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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Sunbed skin cancer risk double that of mediterranean midday summer sun

Thursday 17 January 2013

Cancer Research UK Press Release

The average skin cancer risk from sunbeds is more than double that of spending the same length of time in the Mediterranean midday summer sun – according to new research1 from the University of Dundee and published today in the British Journal of Dermatology.

The study tested levels of ultraviolet (UV) radiation from 400 sunbeds in England and found that nine in ten of the sunbeds tested emitted UV radiation at levels above British and EU standards. The average strength of radiation was approaching twice the recommended limit.

The Cancer Research UK study also compared the skin cancer risk from using these sunbeds with the risk from the Mediterranean midday summer sun. The average skin cancer risk from the sunbeds tested was more than twice that of spending the same length of time in the Mediterranean midday summer sun, with one of the sunbeds producing a skin cancer risk six times higher than the sun.

Professor Harry Moseley, consultant medical physicist at University of Dundee and lead author, said: “The development of high-power sunlamps, along with clear failures of the sunbed industry to regulate themselves effectively, is putting young people at an even greater risk of skin cancer than we previously thought.

“We hope that these findings will make people think twice before using sunbeds as you can’t be sure how much radiation you’re exposing yourself to when you try to top-up a tan. People need to be encouraged to take better care of their skin, otherwise the cases of malignant melanoma, the most dangerous form of skin cancer, will continue to increase in England.”

Yinka Ebo, senior health information officer at Cancer Research UK, said: “It’s worrying to see that so many sunbeds in England are not meeting the safety standards. This strengthens our advice that using a sunbed just isn’t worth it.

“Research has already shown that using sunbeds for the first time before the age of 35 increases the risk of malignant melanoma by 87 per cent. They’re not going to do you any good – the best case scenario is that they’ll age and damage your skin; the worst case scenario is a cancer diagnosis and potentially death.”

The strength of UV from sunbeds was found to be no different in those areas where the licensing of sunbeds is required compared to unlicensed areas.

The British and European standard2 was introduced in 2003 and sets out a maximum level of UV radiation to be emitted by sunbeds used for cosmetic purposes. The findings suggest that there is much more work for local authorities to do to ensure that standards are being met by tanning businesses.

Nina Goad of the British Association of Dermatologists explained: “Product safety standards are there to protect the public and the government needs to step up its regulation of the industry.

“England is sadly trailing behind the rest of the UK in this matter. We need proper regulation, covering issues like safety of equipment and health warnings for clients and enforceable through inspections of premises.”

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For media enquiries please contact the Cancer Research UK press office on 020 3469 8300 or, out-of-hours, the duty press officer on 07050 264 059.

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US researchers warn against apps to diagnose skin cancer

Wednesday 16 January 2013

Smartphone apps that claim to detect skin cancer could delay proper medical diagnosis and potentially life-saving treatment, US expert have warned.

Apps that analyse photographs of the skin to detect possible melanoma skin cancer often give inaccurate results, according to scientists from the University of Pittsburgh School of Medicine.

Researchers used four apps to analyse 188 images of skin lesions. Three of the apps incorrectly classified 30 per cent or more melanomas as 'unconcerning'.

"These tools may help patients be more mindful about their health care and improve communication between themselves and their physicians," said Dr Laura Ferris, one of the researchers.

"But it's important that users don't allow their 'apps' to take the place of medical advice and physician diagnosis."

Every year around 12,800 people in the UK are diagnosed with melanoma, the most serious form of skin cancer. And around 2,200 die from the disease.

The study concentrated on apps that are available on the two most popular smartphone operating systems.

Each of the apps is designed to analyse digital images taken with the phone to advise the user whether their moles are potential melanomas or if they are likely to be benign.

The apps work in different ways. Some returned results based on automated algorithms, whereas one sent images to a skin specialist.

All of the apps featured disclaimers stating they were for educational purposes only, but researchers said there was a risk that patients might rely too heavily on the verdict generated by the phone.

"If they see a concerning lesion but the smartphone app incorrectly judges it to be benign, they may not follow up with a physician," said Dr Ferris.

"Technologies that decrease the mortality rate by improving self- and early-detection of melanomas would be a welcome addition to dermatology. But we have to make sure patients aren't being harmed by tools that deliver inaccurate results."

Dr Claire Knight, health information manager at Cancer Research UK said the finding was worrying.

"Using a mobile phone app may seem like a convenient alternative to visiting the doctor about any changes to your skin, but if the app gets it wrong a potentially deadly skin cancer could be missed," she said.

"If you notice any changes in the size, shape or colour of a mole or any other change to a mole or normal patch of skin, consult your doctor, not your phone."

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NICE recommends new treatments for advanced melanoma

Friday 2 November 2012

Two new treatments for advanced melanoma skin cancer have been recommended for use by NICE, the healthcare guidance body for England and Wales.

Final draft guidance documents have now been issued for both vemurafenib and ipilimumab. Manufacturers of the treatments have agreed to provide discounts.

Vemurafenib, which is also known as Zelboraf and is manufactured by Roche, has been recommended for the treatment of melanoma that has spread. And ipilimumab, marketed by Bristol-Myers Squibb under the name Yervoy, is recommended for the treatment of advanced melanoma in people who have previously received chemotherapy.

Professor Peter Johnson, Cancer Research UK's chief clinician, said: "We're delighted that discounts on the price of these drugs mean that NICE has been able to approve vemurafenib and ipilimumab for routine use on the NHS.

"Although they are not cures, these treatments represent real signs of progress through our understanding of biology for people with advanced skin cancer - a disease where new treatments are long overdue."

The Health Technology Evaluation Centre director at NICE, Professor Carole Longson, said that without the introduction of new treatments, the prospects for patients with advanced melanoma are "very poor". Their quality of life is also likely to be affected by the condition, she added.

Vemurafenib and ipilimumab are the first new drug treatments for advanced melanoma for over a decade. Currently, the disease is managed with a chemotherapy drug called dacarbazine.

In respone to initial negative verdicts from NICE, the manufacturers of both treatments issued additional analysis. This, along with the discounts offered, meant that NICE was able to rule that the treatments represent a cost-effective use of NHS resources.

Cancer Research UK's Professor Johnson added: "This is a good example of NICE and the pharmaceutical companies working together to ensure that effective cancer treatments get from research to the patients who need them. We want to see responsible pricing from the outset so that patients are not left in limbo."

Professor Longson described the new drugs as "breakthrough treatments" for skin cancer and as such represent a major step forwards for patients.

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New route to skin cancer in red-haired people uncovered

Thursday 1 November 2012

The increased risk of developing skin cancer in people with red hair and fair skin may be down to more than a lack of natural protection against ultraviolet (UV) radiation, an American study has found.

In fact, the type of skin pigment predominantly found in red-haired, fair-skinned individuals may itself contribute to the development of melanoma, the most serious form of skin cancer, according to research published in Nature.

But experts were keen to highlight the continued importance of staying safe in the sun, as the vast majority of skin cancers are caused by overexposure to UV radiation from the sun, or from sunbeds.

Our skin contains several types of the pigment melanin. One of these is called eumelanin, a dark brown or black form predominant in individuals with dark hair or skin.

But a lighter blond-to-red pigment called pheomelanin is predominant among those with red hair, freckles and pale skin.

While research has proved that red/blond melanin is less effective at mitigating against the effects of UV damage, a minority of fair-skinned people develop melanomas that can't be explained by their being relatively unprotected against UV radiation.

Researchers at Massachusetts General Hospital (MGH) have discovered one such non-UV-related route to melanoma.

The team looked for additional contributors to melanoma development in mice that were almost genetically identical except for the gene that controls the type of melanin produced.

One group of dark-coloured mice had the typical variant leading to a predominance of dark melanin, while another had the red-blonde type.

