blocks growth of ER-positive breast cancer cells, even in the presence of oestrogen receptors, which usually fuel the disease.

Current standard hormone treatments block the oestrogen receptor or the production of oestrogen. But sometimes patients stop responding to these drugs.

Resistant ER-positive breast tumours often rely on cell signals triggered by the oestrogen receptor to continue to fuel the disease.

The discovery of molecules that block the FOXA1 pathway, which prevents the oestrogen receptor driving the cancer, might provide new approaches to treat patients who are resistant to current approaches.

Dr Jason Carroll, group leader at Cancer Research UK’s Cambridge Research Institute, said: “There’s an urgent need to find new ways to treat breast cancer that is no longer responding to standard treatments, which work by targeting the effect of oestrogen in cancer cells.

“Our team has pinpointed the FOXA1 pathway, which we can target with new treatments to help combat this problem.

“We’ve designed a tailored test that identifies the molecules which switch off the pathway – and which we hope could one day be developed into a new class of drugs.”

The team also discovered that blocking FOXA1 could prevent growth of molecular apocrine breast cancer cells.  Women with this form of breast cancer have limited options for treatment and poor survival.

Dr Keith Blundy, CEO of Cancer Research Technology, said: “We’re proud that the work of Cancer Research UK has already helped to transform breast cancer treatment, leading to significant improvements in survival.

“The FOXA1 pathway is an exciting new area of research and we hope that our cell-based screen will allow us to identify potential new targets for drug development this year.

“We’d be keen to collaborate with industry to screen their library, alongside ongoing research input from our team, to form an effective partnership with exciting opportunities.”

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Age affects risk of being diagnosed with cancer at advanced stage

Friday 2 March 2012

Cancer Research UK Press Release

Older women with breast cancer face a higher risk of being diagnosed with the disease at a late stage, while the risk of an advanced stage diagnosis of lung cancer decreases with age, a new study shows today.

Researchers from the University of Cambridge and the Eastern Cancer Registration and Information Centre (ECRIC) said the study showed that efforts to diagnose cancer early need to be better tailored to different age groups.

The study, published in the British Journal of Cancer*, used ECRIC data on stage – a measure of how advanced the cancer is when diagnosed.

The research aimed to find whether there was a link between age or socio-economic background and being diagnosed with advanced stage cancer.

Researchers looked at around 17,800 women with breast cancer and over 13,200 patients with lung cancer in the east of England who were diagnosed between 2006 and 2009.

They found that compared to women aged 65-69, women aged 70-74 had a 21 per cent increased chance of a late stage breast cancer diagnosis.

The chance of an advanced breast cancer diagnosis became higher as women got older – even accounting for the effect of screening. For example, it was 46 per cent higher in women aged 75-79.**

In contrast, it was less likely that older patients would be diagnosed with advanced stage lung cancer than younger patients.

Compared with people aged 65-69, people aged 70-74 were 18 per cent less likely of be diagnosed with late stage lung cancer and this chance decreased further with age - for people aged 75-79 it was 26 per cent lower.

For breast cancer, the study also found that late stage diagnosis was more common in women from deprived backgrounds. For lung cancer, late stage diagnosis was more common in men.

Dr Georgios Lyratzopoulos, study author based at the University of Cambridge, said: “Patient awareness of the signs of breast cancer is known to be lower among older women and this may explain why breast cancer is diagnosed later among this age group.

“But it is puzzling why older patients have a lower risk of advanced stage lung cancer. More research is needed to better understand this pattern.”

The researchers added that the strong likelihood of older women being diagnosed with late stage breast cancer was worrying given that the risk of the disease increases with age.***

Dr David Greenberg, study author based at ECRIC, said: “Collecting staging data has proved difficult in the past but this data is vital to understanding how to improve the diagnosis of cancer. ECRIC has the most complete information on stage. A modernisation programme for cancer registries aims to improve the collection of such information nationwide by end of 2012.”

Sara Hiom, director of information at Cancer Research UK, said: “If cancer is caught early, patients usually have a better chance of beating the disease as more effective treatment options are available.
“We have made great progress in improving cancer survival rates in the last 40 years, but there is still more work to be done to help more people survive cancer.  
“Collecting information on stage at diagnosis is vital to do this and we must think how to target messages appropriately to the right audiences.
“Cancer Research UK works to raise symptom awareness, and encourage and enable people to go visit their doctor as soon as their notice anything unusual for their bodies.”
 

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EU cancer death rate expected to fall again

Wednesday 29 February 2012

Researchers predict that the proportion of the European Union (EU) population that dies from cancer will continue to drop in 2012.

The falling rates of cancer death are due to a decline in men smoking, and to progress in cancer prevention, early detection and treatment, according to the authors of the report, published in the journal Annals of Oncology.

The new figures were described as "encouraging" by Cancer Research UK, but also highlight a trend of rising lung cancer death rates in women.

Overall, cancer death rates for 2012 will be 139 per 100,000 for men and 85 per 100,000 for women. This is a 10 per cent fall for men and a seven per cent fall for women, compared with rates from five years ago

But the total number of people dying of cancer is set to increase, as the EU population ages.

The report forecasts that around 1.28 million people will die from cancer this year - 717,398 men and 565,703 women. In 2007 this figure was around 1.26 million.

All cancers were included in the overall tally. The researchers also looked individually at cancers of the stomach, intestine, pancreas, lung, prostate, breast, and uterus (including cervix), and leukaemias.