Researchers activated the melanoma-associated cancer gene in patches of the animals' skin, expecting that no melanomas would form without additional environmental stresses like exposure to UV radiation.

To their surprise they found that within months half of the mice with the redhead pigment had developed melanomas, compared to only a handful of the mice with the darker melanin.

A third group of mice that were incapable of producing any pigment, known as "albino redheads", didn't develop melanoma in the absence of UV radiation, leading researchers to conclude that the red-blond pigment could itself be a cause of melanoma.

Professor Julia Newton-Bishop, from the Cancer Research UK Centre at the University of Leeds, said: "This is a very interesting finding and contributes to our understanding of why red-headed, freckly people are particularly prone to skin cancer.

"There's no doubt that the majority of melanomas are caused by UV radiation from the sun - and protecting your skin in the sun is crucial - but this work suggests that there may be other paths to melanoma in red-haired, freckly people."

She also said that the work further emphasises that fair-skinned people with freckles should keep an eye out for any new moles or blemishes on their skin or any changes to existing ones.

Dr David Fisher, chief of the MGH Department of Dermatology, said: "Right now we're excited to have a new clue to help better understand this mystery behind melanoma, which we have always hoped could be a preventable disease."

He added: "The risk for people with this skin type has not changed, but now we know that blocking UV radiation - which continues to be essential - may not be enough.

"It will be important for these individuals to be aware of changes in their skin and never hesitate to have something checked by a dermatologist, even if they have scrupulously protected themselves from sun exposure, which we continue to encourage."

Dr Fisher said that around six out of seven melanomas are treatable if discovered early, adding that the new discoveries could help pave the way for more effective sunscreens.

Cancer Research UK's Professor Newton-Bishop predicted that the research could lead to new ways to prevent melanoma in people with genetic faults that increase their risk of the disease.

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Study links sunbeds to most common forms of skin cancer

Wednesday 3 October 2012

As well as increasing the risk of melanoma skin cancer - the most serious form of the disease - sunbed users are also at increased risk of developing the much more common forms, according to US researchers.

The link between sunbed use and malignant melanoma has been established for some time. But the study confirms recent studies that it can also cause both types of non-melanoma skin cancer: basal cell carcinoma and squamous cell skin cancer.

These cancers are far less dangerous than melanoma, but much more common - an estimated 100,000 people are diagnosed in the UK every year, and the diseases cause around 550 deaths a year.

Scientists from the University of California in San Francisco reviewed 12 studies of 9,328 people with non-melanoma skin cancer.

People who used sunbeds increased their risk of developing the squamous cell type by 67 per cent and their risk of basal cell carcinoma by 29 per cent.

According to the American Cancer Society, around 2 million people are diagnosed with basal and squamous cell skin cancer each year in the US. The study researchers, led by Professor Eleni Linos at the University of California, estimate that sunbeds cause over 170,000 cases of non-melanoma skin cancer every year in the US alone. The study does not provide UK-specific estimates.

The study, published in the journal BMJ, shows there is "a critical period" during early life where exposure to the rays of tanning beds is particularly dangerous.

It found that the risk of basal cell carcinoma was particularly high in people who started using sunbeds before the age of 25.

Cancer Research UK said the study shows that sunbeds are not a safe alternative to sunbathing.

Cancer Research UK's health information manager, Dr Claire Knight, said: "This study adds to the already large body of evidence showing that sunbed use increases the risk of several types of skin cancer. This includes malignant melanoma, the most serious type of skin cancer, but also non-melanoma skin cancer, which although generally less serious is far more common."

In the UK under-18s already face restrictions on sunbed use, and unsupervised tanning salons are banned. Businesses that fail to comply with the regulations and allow under-18s to use sunbeds face fines of up to £20,000.

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New Cancer Research UK trial will shed light on risks and benefits of sun exposure

Wednesday 15 August 2012

Cancer Research UK Press Release

Cancer Research UK has today launched a trial investigating the health benefits and risks of spending time in the sun. It is hoped the trial will help solve years of controversy surrounding vitamin D, the ‘sunshine vitamin’, and how much sun is too much.

The amount of sun exposure needed to make enough vitamin D varies from person to person, largely dependent on skin colour. But at the moment there are no clear guidelines about what level of sun exposure is needed to produce enough vitamin D without causing excessive DNA damage to the skin, which can cause skin cancer.

This Cancer Research UK-funded trial will use simulated sunlight to determine whether certain amounts of sun are beneficial for certain skin types, and how much is too much.

Study leader Professor Lesley Rhodes, from the University of Manchester, said: “There’s no doubt that too much sun can seriously increase skin cancer risk, but we know there are also important benefits to going out in the sun, such as making enough vitamin D. This study is about finding that balance, so we can offer people of all skin colours the best possible advice about how much sun is safe for them.”

Seventy-five healthy volunteers aged 18-45, and with a range of skin colours, are being recruited to take part in the study in the Photobiology Unit, Dermatology Centre at Salford Royal in Greater Manchester.

Wearing standardised clothing, participants will be exposed to simulated sunlight - equivalent to that of a summer’s day in Manchester - for short periods of time. Blood and urine samples will be taken after exposure and examined for chemicals that indicate vitamin D levels and DNA damage. Small skin samples will also be taken from some volunteers and analysed for any signs of DNA damage.

Kalani Hargrove, who is studying a Masters in sociology at the University of Manchester and is one of the first volunteers to take part in the study, said: “Before I signed up for the study I was given an information sheet that explained everything. Taking part has been really simple and straightforward so far and it’s been fascinating to see firsthand how medical research is carried out. I’m delighted to be taking part in research that will hopefully lead to a better understanding of how people of all skin colours can enjoy the sun safely.”

Sara Hiom, director of information at Cancer Research UK, said: “Sun is a really important source of vitamin D, but the amount of sun needed varies from person to person. We know that people with paler skin make vitamin D faster, but burn more easily, than those with darker skin, but it’s still not completely clear where the balance lies in terms of getting enough vitamin D, without excessively increasing skin cancer risk.

“Studies like this, which use simulated sunlight so we can compare the results for people with different skin types, will tell us much more precisely how much sun is safe for different people. In the meantime, continue enjoying the sun, but remember that the amount of time you need to spend in it to make enough vitamin D is always less than would make your skin redden. The best way to protect your skin from sunburn is to use shade, clothing and at least factor 15 sunscreen applied generously and regularly.”

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'Tougher actions' needed to reduce deadly toll of sunbeds

Tuesday 24 July 2012

Every year, sunbeds cause more than one in twenty cases of the most serious type of skin cancer in Europe, French and Italian research has revealed.

The new study estimates that 5.4 per cent of the 63,942 new cases of melanoma skin cancer diagnosed in 2008 were linked to sunbed use.

Cancer Research UK said the study provides "the strongest evidence yet of the link between sunbed use and skin cancer."

Sunbeds are the second most significant environmental cause of skin cancer, after exposure to UV radiation from the sun itself.

The new research looked at data from 27 studies across Europe.

The analysis found that anyone who had used a sunbed had a 20 per cent higher risk of developing skin cancer compared with those who had never used one. This figure rose to an 87 per cent higher risk for people who first used sunbeds before the age of 35, and an additional 1.8 per cent increase in risk for every further sunbed session per year.

The authors say the sunbed industry is not able to "self-regulate effectively" but instead give "information intended to deceive consumers".

The researchers call for tougher regulations governing the use of sunbeds across Europe. They cite Australia, and European countries such as the UK, where under-18s face restrictions on sunbed use and unsupervised tanning salons are banned.

Dr Claire Knight, health information manager at Cancer Research UK, said the study also found that using sunbeds increased the risk of two other less serious but more common types of skin cancer - basal cell carcinoma and squamous cell carcinoma.

"It's now clearer than ever that sunbeds aren't a safe alternative to tanning in the sun. If you really want a tanned appearance it's better to fake it," she added.

Dr Knight also advised that skin cancer is easier to treat when found at an early stage, pointing out the importance of reporting unusual changes to the skin to the doctor without delay.

The study is published in the BMJ and was carried out by experts from the International Prevention Research Institute in France and the European Institute of Oncology in Italy.

• Read in-depth analysis on the Cancer Research UK blog

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Healthy cells around tumours 'may fuel resistance to cancer drugs'

Wednesday 4 July 2012

Tumour cells could be being helped by healthy cells to escape cancer drugs killing them, according to US research.

Healthy cells that make up the 'micro-environment' in and around tumours produce molecules that protect tumour cells from the killing effects of drugs, say experts from the Broad Institute, the Dana-Farber Cancer Institute and Massachusetts General Hospital.

The work, published in the journal Nature, could help to explain why drugs that seem to effectively treat cancer in the lab sometimes only produce partial responses in cancer patients.

Dr John Brognard, from Cancer Research UK's Paterson Institute for Cancer Research in Manchester, said: "We know that tumours can sometimes resist even the most powerful cancer drugs, and understanding what drives this resistance is crucial.

"This fascinating research shows that tumour cells don't just evolve their own ways to combat cancer drugs, but that they might be able to enlist the help of surrounding healthy tissues."

The team grew different types of cancer cells by themselves or together with normal cells to see whether healthy cells could contribute to drug resistance.

They described their results "striking" - drugs that killed cancer cells grown in isolation were rendered ineffective when tumour cells were grown alongside healthy cells.

Dr John Brognard said: "On the surface this is daunting - healthy cells around a tumour could give tumours an innate ability to resist drugs even before the treatment starts. But work like this gives us hope - it shows we can start to unpick these resistance mechanisms early on, even before a new drug is widely used in the clinic."

The researchers went on to focus on melanoma, the most serious form of skin cancer, which is sometimes caused by a fault in a gene called BRAF.

They looked at melanoma cells grown in the lab and found a protein called hepatocyte growth factor (HGF) seemed to help them resist drugs that inhibit BRAF.

The team confirmed the results in melanoma patients. HGF levels in biopsies taken from melanoma patients were low in those who responded well to treatment, and higher in those who responded poorly to treatment.

The research suggests that a combination of BRAF inhibitors alongside HGF-targeted drugs may be effective in fighting melanoma.

Another paper published in the same issue of Nature by Jeffrey Settlemen and colleagues confirms that HGF helps melanoma cells resist drugs that inhibit BRAF.

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New drug is 'greatest advance' for basal cell skin cancer

Wednesday 6 June 2012

A new drug is effective against advanced forms of the most common type of skin cancer, according to US research.

Three new research papers published in the New England Journal of Medicine show that the drug vismodegib (also called Erivedge) can treat and prevent basal-cell carcinomas (BCCs), even those that have spread to other parts of the body.

The drug was approved by the US authorities in January 2012. It is awaiting approval by European regulators.

In the journal's editorial, Dr John Lear from Manchester Royal Infirmary said: "It is a landmark day for patients with basal cell carcinoma and all those involved in their care - the greatest advance in therapy yet seen for this disease."

But he also cautioned that side effects could be unpleasant, including taste loss, hair loss, and muscle cramps.

One paper outlines the results of a clinical trial in which vismodegib was given to patients with Gorlin syndrome, a rare genetic disease in which individuals have tens to hundreds of BCCs.

There is currently no cure for Gorlin syndrome - patients usually undergo regular surgery to remove the tumours. But vismodegib greatly slowed the progress of the disease. On average, people who took the drug developed only two tumours a year, compared with 29 in people who took a placebo.

A second clinical trial published today was the basis for the approval of vismodegib in the US five months ago. The trial shows that the drug is effective for some people with previously 'untreatable' BCCs - advanced tumours that are extremely large ('locally advanced') or have spread (metastasised) to other parts of the body.

The drug caused tumours to shrink in 43 per cent of patients with locally advanced disease, and 30 per cent of patients with metastatic disease.

Vismodegib works by targeting a molecular process inside cells known as the 'hedgehog' signalling pathway, whose precise functioning was unravelled by Cancer Research UK scientists in the 1990s. 

This pathway, which involves a gene known as 'hedgehog', is activated in people with BCC in a way that does not normally occur in healthy cells. Vismodegib limits this effect.

A third research paper outlines the use of vismodegib to treat a man who had BCCs all over his body, but who did not have Gorlin syndrome.

Researchers analysed his genetic material and found faults that suggested he should respond to vismodegib - and he did. 

Dr Safia Danovi, senior science information officer at Cancer Research UK, said: "Cancer Research UK played a key role in the early development of this drug and we're delighted that it has reached this important milestone. If vismodegib is approved in the UK, it will provide advanced BCC patients an alternative to potentially disfiguring surgery, which until now has been the only way of controlling this disease.

"This is great news for patients and it's thanks to the generosity of our supporters that we're able to invest in the kinds of early stage research that can so often spark advances like this."

She added that the charity hopes that this vismodegib will receive its European licence quickly, so that UK patients can benefit as soon as possible from the drug.

Basal cell carcinoma affects about 100,000 people in the UK, and is often caused by excessive exposure to UV radiation such as sunlight.

The vast majority of people are diagnosed at an early stage, before it has spread and when surgical treatment is an effective, although potentially disfiguring, cure.

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Experimental drug could target melanoma that spreads to brain

Friday 18 May 2012

A new drug could be effective for the treatment of melanoma that has spread to the brain, according to an early-stage clinical trial.

Patients from the US and Australia with advanced melanoma - the most serious form of skin cancer - were treated with an experimental drug called dabrafenib.

The drug substantially reduced the size of tumours that had spread to the brain.

Dabrafenib has been developed to treat melanoma in patients whose cancer is caused by faults in a gene called BRAF - first linked to cancer by UK researchers in 2002.

An altered form of this gene is present in about half of people with advanced melanoma and in several other types of cancer including some thyroid, colorectal, ovarian and lung cancers.

The phase I trial - published in the Lancet and funded by drugs company GlaxoSmithKilne - was primarily designed to establish the safe dose of dabrafenib. It involved 184 patients with incurable tumours, 156 of whom had melanoma.

Dr Gerald Falchook from the University of Texas MD Anderson Cancer Centre conducted the study with colleagues at Melanoma Institute Australia and Westmead Hospital in Sydney.

He said: "Brain metastases in most [nine of 10] patients given dabrafenib reduced in size, with four patients' metastases completely resolving.

"Patients with melanoma and brain metastases typically survive for less than five months, yet in this study, all ten patients were alive at this stage One patient remains on treatment at 19 months."

A BRAF-targeting melanoma drug called vemurafenib has already been licensed in the UK.

Dabrafenib not only worked in patients with the type of BRAF fault that vemurafenib has been proven to be effective against, but also against different types of BRAF fault.

Professor Mark Middleton, director of Cancer Research UK's Experimental Cancer Medicine Centre at Oxford, said: "All indications are that dabrafenib could be as effective as the newly licensed melanoma drug vemurafenib, which is available to patients through the Cancer Drugs Fund in England.

"The fact that dabrafenib was also effective for some patients with melanoma that had spread to the brain is really encouraging. This is the first drug to have any activity against these advanced cancers, and this work holds out promise that the whole class of these drugs could be effective for melanoma that's spread to the brain."

"After years of little to shout about, we're finally making progress against this tough cancer."

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Whole-genome sequencing uncovers new skin cancer gene

Wednesday 9 May 2012

US scientists have used high-tech DNA sequencing to uncover a new gene linked to melanoma – the most serious form of skin cancer.

The link between the PREX2 gene and melanoma was identified by scientists from the Broad Institute and Dana-Farber Cancer Institute, in a study published in the journal Nature.