The report predicted substantial reductions in breast cancer death rates, not just in middle-aged and older women, but also in younger women.

Overall breast cancer death rates are tipped to fall by nine per cent to 14.9 per 100,000 women, while deaths among women aged 20 to 49 will fall by 13 per cent to 6.3 per 100,000 women.

Study leader Professor Carlo La Vecchia, from the University of Milan, said: "The fact that there will be substantial falls in deaths from breast cancer, not only in middle age, but also in the young, indicates that important advancements in treatment and management are playing a major role in the decline in death rates."

A total of 88,000 women in the EU are expected to die of breast cancer in 2012, making it the leading cause of death overall in women.

But they predict lung cancer will be the biggest cause of death among women in the UK and Poland, with rates of 21.4 and 16.9 per 100,000 women respectively.

And lung cancer will continue to be the biggest cause of death among men in the EU with a rate of 37.2 per 100,000. But this is a 10 per cent fall on the 41.3 figure from 2007.

Catherine Thomson, head of statistical information at Cancer Research UK, said the study is in line with previous research "which shows that generally death rates from cancer in the UK are predicted to fall".

She added: "This is true for breast and bowel cancers and lung cancer in men - reassuring news that highlights the impact of men stopping smoking, the introduction of new therapies and diagnostics, and how the NHS has improved treatment delivery.

But she said that climbing lung cancer death rates in women were worrying.

"Smoking prevention is the key to reducing lung cancer rates as over eight out of 10 lung cancer cases are caused by smoking. Most smokers start under the age of 18, so efforts to dissuade both boys and girls from starting to smoke in the first place must be continued," she continued.

"One important step is to remove the displays of cigarettes in shops - which is being rolled out in large stores and supermarkets in April. Tobacco companies have used the cigarette pack to appeal to new smokers over recent years. Cancer Research UK is also urging the government to remove all branding from tobacco packets and sell this deadly product in plain, standardised packets with large health warnings front and back."

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Hundreds more breast cancer patients should be tested for BRCA1 gene

Wednesday 15 February 2012

Cancer Research UK Press Release

Leading breast cancer experts are calling for women under 50 who are diagnosed with triple-negative (TN) breast cancer to be offered testing for faults in the BRCA1 gene, according to a report published in the British Journal of Cancer.

The researchers – funded by Cancer Research UK and led by scientists at The Institute of Cancer Research – looked at more than 300 women with TN breast cancer and found BRCA1 mutations in nearly one in five women diagnosed under 50.

But due to the cost of testing for the BRCA1 mutation, NICE guidance recommends that BRCA1 should be offered if the likelihood of detecting a mutation is greater than 20 per cent, although many testing centres offer it if the likelihood is between 10-20 per cent.

Centres use a range of criteria and methods to determine if a patient is eligible for testing. But this requires specialist knowledge and software and potentially misses hundreds of women a year.

Based on their findings the researchers estimate more than one in three women with TN breast cancer caused by BRCA1 mutations would not have been tested using the current criteria.

Lead author Professor Nazneen Rahman, a Cancer Research UK funded researcher at the Institute of Cancer Research and the Royal Marsden Hospital, said: “Our findings show that women diagnosed with triple-negative breast cancer under 50 should be offered BRCA1 testing. Using a simple age criteria for testing will provide a clear and understandable guide for doctors and women to follow, and should result in many more women benefitting from the optimised care that genetic information makes possible.”

Changing the current testing guidelines could mean an extra 1,200 tests a year, which the researchers acknowledge will place an extra burden on current genetic testing services.

Professor Rahman added: “There are hurdles to overcome so that NHS testing services can cope with more BRCA1 testing, but we’re moving towards an era of faster and cheaper genetic testing, so it will soon be possible.”

Women carrying the BRCA1 mutation have up to a 65 per cent chance of developing breast cancer by the time they are 70. But only around one in 900 women in the general population carry a BRCA1 mutation.

Breast cancers with BRCA1 mutations can respond well to treatment with platinum-based drugs, such as carboplatin and cisplatin, and also to radiotherapy. But they can develop resistance to the treatment and start to grow again.

Rowena Kincaid, 36, from Cardiff, was diagnosed with breast cancer in July 2009 after finding a lump. It was confirmed as triple negative and she underwent a lumpectomy followed by four months of chemotherapy and radiotherapy. She is now doing well, is back at work and took part in Race for Life in 2011.

She said: “I am interested to know about the genetic testing, as I know there has been cancer in the family. To be offered the chance to find out if I carry the BRCA1 mutation would not only give me insight to my own disease but also allow me and my family to discuss with our doctors if we carry the mutation what the next steps would be.”

Professor Peter Johnson, chief clinician at Cancer Research UK, said: “It’s important that we identify women and their families who carry BRCA1 mutations. They’re more likely to develop breast and ovarian cancer, so armed with this knowledge doctors can offer targeted screening and tailored treatments to these women.

“The NHS needs to adapt so that tests for BRCA1 can be offered to women who are likely to carry the mutation. This approach will be cost-effective for the NHS in the long-term, leading to a substantial reduction in the number of breast and ovarian cancers by offering preventative treatments for those women and their families who are at greatest risk.”

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CBT is effective for menopausal symptoms after breast cancer treatment

Wednesday 15 February 2012

Research funded by Cancer Research UK suggests that cognitive behavioural therapy (CBT) can help women who have had breast cancer treatment manage the common side-effects of hot flushes and night sweats.