They found that PREX2 was damaged in tumour samples from 44 per cent of 25 melanoma patients involved in the study.

The scientists sequenced the whole genomes - the complete set of DNA in a cell – in tumour samples from the patients, and also sequenced the DNA in samples of their blood, as a reference.

By comparing the tumours’ DNA to the ‘normal’ DNA in the blood, the researchers showed that the degree of genetic damage in tumours’ DNA was greatest in patients who had been in the sun most, confirming that chronic sun exposure has a major role in skin cancer.

They also confirmed the importance of faults in two other genes - BRAF and NRAS - in melanoma. These genes, known to be important in sending cell growth signals, and previously linked to melanoma, were damaged in 24 of the 25 tumours studied.

But significantly, PREX2 was also altered in many of the samples.

When looking at PREX2 in a further 107 tumour samples, the researchers found 14 per cent of them contained the altered gene.
Faults in PREX2 have been previously associated with breast cancer.

Mouse experiments suggested that PREX2 mutations spurred tumour growth in ways yet to be determined.

"We still can't say we know exactly how it works," Dr Levi Garraway, senior author, said. "PREX2 may be in a very interesting new category of mutated cancer genes that point us to at least one and maybe more pathways that would be worth targeting therapeutically in melanoma," he added.

Professor Mark Middleton, director of Cancer Research UK’s Experimental Cancer Medicine Centre at the University of Oxford, said: “After the recent success of drugs targeting the faulty BRAF gene in melanoma, we’re very keen to find other genetic mutations that are important in its growth. This research increases our understanding of the disease, the most deadly form of skin cancer, and suggests new ways to treat it.”

The discovery that BRAF mutations are common in melanoma directly led to the development of a drug, vemurafenib, to target these mutations. The drug is currently being assessed by NICE.

Professor Middleton asaid the study also highlighted the important role played by sun damage in melanoma, and emphasises the need to follow simple measures to enjoy the sun safely.

He advised people to use a combination of shade, clothes and SPF 15 sunscreen to protect their skin in strong sunlight.

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Diabetes treatment doubles skin cancer drug's effectiveness

Saturday 31 March 2012

Cancer Research UK Press Release

COMBINING the experimental drug Avastin (bevacizumab) with the diabetes drug Metformin almost doubles its ability to reduce skin cancer growth, according to a study in Cancer Discovery1.

The researchers – funded by Cancer Research UK, the AICR and based at The Institute of Cancer Research (ICR) - found that treating aggressive skin cancer in mice with just Avastin suppressed tumour growth by 34 per cent.

But, when combined with Metformin, tumour growth was reduced by 64 per cent.  

Professor Richard Marais, lead researcher and director of Cancer Research UK’s Paterson Institute at the University of Manchester, said: “Our results are surprising because combining Metformin with drugs such as Avastin has a much greater effect in suppressing tumour growth than would be expected when looking at the effect of either drug on its own. If we can now show this effect holds true in patients, it could help overcome the resistance we often see in skin cancer patients.”

Intriguingly, melanoma cells – the most aggressive form of skin cancer - treated with just Metformin grew more quickly.

Metformin caused melanoma cells with a BRAF mutation form new blood vessels and accelerate tumour growth.

BRAF mutations are found in around 70 per cent of all melanomas. Professor Marais and colleagues, with support from Cancer Research UK, were the first to discover their role in causing the disease.

Professor Marais added: “Recent research has shown that the common diabetes drug metformin has anticancer properties. But we need to understand the effect it’s having on BRAF melanomas and whether prescribing metformin by itself could potentially worsen the disease.”  

Each year around 11,800 people are diagnosed with melanoma in the UK. Over the last 25 years, rates of malignant melanoma have risen faster than any of the most common cancers.

Professor Nic Jones, Cancer Research UK’s chief scientist, said: “This research points the way to a potentially very effective drug combination to treat the most aggressive form of skin cancer. We now need to see if this combination benefits patients in clinical trials with the hope of making new treatments for skin cancer even more effective.

“Professor Marais’ team, funded through the public’s generous support of Cancer Research UK, are making great strides in turning their discoveries in BRAF into new treatments that could make a real difference for patients with melanoma.”

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Scientists uncover reason for second cancers after targeted melanoma treatment

Thursday 19 January 2012

An international study has uncovered how secondary skin cancers sometimes develop in malignant melanoma patients who are treated with an experimental drug.

The study, published in the New England Journal of Medicine, shows that it might be possible to prevent these extra cancers.

Melanoma is the most serious form of skin cancer, and more than 10,600 people are diagnosed with the disease each year in the UK.

Around half of these patients' cancers have faults in a gene called BRAF, and inhibitor drugs that target these cancers, such as vemurafenib (Zelboraf), have shown tremendous promise in trials.

But between 15 and 30 per cent of patients treated with BRAF inhibitors develop another, less serious form of skin cancer, called squamous cell carcinoma, which needs to be surgically removed.

The study, which involved Cancer Research UK-funded researchers at The Institute of Cancer Research, looked at squamous cell carcinoma tissue taken from 21 malignant melanoma patients who had been treated with vemurafenib in a clinical trial.

It found that almost all of these samples had mutations in a second gene, known as Ras.

These Ras mutations are likely to have been caused by prior skin damage from sun exposure, explained author Dr Antoni Ribas, from UCLA's Jonsson Comprehensive Cancer Centre in the US.

"What vemurafenib does is accelerate the appearance of these skin squamous cell cancers, as opposed to being the cause of the mutation that starts these cancers," he said.

"This is one of the very few times that we understand molecularly why a side effect to cancer treatment is happening. The side-effect in this case is caused by how the drug works in a different cellular setting. In one case it inhibits cancer growth, and in another it makes the malignant cells grow," he added

Professor Richard Marais from The Institute of Cancer Research, who worked on the study and was part of the team that initially linked BRAF mutations and cancer, said the results may enable more patients to benefit from the drug.

"By determining the mechanism by which these [secondary skin tumours] develop, we have been able to devise a strategy to prevent the second tumours without blocking the beneficial effects of the BRAF drugs," he said.

The researchers suggest that a second type of drug, called a MEK inhibitor, could be given alongside vemurafenib, and that this could prevent second cancers. This is now being tested in trials.

Dr Julie Sharp, Cancer Research UK's senior science information manager, said: "This research reveals a possible new approach to avoid the second cancers that affect some malignant melanoma patients taking BRAF inhibitors. The next stage will be to explore these results in more patients in clinical trials to see if this drug combination could treat the original cancer while preventing new cancers from forming."

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'Detox' immune cells linked to skin cancer development

Friday 6 January 2012

A study funded by Cancer Research UK has provided a surprising insight into the development of a form of skin cancer called squamous cell carcinoma, or SCC.

Researchers based at the charity's London Research Institute and King's College London, working with colleagues at Yale University in the US, found that a supposedly beneficial immune cell appears, under some circumstances, to be involved in SCC development.

The cells, known as Langerhans cells, are widely thought to help protect the body from the disease by removing naturally occurring toxins from tissues.

However, the new research suggests the immune cells also have a darker side.

Skin cancers, including SCC, are caused by damage to DNA by various factors. Ultraviolet light is a major cause of DNA damage, but chemical carcinogens like tobacco smoke and industrial pollution also play a role.

Researchers studies mice that lacked Langerhans cells, and found they were completely resistant to DNA damage when exposed to synthetic toxins. As a result, the mice did not develop skin cancer.

The team then confirmed this finding in human tissues, finding the same effect as that seen in the mice. The research was published in the journal Science.

Professor Adrian Hayday, based both at King's College London and Cancer Research UK's London Research Institute, said the results of the research could influence the approach to treatments of certain types of cancer.

He said: "Langerhans cells may activate immunoprotective components of the immune system and so are often regarded as useful in preventing cancer.