The research, published in The Lancet Oncology, found that CBT is a safe and effective form of treatment for the 65 to 85 per cent of women affected by such symptoms after having breast cancer treatment.

Hormone replacement therapy (HRT) is not generally prescribed for women with menopausal symptoms who have had breast cancer, as it can  increase the risk of cancer coming back. Also, symptoms can return in women who stop HRT.

To test if CBT is an effective treatment, the researchers recruited 96 women from breast clinics in London, UK, who had problematic hot flushes and night sweats after breast cancer treatment.

The women were randomly split into two groups: one that received usual care only (49 women), and one that received CBT and 'usual care' (47 women).

'Usual care' included having access to nurses and oncologists, as well as telephone support programmes and other cancer support services.

CBT consisted of one 90 minute session a week for 6 weeks, and included psycho-education, paced breathing, and cognitive and behavioural strategies to manage symptoms.

Women were asked to rate the extent to which symptoms were bothersome and interfered with their life during the course of the study. The CBT group had significantly reduced hot flushes and night sweats ratings after nine weeks compared with usual care.

These improvements were then shown to be maintained at 26 weeks.

The authors, led by Professor Myra Hunter of the Institute of Psychiatry at King's College London, said: "Our findings show that group CBT can reduce the effect of hot flushes and night sweats for women who have had breast cancer treatment. These reductions were sustained and associated with improvements in mood, sleep, and quality of life.

"Group CBT seems to be a safe, acceptable, and effective treatment option which can be incorporated into breast cancer survivorship programmes and delivered by trained breast cancer nurses."

Martin Ledwick, head information nurse at Cancer Research UK, said: "We know that many women can have problems with hot flushes and night sweats following treatment for breast cancer and that this can be distressing, particularly when they have not previously suffered from these symptoms.

"Although certain drugs can help, many women prefer to seek alternatives where possible. We hope this new approach will provide these women with a more acceptable way of managing these symptoms."

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Change4Life warns of cancer risk from drinking 'a little too much'

Tuesday 7 February 2012

People are at risk from serious illness including cancer, heart disease and stroke if they drink just slightly more than they should, Andrew Lansley has warned.

The Health Secretary was speaking at the launch of the nationwide Change4Life campaign which tells the public that drinking just a little bit over the lower-risk alcohol guidelines can seriously impair long-term health.

The campaign was welcomed by Cancer Research UK, which said major benefits can be achieved by small lifestyle changes such as having a few designated alcohol-free days each week.

A Change4Life TV ad highlights the risk associated with regularly drinking two large glasses of wine or two strong pints of beer a day, which triples the risk of developing mouth cancer and doubles the risk of developing high blood pressure.

Heightened awareness of the risks linked to drinking more than the NHS recommends is urgently required, according to the findings of a new survey.

It found that 85 per cent of people do not realise it increases the risk of developing breast cancer; 66 per cent are not aware of its link to bowel cancer and 63 per cent do not realise it raises the chances of developing pancreatitis (inflammation of the pancreas).

The poll also revealed that 59 per cent do not realise it increases the risk of mouth, throat and neck cancer; 37 per cent do not realise it reduces fertility; and 30 per cent are not aware that it increases the risk of high blood pressure.

The Change4Life website features an online calculator to help people check how much they are drinking and work out whether they need to cut down.

The campaign advocates having alcohol-free days, not drinking at home before an evening out and switching to smaller glasses or low-alcohol drinks.

Chief Medical Officer Professor Dame Sally Davis said: "Drinking too much is a major public health issue. This campaign highlights how easy it can be to use a glass of wine or beer to unwind at the end of a busy day but these drinks stack up and can increase your risk of high blood pressure, cancer or liver disease.

"The campaign with its new online calculator is available on the Change4Life website to help and encourage people to check how much they are drinking and, if they find they are drinking over the guidelines, help them cut down."

Sarah Lyness, executive director of policy and information at Cancer Research UK, said: "Alcohol can increase the risk of seven types of cancer, including two of the most common kinds - breast and bowel cancers.

"A recent study showed that nearly 12,500 cancers in the UK each year are caused by alcohol.

"The risk of cancer starts to go up even at quite low levels of drinking, but the more people cut back on alcohol, the more they can reduce the risk.

"Small changes can really make a difference, so try swapping a glass of wine or beer for a soft drink or having a few alcohol-free days a week."

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Promising breast cancer prevention drug 'weakens bones'

Tuesday 7 February 2012

The drug exemestane, which is used to treat breast cancer and is also in trials to prevent the disease developing in postmenopausal women, significantly worsens age-related bone loss, according to a study from Canada.

The findings, published in The Lancet Oncology, suggest that the cancer-protective effects of the drug need to be weighed against the risk of bone fracture, and that any women prescribed the drug to prevent breast cancer in the future will need to be carefully monitored for bone effects.

Exemestane - also called Aromasin - is a type of hormonal therapy called an aromatase inhibitor and is used to treat oestrogen-receptor-positive breast cancer in women who have been through the menopause.

The drug works by blocking the production of oestrogen, which fuels the growth this type of cancer.

Clinical trials are being carried out to assess whether exemestane is also effective at preventing breast cancer in postmenopausal women at high risk of developing the disease.

Concerns have been raised about the effects of aromatase inhibitors on bone loss and increased fracture risk, but previous studies were conducted against a comparison with tamoxifen, a treatment with known beneficial effects on bone in postmenopausal women.

Preliminary research suggested that exemestane might cause less bone loss than other aromatase inhibitors and could even stimulate bone formation.

In this latest work, Dr Angela Cheung and colleagues from the University Health Network, Toronto, studied women from the MAP.3 trial in order to measure the effect of exemestane on bone-mineral density (BMD) and structure in postmenopausal women.

The trial is looking at the effect of exemestane at preventing breast cancer in more than 4,500 healthy postmenopausal women with a family history of breast cancer.

Study results published last year showed that exemestane reduced the risk of developing breast cancer by 65 per cent compared with placebo.

In the latest analysis, 351 women without osteoporosis were included, 176 given exemestane and 175 given placebo.

After two years of treatment, women given exemestane had a significant loss of BMD at the distal tibia and distal radius, common sites for fractures related to osteoporosis.

Cortical thickness (the tissue that usually makes up the outer shell of bone) and area had also declined by almost eight per cent compared with a one per cent decline in the placebo group over the two-year period.

The study found that exemestane substantially affected the loss of cortical bone compared with trabecular - spongy - bone. This finding is important because 80 per cent of fractures in old age are caused by greater loss of cortical (rather than trabecular) bone and account for most disability.

Dr Cheung, said: "Exemestane worsens age-related decreases in bone mineral density by about three times, even in the setting of adequate calcium and vitamin D intake."

In conclusion, the authors said: "Women considering exemestane for the primary prevention of breast cancer should weigh their individual risks and benefits. For women taking exemestane, regular bone monitoring plus adequate calcium and vitamin D supplementation are important."

They added: "Long-term studies are needed to assess the effect of our findings on fracture risk."

Dr Julie Sharp, senior science information manager at Cancer Research UK, said: "Exemestane is not routinely used as a breast cancer prevention drug, as we don't have enough information about its risks and benefits, but it is being tested in clinical trials.

"For women already given these types of hormone drugs to prevent their breast cancer coming back doctors already look out for the bone-weakening effects, and if suitable, prescribe drugs to strengthen the bones. This new study shows that monitoring of women treated with exemestane and other similar drugs is really important.

"Cancer Research UK is supporting a breast cancer prevention trial - IBIS-II - with another aromatase inhibitor called anastrozole. Results from this study, and the longer-term follow up of exemestane, will be important to measure the protective effects and side effects of the aromatase inhibitors."

Professor Jack Cuzick, a Cancer Research UK epidemiologist based at Queen Mary, University of London, said: "In IBIS -II we measure bone density before starting trial medication and if it is low we recommend use of bisphosphonates at the same time. Our initial studies have shown that this will actually increase bone density even when given with an aromatase inhibitor."

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Researchers defend HRT breast cancer study

Tuesday 17 January 2012

The authors of a study showing that hormone replacement therapy (HRT) increases the risk of breast cancer have defended their findings, following criticism from a team of experts linked to pharmaceutical companies that make the treatment.

The Million Women Study, part-funded by Cancer Research UK, began recruiting women in 1996. In 2003, it found that using HRT that combines oestrogen and progesterone increases a woman's risk of developing breast cancer. Several subsequent analyses including a follow-up paper in 2011 found similar results, including a "rapid fall in risk" after HRT is stopped.

Although more than 20 further independent studies have also found an increased risk of breast cancer in women who use HRT, especially the combined form, such a link has proved controversial, with some suggesting that the findings have been exaggerated.

In the latest critique, the original research has been analysed by a team led by Professor Samuel Shapiro of the University of Cape Town Medical School, and published in the Journal of Family Planning and Reproductive Health Care.

The researchers claim that the Million Women Study does not in itself establish HRT as linked to breast cancer. But they don't rule out the possibility that HRT may indeed increase risk of the disease.

The critique's authors, from South Africa, Germany and the UK, admitted that they had all acted (or continue to act) as consultants for pharmaceutical companies that make HRT.

Prof Shapiro's team wrote: "HRT may or may not increase the risk of breast cancer, but the Million Women Study did not establish that it does."

His team examined criteria applied to scientific research to show a causal link, and identified several flaws it claims would have skewed the findings.

Researchers said that cancers detected within a few months of the study's start would have already been present when the women were enrolled in the research, but these women were not excluded from the analysis.

And they said inviting women to join the study would, in itself, have increased the number who were already aware of breast lumps or pre-cancerous changes, leading to higher numbers of cancers being detected.

This claim is borne out by a higher rate of cancers among the study participants than in the general population, irrespective of whether or not they used HRT, they said.

And they point out that crucial data was often missing, and in the third report from the Million Women Study they said follow-up data on HRT use was not available for at least 57 per cent of participants.

Prof Shapiro's group added: "The validity of any study is dependent on the quality of its design, execution, analysis and interpretation. Size alone does not guarantee that the findings are reliable."

The Million Women Study was an observational study and "if the evidence was unreliable, the only effect of its massive size would have been to confer spurious statistical authority to doubtful findings," they said, adding that the study evidence "was indeed unreliable."

Defending the findings, Cancer Research UK's Professor Dame Valerie Beral (pictured), head of the Cancer Epidemiology Unit at the University of Oxford, said the paper was a re-statement of previously refuted views from "many consultants to HRT manufacturers, as these authors are, attempting to dispute evidence" about its adverse effects.