"Here we have actually shown that the opposite is also true - they can also play a role in facilitating development of the disease.

"It is seldom recognised that Langerhans cells are primarily 'scavenging garbage collectors', that identify and try to break down harmful compounds.

"They successfully deal with natural toxins that we come into contact with all the time, such as many in food, but they cannot deal well with some common synthetic toxins from sources such as industrial air pollution.

"This study showed that when these cells attempt to process synthetic toxins, their role changes and their attempt to break down these toxins instead creates even more harmful carcinogenic products that spread to neighbouring cells.

Dr Safia Danovi, senior science information officer at Cancer Research UK, said: "We're used to thinking that cancer arises from one rebel cell working alone, but this research challenges that view and shows that the immune system can sometimes trigger skin cancer when the skin is exposed to certain toxins.

"So although immune cells usually help protect us against diseases, the system isn't foolproof and things can go wrong. We need to study this glitch and perhaps, in the future, we'll be able to harness this knowledge to help cancer patients."

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Protein linked to spread of skin cancer

Tuesday 22 November 2011

An international team of researchers working together on both sides of the Atlantic have pinpointed a protein, called P-Rex1, that seems to play a key role in the spread of malignant melanoma - the most deadly form of skin cancer, according to a paper in Nature Communications.

The team, led by researchers from the Cancer Research UK-funded Beatson Institute of Cancer Research in Glasgow, were studying cells called melanoblasts - highly mobile cells involved in the early development of the skin.

Researchers believe that the way melanoblasts move around body tissues very similar to how melanoma cells spread. The major cause of death from melanoma is due to it spreading, or metastasising, from the initial tumour.

The discovery came when the team noticed that mice which lacked the gene that which makes the P-Rex1 protein, had skin cancers that did not spread.

Armed with this knowledge, the research team then tested human melanoma cells and tumour tissue and discovered raised levels of P-Rex1, suggesting that the protein was involved in the movement of the cells.

The discovery will give researchers a better understanding of how the cells work, which in turn enables them to better select a target for developing new treatments.

Researcher Channing Der, a member of the team based at the Lineberger Comprehensive Cancer Center the US, said: "We know that mutations in a gene called BRAF are important for the development of melanoma and several years ago we published a collaborative paper listing 82 proteins that seem to be affected by this genetic pathway. From that list, we focused on P-Rex1."

The BRAF gene was discovered to be involved in melanoma by Cancer Research UK scientists, and this year a drug - vemurafenib - was developed that targets melanomas in which the BRAF gene is defective. This is thought to be the case for around 80 per cent of patients.

The discovery that P-Rex1 is 'downstream' of BRAF - in other words, signals coming from BRAF need to 'pass through' P-Rex1 - is significant because it suggests that drugs that target P-Rex1 could - in theory - help the 20 per cent of people with melanoma whose cancer doesn't have a faulty BRAF gene.

Nell Barrie, senior science information manager at Cancer Research UK, said: "Cancer is difficult to treat once it has spread, and research that helps us to understand how cancer cells travel around the body is helping scientists to target this process with new drugs. Studies like this give us more ammunition against melanoma and other types of cancer, but it's important to remember that it can take years to turn a discovery in the lab into a treatment for patients."

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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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Scientists uncover how cancer stem cells are regulated in common skin cancer

Thursday 20 October 2011

Belgian scientists have discovered that a molecule already targeted by several cancer therapies may play a crucial role in a common form of skin cancer.

The work could spark research into new ways to prevent and treat the disease.

Previous studies suggest that squamous cell skin cancer, like several other types of cancer, contains cells known as cancer stem cells, which are able to continually grow and divide to sustain the growth of tumours.

Squamous cell skin carcinoma is the second-most common form of non-melanoma skin cancer, affecting approximately 10,000 people per year in the UK. Although not as serious as melanoma, it can still spread if left untreated.

The latest study, published in the journal Nature, looked at the activity of a molecule called VEGF in controlling cancer stem cells in the skin. VEGF is known to regulate the growth of new blood vessels - a process known as angiogenesis - by activating a second group of proteins, known as VEGF receptors (VEGFR).

Researchers have already developed several drugs that target this process in cancer patients, with the intention of cutting off the tumour's nutrient supply.

In this latest research in mice, the researchers blocked the activity of VEGF receptors by using an antibody, and found that this not only slowed down blood vessel growth, but also stopped skin cancer stem cells from growing, causing tumours to shrink.

The researchers followed this up by genetically removing VEGF from the skin cancer stem cells and found that this created a defect in their ability to multiply, also causing tumours to shrink.

Researcher Benjamin Beck said: "It was extremely exciting to see the complete disappearance of these tumours only two weeks after the treatment."

The study also found that a VEGF receptor called Neuropilin , or Nrp1, has a crucial role in controlling the growth of cancer stem cells and the formation and growth of tumours.

Oliver Childs, senior science information officer at Cancer Research UK, said: "This is a great example of why high-quality laboratory work to understand the inner working of cancer cells is vital if we're to beat cancer.

"By uncovering a new way that VEGF works in squamous cell skin cancer, this study opens up the possibility of new ways to prevent and treat this cancer. There's a long way to go before any new treatment is available, but this kind of lab work is laying the foundation for tomorrow's cancer drugs."

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• Image (c) Nature Publishing Group, used with permission; taken from Nature: News & Views, 2011

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Advanced skin cancer drug 'not cost-effective' for NHS

Friday 14 October 2011

A new skin cancer drug is not suitable for use on the NHS as its benefits are outweighed by its cost and possible side-effects, according to draft guidance by the National Institute for Health and Clinical Excellence (NICE).

Ipilimumab (Yervoy) is designed to treat patients with advanced malignant melanoma - the most serious form of skin cancer - who have already received chemotherapy.

But NICE said the cost of the treatment - around £80,000 per patient - did not justify its potential benefits.

Trials have shown that the drug is only effective in a small number of patients, and can cause severe side effects.

The draft guidance, which is now open to consultation, highlights doubts over clinical evidence submitted by the drug&aposs manufacturer Bristol-Myers Squibb.

NICE chief executive Sir Andrew Dillon said a trial had shown that the drug could potentially be very effective in a small minority of patients with advanced or metastatic melanoma (cancer that has spread).

But, he said the follow-up from the trial had been too short to determine how long the effect lasted.

Trials have suggested that ipilimumab improves survival rates among just 30 per of suitable patients, with only one in ten likely to experience long-term benefits.

In one trial presented at this year&aposs American Society of Clinical Oncology conference in the US, 20.8 per cent of those given ipilimumab, in combination with cancer drug dacarbazine, were still alive after three years. This compared with 12.2 per cent of patients given just dacarbazine.

Sir Andrew said: "We need to be sure that new treatments provide sufficient benefits to patients to justify the significant cost the NHS is being asked to pay.

"Unfortunately, no patient characteristics or biomarkers have yet been identified to help identify this small group of people most likely to gain long-term benefit from receiving ipilimumab.

"The drug is also associated with a number of adverse reactions including diarrhoea, rash, fatigue, nausea, vomiting, decreased appetite, and abdominal pain which can significantly affect a patient&aposs quality of life.

"The Committee considered all these factors and concluded that, on the basis of the evidence provided so far, ipilimumab could not be considered a cost effective use of NHS resources."

Ipilimumab could still be available to some NHS patients, with health trusts able to make local decisions on funding the treatment.

Once NICE issues its final guidance, this will replace local recommendations. But, the drug may still be available for some patients in exceptional cases, or via the Cancer Drugs Fund.

Sir Andrew said the manufacturer, healthcare professionals and the public would be able to comment on the preliminary NICE guidelines.

"The manufacturer can also consider whether it wishes to reduce the acquisition cost to the NHS of the drug by proposing a patient access scheme. Ipilimumab currently costs around £80k per patient whether the treatment is effective for them or not," he said.