"The authors omit to say that Million Women Study findings, of an increased risk of breast cancer in users of HRT, especially of oestrogen-progestagen combinations, have been replicated in over 20 other studies. The totality of the worldwide evidence is now overwhelming."

Professor Beral's colleague Professor Sir Richard Peto added that although the report raises valid criticisms of certain aspects of the Million Women Study, it fails to challenge its central finding: that HRT is a major cause of breast cancer, and that women can reduce their risk by stopping taking it.

Sir Richard, Professor of Medical Statistics and Epidemiology at the University of Oxford, said the results were biologically valid.

"Ordinary breast cells can be stimulated to divide by the female hormone, oestrogen. Even when one cell from the breast has gone wrong and has turned into the seed of a growing cancer, that cancer can still be dependent on the continued stimulation by the body's own oestrogen.

"Hormone-sensitive breast cancers can, however, be shrunk (and sometimes cured completely) by drugs such as tamoxifen, which block the action of oestrogen on the breast cancer cells.

"In women who have had a hormone-sensitive breast cancer apparently completely removed from their breast, invisibly small deposits of cancer cells may remain either nearby or in distant parts of the body". These, he said, could cause the cancer to return.

"In the Million Women Study participants were recruited just before they attended a breast screening clinic, at which some cancers were detected.

"But, even if attention is restricted to cancers that were detected only later, hormone-sensitive cancers are still three times as common in HRT users as in non-users or ex-users. Thus, the Million Women Study provides strong, biologically plausible evidence of causality.

Sir Richard concluded that there is clearly an increased chance of getting breast cancer among otherwise similar women and a rapid decrease after they stop.

Hazel Nunn, head of health information at Cancer Research UK, said that women shouldn't be unduly worried by the new criticisms.

"HRT can be an effective short-term treatment for menopausal symptoms - women taking it should try and use the lowest dose possible for as short a time as they need it.

"If you are considering starting or stopping HRT, or using it for a long time, you should discuss it with your doctor. The issues are different for every woman and your doctor will be able to help you weigh up the benefits and risks of different types of HRT and make the right choice based on your own circumstances.

"In the UK, HRT use has been falling since the start of the Millennium. Studies suggest that in 2005 there were 1,400 fewer cases of breast cancer in the UK among women aged 50-59 than would have been if there had been no drop in HRT use," she added.

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Reprogrammed oestrogen binding linked to more aggressive breast cancer

Wednesday 4 January 2012

Cancer Research UK Press Release

SCIENTISTS based at Cancer Research UK’s Cambridge Research Institute have discovered how receptors for the female sex hormone oestrogen attach to a different part of the DNA in breast cancer patients who are more likely to relapse, according to a study published in Nature today.

Crucially, they also found that within these more aggressive breast cancers, the oestrogen receptor (ER) was being ‘redirected’ to a different part of the genome by a protein called FOXA1. So drugs that specifically block FOXA1 could help treat patients who do not respond to conventional hormone treatments, such as tamoxifen.

The researchers used state of the art technology, called ChIP sequencing, to analyse ER-genome interactions in frozen breast tumour samples* and create a map of all of the sites in the human genome where ER attaches itself to the DNA and switches on particular genes.

This map was used to compare where in the genome ER attached in tumours from people that responded well to treatment, versus those that went on to relapse or were resistant to treatment from the start.

This revealed almost 500 contact points that were common across all the samples analysed, but also a distinct set that were specific to patients with different clinical outcomes – of which 599 were associated with good response to treatment and 1,192 with poor response.

Studying patterns of gene activity in these two areas of the genome allowed the researchers to identify a subset of genes that are more active in tumours that return and spread.

Cancer Research UK’s Dr Jason Carroll, who jointly led the study with Professor Carlos Caldas, said: “These findings suggest that ER binds to different regions of the genome DNA in breast cancer patients that respond to treatment, compared to those that relapse and whose cancer spreads.

“We know from previous studies involving breast cancer cells growing in the lab that a protein called FOXA1 is needed for oestrogen receptors to interact with the DNA and switch on genes that fuel cancer growth. But this is the first time we’ve examined frozen tumour samples and shown that FOXA1 redirects ER to different locations within the DNA in patients with different outcomes. This switches on different sets of genes, which in turn affect the outcome of the patient. We now hope to develop ways of blocking FOXA1 to help treat patients who no longer respond to standard treatments.”

Carlos Caldas, Professor of Cancer Medicine at the Department of Oncology at the University of Cambridge and the Cancer Research UK Cambridge Research Institute said: “Some breast cancers are treated with hormone treatments, such as tamoxifen, which work by blocking oestrogen receptors. But we know that about a third of patients either fail to respond to this type of treatment, or go on to relapse at a later date.

“Understanding the genetic differences that determine who will or won’t respond to a given treatment is a vital step in being able to choose the right drugs for individual patients. The next step will be to see if these findings can be repeated in larger groups of patients.”

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Scientists move a step closer to targeting key cancer process

Friday 9 December 2011

Scientists in the US are closer to working out how to target cancer cells that are driven by a hyperactive gene called Myc, according to a report in the journal Science.

Researchers estimate that 20-40 percent of all cancers are driven by mutations in this gene, and are often aggressive.

Researchers at Baylor College of Medicine and Harvard Medical School showed that a second cellular process, called SUMOylation, was responsible for allowing cancer cells to survive when their Myc gene was hyperactive.

In a series of lab experiments, they also showed that switching SUMOylation off caused these cells to die, since the stresses that the hyperactive gene caused them were too great.