Professor Peter Johnson, chief clinician at Cancer Research UK, said: "It is disappointing that the high cost of Ipilimumab makes it impossible for NICE to recommend its routine use in the NHS. This is a novel and potentially effective treatment for some people with melanoma, but we still do not have a good way to identify those most likely to benefit and those at risk of the occasionally severe side effects."

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Protein prompting cells to sprout legs could cause skin cancer to spread

Wednesday 14 September 2011

Cancer Research UK Press Release

Cancer Research UK scientists have discovered that a protein called Rac1 prompts pigment cells to sprout long ‘legs’ that could propel skin cancer cells, allowing them to spread, according to research published in Developmental Cell today.

The team from Cancer Research UK’s Beatson Institute for Cancer Research at the University of Glasgow showed that when Rac1 is switched on in mice it signals healthy pigment cells, called melanoblasts, to grow legs and ‘travel’ during their early development. When Rac1 was ‘switched off’ the cells were only able to sprout short buds and had difficulty moving.

• Click for a larger version of this graphic

Melanoblast cells mature to develop into melanocytes – pigment-producing cells that define skin and hair colour. Melanocytes can form moles, or naevi, and if they contain genetic faults these cells can develop into melanomas – the most dangerous form of skin cancer.

Immature melanoblasts move through the developing skin layers of an embryo to find the correct place to settle and grow. Once they have matured and anchored in position, they no longer travel.

But cancer cells sometimes mimic the characteristics of immature embryonic cells such as melanoblasts and ‘re-learn’ forgotten skills – such as the ability to move. Studying these immature cells helps scientists understand how cancer develops and spreads.

Lead author, Professor Laura Machesky at Cancer Research UK’s Beatson Institute, said: “We’ve discovered that a protein called Rac1 triggers the growth of long ‘legs’ which can propel cells during the early stages of skin development.

“But once cells have matured these ‘shape-shifting’ abilities are lost.

“Our study reveals fresh understanding of how melanoma cells could re-learn forgotten skills, such as being able to change shape, and use these abilities to break away from a tumour and move around the body.”

There are around 11,770 new cases of malignant melanoma diagnosed each year in the UK and it is mainly caused by over exposure to UV light. Almost one third of all cases of malignant melanoma occur in people under 55.

Dr Lesley Walker, Cancer Research UK’s director of cancer information, said: “Our scientists are carrying out pioneering work to understand the biology of skin cancer and to find new and better ways to treat the disease.

“Melanoma can be successfully treated if caught early, but can be deadly if it spreads to new areas.

“It’s critical to understand how this happens so we can develop drugs to block this process.”

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Sunburn rife as men skimp on sunscreen

Monday 29 August 2011

Cancer Research UK Press Release

Nearly 90 per cent of British adults admit their skin has been sunburnt – with almost half* experiencing pain as result of being in the sun.

And among men fewer than half (47 per cent) use at least factor 15 sunscreen compared to two thirds (66 per cent) of women, to protect their skin in the sun.

Men are also less likely than women to protect their skin in other ways – like spending time in the shade or cover up with clothing.

The YouGov survey** commissioned by Cancer Research UK reveals today (Monday) that nearly all Brits (96 per cent) are aware that getting sunburnt increases the risk of skin cancer.

Yet for many reasons Brits are still putting themselves at risk of skin cancer by getting sunburnt.

The survey showed that 20 per cent of Britons often don’t plan for the weather and get caught without protection if it is sunny while more than a fifth (22 per cent) want to be tanned.

David Denton, 34, from near Halifax in Yorkshire, was diagnosed in February 2009 with malignant melanoma on his face after his dentist persuaded him to get a strange-looking mole checked out.

“I never really thought about the possibility of getting skin cancer even though I’m fair skinned and burn easily – and I think many men are the same.

“I’m not a sun worshipper, but as a construction site worker I spend about 40 per cent of my working life outdoors. The company I worked for said we had to wear T shirts and long trousers to help protect our skin, but it was still easy to get caught out and forget the strength of the sun sometimes.”

David had surgery to remove the melanoma from the side of his face leaving him with a large scar and stretched skin which, he says, looks “as if he’s been glassed”.

“Whatever they might think, men don’t look like wimps if they use sun protection and they certainly don’t look good resembling a boiled lobster.

“I am definitely more aware of protecting my skin from sunburn now, and always remind my mates to put on sunscreen, stick a cap on and keep an eye on their skin.

“I’m lucky that my melanoma was spotted early but the disease can be deadly. Men as well as women should ensure they look after their skin to keep the risk of this awful cancer to a minimum.”

Caroline Cerny, Cancer Research UK’s SunSmart campaign manager, said: “There’s a big gap between what people know and how they behave in the sun. And this report highlights one of the challenges we face in halting the rise in melanoma rates.

“These results indicate that men seem to be worse than women at protecting their skin in the sun.

“Traditionally it’s been women who want to sport a suntan but this survey suggests men crave this look as well but are forgetting to protect their skin.

“Sunburn is a sign that the DNA in your skin has been damaged and people know that getting sunburn can increase the risk of skin cancer but many don’t bother to protect their skin from burning.”

Over the last 25 years in Britain, rates of malignant melanoma – the most serious form of skin cancer - have risen faster than any of the most common cancers in males and females.

This survey showed that generally women are better at protecting their skin – using sunscreen with at least SPF 15, spending time in the shade and wearing sunglasses.

Five times as many men compared to women said they rely on their partner to remind them to protect themselves in the sun.

Over 50 per cent more men than women forget to protect their skin and, worryingly, 75 per cent more men than women are not worried about getting sunburnt.

Despite more women being diagnosed with melanoma, more men die from the disease.***

Public Health Minister Anne Milton said: "We should all enjoy the sun but we all need to be aware of the dangers of too much sun and the increased risk of developing skin cancer. These findings clearly show the importance of men, and women, protecting their skin from sun damage by using sun cream, covering up and spending time in the shade during the hottest part of the day."

Sara Hiom, director of health information at Cancer Research UK said: “Your skin doesn’t have to be red-raw, peeling or blistering to have sunburn damage. If your skin has gone red in the sun, it’s sunburnt.

“We all need sunshine for good general health but many cases of melanoma could be prevented if people took more care in the sun. A good way of doing this is to get to know your skin and avoid it going red.

“The British weather causes a dilemma because we don’t tend to get many sunny summer days, so when it does shine people tend to overdo it, not realising you can burn even when it’s cool or slightly cloudy. Whether at home or abroad, people should think how to use shade, clothing and sunscreen, applied generously and regularly, to protect themselves.”

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European licence for drug to treat advanced melanoma

Tuesday 23 August 2011

A European licence has been granted to drug manufacturers Bristol-Myers Squibb to market the cancer drug ipilimumab (also known by its brand name, Yervoy) for the treatment of advanced melanoma, the most dangerous form of skin cancer.

Ipilimumab has shown in trials that it can extend the lives of patients with advanced melanoma who have already received another treatment.

It helps to fight cancer by boosting the body's immune system, interfering with a protein called CTLA-4, whose normal function is to stop the immune system from attacking itself, but which also stops it from spotting and attacking cancer.

A recent trial presented at a US conference earlier this year showed that 47.3 per cent of patients given ipilimumab in combination with the current treatment - dacarbazine - were still alive a year later, compared to 36 per cent of patients who were given dacarbazine alone.

The drug is given as a series of four injections, each costing around £18,000. The average cost per patient is thought to be around £75,000.

The manufacturer has submitted data to the National Institute for Health and Clinical Excellence (NICE), so they can make a decision as to whether the treatment should be routinely available on the NHS.

Patients may be able to access the drug through the government's Cancer Drugs Fund, which pays for non-NICE approved treatments under certain circumstances.

Every year more than 2,000 people in the UK die from malignant melanoma, and more than 11,000 people develop the disease.

Dr Paul Lorigan, senior lecturer in medical oncology from the Christie NHS Foundation Trust in Manchester, said: "The authorisation of ipilimumab represents a real advance in the treatment of patients with advanced melanoma as this is the first treatment for 30 years in the UK to extend patients's life expectancy.

"After years of no progress in the treatment of this terrible illness, we have now made a stride forward."

Sarah Woolnough, Cancer Research UK's director of policy, said: "It's exciting that ipilimumab is now licensed for use in the UK, as this means it is one step closer to becoming available for patients with melanoma - the most dangerous form of skin cancer.

"This is one of the first effective treatments we have for advanced melanoma and it's important that NICE makes a decision as quickly as possible on whether or not the drug should be made routinely available to all appropriate patients.

"In the meantime decisions about whether patients can get this drug will have to be made through the Cancer Drugs Fund or through other means locally."

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Contact allergies 'may be associated with reduced risk of some cancers'

Tuesday 12 July 2011

People with contact allergies to common metals and chemicals may be less likely to develop certain types of cancer, according to a study by Danish scientists.

However, the study only looked at retrospective data rather than actively tracking people's habits over time, so further studies are needed to clarify the apparent links between contact allergies and the risk of cancer.

The research was carried out by scientists at the National Allergy Research Centre in Copenhagen, Denmark.

Scientists analysed data on 16,922 Danish adults, all of whom were tested between 1984 and 2008 to see whether they were allergic to any common contact allergens.

Thirty-five per cent of people reacted to at least one allergen, including 41 per cent of women and 26 per cent of men.

The researchers looked to see whether any of these individuals were recorded on the Danish Cancer Registry, which contains data on all instances of cancer in the country.

They found that 19 per cent of participants had developed a growth (cancerous or non-cancerous), and that 38 per cent of these individuals had a contact allergy.

Overall, the researchers found a strong link between contact allergies and cancer, though from this analysis alone, they were unable to say whether contact allergies were the direct cause of the reduced cancer risk.

Breast cancer and non-melanoma skin cancer were both significantly less common among people with contact allergies, and brain cancer was less likely to develop in women with an allergy.

The researchers suggest that the findings may be explained by the so-called 'immunosurveillance hypothesis', which states that people with allergies may be less likely to develop cancer because their immune systems are highly responsive.

In contrast, the researchers observed that people with contact allergies had an elevated risk of bladder cancer - a trend they believe may be due to higher levels of chemical break-down products in the bladder.

The study, published in the journal BMJ Open, cannot be used to draw conclusions about allergies and individual cancer risk - further research is needed.

Dr Caetano Reis e Sousa, a Cancer Research UK immunology expert, said: "This is an interesting study, but it doesn't tell people with allergies anything about their individual cancer risk. Firstly, the researchers only looked at a specific type of allergy, so this work doesn't apply to other common allergies such as hay fever. Secondly, the study only demonstrated a statistical link, not the actual cause of this relationship. So further work needs to be carried out before scientists can give solid reasons for these associations.

"Nevertheless, this work highlights the value of good quality databases to help scientists explore possible causes of cancer. It opens the door for further research looking at the role of the immune system in allergies and cancer."

The researchers said: "More refined analyses, adjusting for social class and smoking, for instance, and studies focusing on specific chemical exposures are required to further our understanding of the role of contact allergies in the development of cancer.

"However, if these relations are aetiological, there are implications for understanding how contact allergy can affect cancer development, and vice versa."

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Study reveals 16 to 30-year-olds are worst at skin cancer prevention

Tuesday 5 July 2011

People aged 16 to 30 years tend to have the poorest understanding of ways to avoid skin cancer and are more likely to get sunburnt than older age groups, new research shows.

The survey, which was presented at the annual conference of the British Association of Dermatologists, involved 1,000 adults who were questioned about their sun safety knowledge and behaviour while visiting their GP.

Researchers at Oxford Radcliffe Hospitals NHS Trust and the Royal Free Hampstead NHS Trust found that 16 to 30-year-olds had the worst understanding of skin cancer prevention.

They were more likely to get sunburnt and less likely to avoid the midday sun than older age groups, with 17 per cent admitting that they never avoid the sun between the hours of 11am and 3pm, when the sun is strongest.

More than half of 16 to 30-year-olds said they are exposed to sun on a daily basis, compared with 44 per cent of 31 to 45-year-olds.

And 19 per cent of younger people said that they burn more than once a year, compared with just three per cent of over-60s.

Overall, the findings indicate that 16 to 30-year-olds are the worst at protecting their skin in the sun, despite the fact that melanoma - the most serious form of skin cancer - is the second most common cancer in this age group.

The survey also suggests that young people who have previously had skin cancer or have a family history of the disease are no less likely to avoid or cover up in the sun than people with no history of the disease.

Dr Antonia Lloyd-Lavery, from Oxford Radcliffe Hospitals NHS Trust Dermatology Department, said: "Our results indicate that younger patients are less likely to practise safe sun exposure. Furthermore, our results suggest that those with a personal or family history of skin cancer may not have received critical education on safe sun exposure from the medical profession.

"UK-based health awareness programmes should therefore particularly target younger age groups. In addition, healthcare professionals must ensure that opportunities are taken to reinforce the importance of safe sun exposure among patients."

Nina Goad, from the British Association of Dermatologists, described the findings as a "real worry".

She said: "We definitely need to look more at what will help encourage young people to adhere to anti-sunburn advice."

Dr Claire Knight, health information officer at Cancer Research UK, said: "This research highlights the need for more efforts to encourage people to change their behaviour so they enjoy the sun safely and avoid sunburn whatever their age. Rates of malignant melanoma, the most serious form of skin cancer, have more than quadrupled in Britain in the last 30 years.

"But the good news is that most cases of melanoma could be prevented by avoiding overexposure to UV rays, from the sun or sunbeds. To reduce the risk of skin cancer, protect yourself from strong sun by covering up with clothing, spending some time in the shade, and applying at least SPF 15 sunscreen with 4 or more stars generously and regularly."

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US trials show continued promise for two new skin cancer treatments

Wednesday 8 June 2011

Two clinical trials presented at the largest annual cancer conference have raised hopes for new drugs designed to treat malignant melanoma, the most serious form of skin cancer.

The first was a Phase III trial of an immunotherapy drug - treatment that harnesses the power of the immune system to fight cancer. The trial found that previously untreated patients with advanced skin cancer who were given a combination of the immunotherapy drug ipilimumab and the chemotherapy drug dacarbazine lived longer than those who were only given dacarbazine.

The study, which was presented at the annual meeting of the American Society of Clinical Oncology, is the first to show that a combination of immunotherapy and chemotherapy is safe and effective in patients with advanced melanoma.

Researchers recruited 502 patients for the trial - half were given ipilimumab and dacarbazine, while the others took dacarbazine and a placebo (dummy treatment).

They found that patients who received ipilimumab lived for an average of 11.2 months, compared with 9.1 months for those only taking dacarbazine.

After one year, almost half of the patients (47.3 per cent) who took the combination of drugs were still alive, compared with 36.3 per cent of those on dacarbazine alone.

And, after three years, the overall survival rate was 20.8 per cent for the two drugs, compared with 12.2 per cent for dacarbazine alone.

Lead author Dr Jedd Wolchok, director of immunotherapy clinical trials and associate attending physician at Memorial Sloan-Kettering Cancer Centre in New York, said: "This trial's three-year endpoint is significant. No randomised trial for metastatic melanoma has followed patients for this long, and it demonstrates the durability of this survival benefit, now out to three years in this population, and even four years in some cases.