"The tumours stopped growing and many of them melted away," said Dr Thomas Westbrook, a senior author of the report.

"For 30 years, scientists have tried to attack [the Myc gene]. However, it has not been amenable to the drugs we have", he added.

"Now we have to take advantage of the stresses the oncogene puts on the cancer cell and determine if we can ramp those up to kill the tumour"

Victoria Cowling, a Cancer Research UK-funded scientist at the University of Dundee, said: "Myc is a gene found in every cell in our bodies. Over 20 years ago, researchers discovered that it was hyperactive in cancer cells, and we now know that this hyperactivity is involved in many types of cancer.

"Developing treatments to directly switch off hyperactive Myc is notoriously difficult, so many experimental approaches focus on working out why cancer cells tolerate the stress of having a hyperactive gene rather than die off. For a cell to survive with high levels of Myc and divide uncontrollably - i.e. become cancerous - it must adapt.

"This early lab research found that human breast cells can only cope with high levels of Myc if they also switch on a process called SUMOylation, which alters the behaviour of many cellular proteins. Significantly, by stopping this process, the researchers switched off Myc's cancer-causing activity, but did not affect healthy cells.

"It will be exciting if this approach can be developed into a way to treat people whose cancers are driven by hyperactive Myc genes. Although this is a long way off, it could one day prove a powerful weapon against cancer."

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Triple drug combination effective in HER2-positive breast cancer

Wednesday 7 December 2011

Italian researchers have shown that the effect of treating women before surgery with trastuzumab (Herceptin) and docetaxel for HER2-positive breast cancer is improved by adding another 'Herceptin-like' drug called pertuzumab.

Experts at the San Raffaele Cancer Centre in Milan found that adding pertuzumab to a woman's treatment improved the rate at which her cancer completely disappeared by more than half after just four cycles (12 weeks) of treatment, compared with the treatment with just trastuzumab and docetaxel.

The phase II study - published in the Lancet Oncology - involved 417 previously untreated women with an aggressive type of early HER-2 positive disease.

About one in five women with breast cancer have HER2-positive disease, meaning that their tumour produces too much of the HER2 protein. Trastuzumab is a monoclonal antibody that blocks the cancer-causing activity of HER2. It's a standard treatment for women with this type of breast cancer.

Pertuzumab is an experimental drug that also targets HER2, but in different way to trastuzumab.

Almost half (46 per cent) of women in the study who received the new triple combination before surgery had a pathological complete response - defined as complete absence of tumour cells in surgically removed breast tissue. This compared with 29 per cent of women given standard therapy.

The study also revealed that 17 per cent of women benefited from a combination of pertuzumab and trastuzumab without the addition of chemotherapy. That raises the possibility of a potential non-chemotherapy treatment for HER2-positive breast cancer patients in the future.

The study's lead author, Luca Gianni, said the tumour response to the new triple combination is one of the highest reported to date, despite just a short treatment time. But he cautioned that further investigation is needed before a chemotherapy-free HER2 targeted therapy can be established.

The study also found that the new triple combination did not significantly increase side effects compared with the other regimens.

Dr Carlo Palmieri, a Cancer Research UK-funded breast cancer expert at Imperial College London, said: "This interesting study shows the benefits of using another HER2-directed treatment called pertuzumab alongside trastuzumab (Herceptin) in women with HER2-positive breast cancer.

"It's particularly interesting that a small number of women on this study benefited from combination antibody treatment without chemotherapy. This holds the potential in the future for a possible non-chemotherapy treatment for HER2-positive breast cancer. But we''ll need to develop tests to pinpoint such women in the clinic.

"Further work will show if these impressive tumour responses translate into better survival rates. This will involve larger trials using pertuzumab with trastuzumab after surgery, not before as in this study."

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Chemo after breast cancer surgery cuts deaths by one-third

Tuesday 6 December 2011

Women with breast cancer who were given chemotherapy following surgery fared better than women who were given no chemotherapy, according to a large University of Oxford study funded by Cancer Research UK and others.

The study looked at 123 trials involving around 100,000 women with breast cancer over the last 40 years and revealed that mortality rates were one-third lower among women given both treatments.

The findings - also supported by the Medical Research Council and the British Heart Foundation - have been published in the Lancet journal.

The researchers studied the trials of various older chemotherapy regimens, and found that standard 1980s chemotherapy reduced breast cancer deaths by around one-quarter. More modern treatments further reduced this risk.

The reduction appeared to apply to all women, irrespective of age, how big the tumour was, whether it had started to spread to the local lymph nodes and of whether or not it was oestrogen-receptor (ER)-positive.

The researchers also found that chemotherapy plus hormone therapy was even more effective than hormone therapy alone.

Study leader Sir Richard Peto said: "Most breast cancers are ER-positive, and for ER-positive disease that appears to have been completely removed by surgery the 10-year risk of recurrence and death from breast cancer can be reduced by at least half by giving a few months of modern chemotherapy plus 5 years of endocrine [hormone] therapy."

Kate Law, director of clinical and population research at Cancer Research UK, said: "This large and comprehensive analysis confirms that more widespread use of chemotherapy to treat breast cancer after surgery has had a major impact on saving lives.

"In the UK we've seen a dramatic drop in death rates for breast cancer since the 1980s and this research shows us just how improved treatments have contributed to this success.

"Modern day treatments are not without side effects but we hope that current research will make treatment more tailored to individual cancers leading to further improvements in the future."

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Powerhouse of cells 'hyperactive in cancer'

Thursday 1 December 2011

New US research suggests that the way cancer cells produce energy may be different than previously thought, and that an already available drug could kill tumours by depriving them of their power supply.

Mitochondria are the 'powerhouses' of normal cells - they create chemical energy used to fuel the cell.

It's thought that cancer cells mostly generate energy in a different, more inefficient, process that doesn't use mitochondria, known as the Warburg Effect.

It's been debated for decades how much cancer cells also depend on their mitochondria for their energy.

Earlier work by the same team suggests that the inefficient 'Warburg' energy production actually takes place in the normal cells that surround a tumour, rather than in cancer cells themselves. And this process then provides fuel for mitochondria in cancer cells, feeding the growth and spread of tumours spread.

They've coined this the "Reverse Warburg Effect," the opposite of the existing paradigm.

In the new research, published in the journal Cell Cycle, Professor Michael Lisanti at Thomas Jefferson University took tissues samples from breast cancer patients and showed that that tumour cells have increased mitochondrial activity, whereas other nearby cells do not.

Dr Lisanti said: "We and others have now shown that cancer is a 'parasitic disease' that steals energy from the host - your body - but this is the first time we've shown in human breast tissue that cancer cell mitochondria are calling the shots and could ultimately be manipulated in our favour."

The researchers also suggest that the disease could potentially be tackled by blocking this process with chemicals that interfere with mitochondria, such as metformin, an off-patent generic drug currently used to treat diabetes.

The team also looked at the activity of genes in more than 2,000 human breast cancer samples to compare the activity of mitochondria in cancer cells with their activity in normal cells. 

They found that human breast cancer cells had increased levels of mitochondrial activity, whereas surrounding tissues had little or no mitochondrial activity.

Dr Lisanti said: "Mitochondria are the 'Achilles heel' of tumour cells and we believe that targeting mitochondrial metabolism has broad implications for both cancer diagnostics and therapeutics, and could be exploited in the pursuit of personalised cancer medicine."

Dr Patrick Pollard, a Cancer Research UK cancer metabolism expert at the University of Oxford, said the work showed how important research into cancer energy metabolism was. 

"This study suggests that some breast cancer cells can hijack nutrients from neighbouring cells and metabolise them through their own mitochondria – the powerhouse of most normal cells - giving the cancer a strong growth advantage. 

"Results of studies like this vary at the moment. But this work highlights the importance for us to keep increasing our understanding of metabolism in normal cells compared to cancer cells, which may help to define new routes to therapy for some breast cancers,” he added.

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Drug boosts survival when breast cancer spreads to brain

Wednesday 30 November 2011

Cancer Research UK Press Release

Treatment with lapatinib could extend survival in women with Her2-positive breast cancer that has spread to the brain, according to research published today (Wednesday) in the British Journal of Cancer1.

Researchers at the Medical University of Vienna looked at the average survival of a group of 43 women with Her2-positive breast cancer that had spread to the brain – 28 had been treated with herceptin and 15 had also received lapatinib. While the women treated with herceptin survived for 13 months on average, more than half who were treated with lapatinib were alive after two years2.

This group were all compared with a control group of 37 women who were treated before the use of herceptin became routine and received no targeted treatment. In this group women treated with chemotherapy survived for nine months on average and those given radiotherapy only survived an average of three months.

Her2-positive breast cancer is more likely to spread to the brain and this problem has been increasing in the last decade. Lapatanib is a type of biological therapy called a protein tyrosine kinase inhibitor, which blocks a group of proteins that stimulate cancer cells to grow.

Unlike many other drugs, lapatinib is a small molecule that is more likely to cross the blood-brain barrier.

Professor Guenther Steger, study author based at the Medical University of Vienna, said: “These results are very promising, but we’ve only studied a small and very specific group of women. We now need to look at the effect of lapatinib in a larger group of women with Her2-positive breast cancer to see if the same improvements in survival are seen.”

Dr Julie Sharp, senior science information manager at Cancer Research UK, said: “Women with Her2-positive breast cancer appear to have a greater risk of their disease spreading to the brain, which is very difficult to treat.. If lapatinib is proven to work in a larger group of women we could have a powerful new approach to prevent and treat the spread of breast cancer to the brain.”

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First patients enrolled in project to improve NHS cancer gene testing

Monday 21 November 2011

Cancer Research UK Press Release

Cancer Research UK has started recruiting patients for a pioneering initiative to demonstrate how genetic tests could be used within the NHS to help match cancer patients to the most appropriate treatment, while building a database of information for research into new targeted therapies.

The charity’s multi-million pound Stratified Medicine Programme ultimately aims to establish a world-class NHS genetic testing service for cancer patients in the UK. This means that, as and when new targeted treatments become available, doctors will have access to the tests they need to help them decide which drugs are best for their patients.

Medical staff in seven of Cancer Research UK’s existing Experimental Cancer Medicine Centres (ECMCs) will be asking up to 9,000 patients to participate in the first phase of the Programme, which covers six different tumour types: breast, bowel, lung, prostate, ovarian and melanoma skin cancer.

The ECMCs are: The Institute of Cancer Research (ICR) in London, Leeds, Edinburgh, Cambridge, Cardiff, Glasgow and Manchester, collectively covering more than 20 hospitals across the UK.

Patients will be asked to give consent for a small sample of their tumour to be sent to one of three leading NHS genetic testing labs – based at The Institute for Cancer Research in London, Cardiff All Wales Regional Molecular Genetics Laboratory and the West Midlands Regional Genetics Laboratory in Birmingham – where DNA will be extracted and analysed for a range of molecular faults linked to cancer.

This information will be stored alongside other relevant clinical information to allow researchers to compare the success of different treatments in relation to specific faults within cancer cells.

So although the Programme will not alter patients’ treatment at this stage, it’s hoped it could help scientists design better targeted treatments in the future.

Wendy Payne, 55, who is being treated at Addenbrooke's Hospital in Cambridge, is one of 240 patients who are so far taking part in the programme. She was diagnosed with ovarian cancer in March 2011 after a CT scan.

Mrs Payne said: “I was very keen to take part in the Stratified Medicine Programme because I think much more can and should be done to help patients get the right drugs in future.

“Finding out I had cancer was terrifying but it’s incredible to think that the tumour which could have killed me can now be used to develop more targeted drugs in future. Even though I won’t benefit from that research, it’s comforting to think that my experience with cancer will be helping others who are diagnosed in future.”

Cancer Research UK, AstraZeneca and Pfizer are funding the £5.5 million programme. The charity’s share is being funded through its Catalyst Club - a pioneering venture to raise £10 million to propel forward the use of personalised cancer treatment, including Cancer Research UK’s Stratified Medicine Programme.

The initiative is closely aligned with the government’s Technology Strategy Board (TSB)’s £6 million investment in the development of tests for analysing a tumour’s genetic profile and secure software that can link this information to relevant clinical information.

James Peach, director of Cancer Research UK’s Stratified Medicine Programme, said: “In the ten years since the Human Genome Project was completed we’ve made huge progress in unraveling the genetic basis of cancer and understanding what drives it at a molecular level. We know that prescribing certain drugs according to the genetic basis of the tumour can improve the chances of successful treatment. And by hardwiring research into the day-to-day care of cancer patients, we can harness the power of the NHS to bring personalised medicine a step closer to reality.

“This programme marks the beginning of the journey, and there is much to be done before we can bring the benefits of personalised medicine to every cancer patient. But I’m confident that within the next few years we’ll see personalised medicine changing the face of cancer treatment and saving many more lives from cancer.”

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Cancer Research UK launches nine high-tech gene projects

Friday 18 November 2011

Cancer Research UK Press Release

Unravelling the genetic secrets behind a range of cancers - from understanding how certain genes control cancer to determining how the disease evades treatment - is the aim of a new initiative from Cancer Research UK.

The Genomics Initiative will use the latest high-tech gene sequencing machines to address specific research questions that until now were impossible to answer.

The latest sequencing technology allows researchers to scan all of the genes in a cancer – like reading an instruction manual for the disease – and identify each of the cancer causing faults a million times faster than the Human Genome Project ten years ago.

The genes involved in cancer not only cause the disease but also drive its changes between different forms, influence how aggressive it is and whether certain treatments will work.

Armed with this knowledge, the researchers will be able to piece together information that will tell them about people at greater risk of cancer, pick the right treatments for the disease and start developing new drugs.

The Genomics Initiative is being funded by Cancer Research UK’s Catalyst Club – a pioneering venture to raise £10 million for various research projects, including the Genomics Initiative, on personalised medicine for people with cancer.

One of the projects will look at rare types of skin cancer. The study, led by Professor Richard Marais at The Institute of Cancer Research, will look for the genes that make certain types of skin cancer more aggressive with the ultimate aim of improving treatments for patients with these rare forms of the disease.

Professor Marais said: “We urgently need new drugs to treat these rare but very aggressive forms of skin cancer. This project will let us build a bigger picture of the genes that are involved in the disease giving us an insight into the inner workings of skin cancer.”

Another project will attempt to understand why kidney cancer has unique genetic defects in different parts of the same tumour. This can result in a tumour biopsy not giving the full picture of what is going on in the cancer. Professor Charles Swanton, at Cancer Research UK’s London Research Institute, is trying to understand why this happens and hopes to find new markers that predict who will benefit from targeted treatments.

Professor Swanton said: “Attempts to identify markers to predict if patients with kidney cancer will respond to distinct targeted drugs have so far been unsuccessful. Our research is investigating whether this may result from the genetic variation within single tumours, such that an oncologist may not be able to fully trust the genomic information present in a single biopsy. We hope to be able to find markers for drug resistance that are common across multiple biopsies in the same tumour, that may guide the treating clinician to determine the right treatments are given to each patient."

The other seven projects are:

• Finding genes that put people at a higher risk of developing pre-cancerous growths called polyps and bowel cancer

• How follicular lymphoma transforms into the more aggressive B cell lymphoma

• Sequencing the genes in an aggressive form of childhood brain cancer

• Looking for the genes that affect how pancreatic cancer patients respond to treatment

• Identifying key genes in skin cancer in people with no family history

• Studying 1,000 women to find new genes linked to breast cancer

• Understanding how stem cells in leukaemia pick up new genetic faults

Dr Harpal Kumar, Cancer Research UK’s chief executive, said: “We’re delighted to launch the Genomics Initiative, which takes advantage of powerful new technologies to drive an exciting area of cancer research. We know that mistakes in genes are behind cancer, and they also drive how cancer act and respond to treatment. Understanding this better will bring real benefits for patients in the future, playing an essential role in the push towards personalised cancer treatment.”

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