"It's one of the advantages of immunotherapy. The immune system is a 'living drug', able to adapt itself to changes in the tumour that might otherwise lead to resistance when treated with chemotherapy or a pathway inhibitor."

A second Phase III trial focused on a new treatment called vemurafenib, which is a type of drug called a BRAF inhibitor.

All patients on the trial had advanced melanoma with a specific fault (V600E) in their BRAF gene. Vemurafenib is designed to target this specific fault, which is not found in healthy cells.

Half of the 675 patients were given vemurafenib, while the other half received dacarbazine.

After six months, 84 per cent of vemurafenib users were still alive, compared with 64 per cent of patients in the dacarbazine group.

An early analysis revealed that vemurafenib was associated with a 63 per cent reduction in the risk of dying, compared with dacarbazine, as well as a 74 per cent reduction in the risk of disease progression (or death). And, as these results were so promising, patients who had initially been taking dacarbazine were advised to switch to vemurafenib.

Lead author Dr Paul Chapman, attending physician at Memorial Sloan-Kettering Cancer Centre, said: "This is a really huge step toward personalised care in melanoma.

"This is the first successful melanoma treatment tailored to patients who carry a specific gene mutation in their tumour, and could eventually become one of only two drugs available that improves overall survival in advanced cancers."

Professor Peter Johnson, Cancer Research UK's chief clinician, said: "For the first time, we have effective treatments becoming available for melanoma. Vemurafenib, which targets a molecular abnormality in the melanoma cells, and ipilimumab, which allows the body's immune system to attack them freely.

"Both show how the research we have been doing is feeding through into help for patients. It is a first step but a vitally important one, and it encourages us to redouble our efforts for people with this most dangerous type of skin cancer."

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New law protects under-18s from sunbed dangers

Friday 8 April 2011

New laws have come into force today (April 8th) which will prevent under-18s in England and Wales from using sunbeds, and punish businesses that fail to comply with the regulations.

The Sunbeds (Regulation) Act 2010 is designed to protect under-18s from overexposure to ultraviolet (UV) radiation, which is the main cause of skin cancer.

A study by Cancer Research UK shows that six per cent of 11 to 17-year-olds in England - including half of all 15 to 17-year-olds in Liverpool and Sunderland - use sunbeds to achieve a year-round tan.

According to the charity's SunSmart campaign, two people under the age of 35 are diagnosed with melanoma skin cancer each day - and a proportion of these cases are thought to be linked to sunbed use.

Under the new regulations, under-18s are now banned from using tanning salons and sunbeds at beauty salons, leisure centres, gyms, hotels and other premises.

It is now illegal to offer an under-18 the use of a sunbed, and young people are no longer allowed in areas that are reserved for sunbed users.

Businesses that fail to comply with the regulations and allow under-18s to use sunbeds will face fines of up to £20,000, and local authorities will be responsible for inspecting businesses and enforcing the Act.

Public health minister Anne Milton said: "Cases of skin cancer continue to rise each year. This new law will go some way to help reduce one of the biggest cancers among 15 to 24-year-olds.

"My message to young sunbed users is clear: you are putting your health at risk. Intense bursts of UV radiation can cause damage to your skin, even after just one use."

Professor Dame Sally Davies, England's chief medical officer, revealed that about 100 deaths a year from skin cancer are thought to be the result of sunbed use.

She said: "Damage to the skin from artificial or natural sunlight can take years to develop and young people are particularly vulnerable, which is why I welcome this new law that protects the under-18s."

Cancer Research UK, which has just launched its annual SunSmart campaign to raise awareness of skin cancer prevention, welcomed the new legislation.

Sarah Woolnough, the charity's director of policy, said: "As well as protecting under-18s from sunbed use, we hope the legislation sends a clear message to all that using a sunbed increases the risk of skin cancer. The World Health Organisation has classified sunbed use in its highest risk category for cancer, alongside tobacco.

"Skin cancer rates continue to rise rapidly, especially among under-35s as shown by our SunSmart campaign earlier this week, so we encourage people to take care in the sun and avoid using sunbeds. The safest way to get a tan is to fake it."

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Two young adults diagnosed with skin cancer every day

Wednesday 6 April 2011

Cancer Research UK Press Release

Each day more than two people under 35 in Britain are diagnosed with malignant melanoma – the deadliest form of skin cancer - according to new figures from Cancer Research UK.

The charity’s 2011 SunSmart campaign, launched today (Wednesday), reveals an alarming tripling in melanoma rates among British 15-34 year olds since the late seventies.

In the late seventies, there were around 290 cases of melanoma among 15-34 year-olds. Now more than 900 young Britons are being diagnosed with the disease each year - more than two a day.*

Thirty years ago, there were 1.8 cases of melanoma per 100,000 people in this age group. Now there are 5.9 cases per 100,000.

And the numbers continue to increase. Latest available figures show that the total number of cases of malignant melanoma for all ages increased from 10,800 in 2007 to 11,700 in 2008 – a rise of 8.5 per cent.

Caroline Cerny, Cancer Research UK’s SunSmart campaign manager, said: “It’s very worrying to see that the number of young adults being diagnosed with this potentially fatal disease has risen so dramatically, especially since cancer is typically a disease that affects older people.

“With summer approaching after such a harsh winter, everyone is looking forward to enjoying some sunshine. But it’s more important than ever to be aware of the dangers of getting sunburnt.

“Nor are sunbeds a safe alternative to tanning. In fact using a sunbed before the age of 35 can increase your risk of melanoma by 75 per cent.

“Young women in particular need to take care since they are more than twice as likely to be diagnosed with melanoma than young men. The good news is that the majority of cases could be prevented by making sure you don’t get sunburnt.”**

Lindsey Coane, 27, an architectural assistant from Preston, was diagnosed with malignant melanoma on her leg at just 21 while she was at university in Liverpool.

“I used sunbeds for six to nine minutes at a time every week for nearly two years while at university. I was really keen to have a tan and used to get sunburnt while on holiday with my friends. I’m convinced that both these things caused my malignant melanoma,” she said.

“I’m very lucky that the cancer was caught when it was. But a lot of skin and tissue still needed to be taken out of my leg, cutting through some of my nerves which left my leg partially numb.

“I had to learn to walk again and then run. The first event I took part in was Race for Life – it was such a big achievement for me. As far as I’m concerned now, pale skin is interesting.

“I am very fair and I only have to be in the sun for a few minutes to burn, which is why it was so silly of me to go on sunbeds.”

Sara Hiom, director of health information at Cancer Research UK, said: “While some sunshine is good for us, going red and burning can be dangerous.

“The most important thing people can do to reduce their chances of developing skin cancer is to make sure they don’t get red or burn. And the best way to do that is to get to know your skin and how long you can safely stay in the sun, and also avoid sunbeds.

“Sunburn means that UV rays have penetrated the skin cells causing damage which builds up over time and increases the risk of skin cancer.

“The explosion in melanoma rates we are seeing now reflects people’s tanning behaviour in the past and the desire to sport a suntan – a trend which began in the seventies with the dawn of cheap package holidays.

“But all too often holiday-makers thought getting sunburnt was part of the process of getting a tan.

“Everyone is different so know your skin type - if you are fair, freckly, have lots of moles or a family history of skin cancer then you need to take extra care in the sun.

“Our message is clear – enjoy the sun safely and protect yourself from sunburn.”

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Lab tests suggest arthritis drug could slow melanoma skin cancer growth

Wednesday 23 March 2011

In research published in Nature, an international team of scientists have shown that an existing rheumatoid arthritis drug can slow down the growth of malignant melanoma, the deadliest form of skin cancer. The research was done in zebrafish and mice.

Researchers at the University of East Anglia (UEA) and Children's Hospital Boston in the US found that the drug leflunomide slowed down the growth of tumours over a short period of time.

Drs Grant Wheeler and Matt Tomlinson worked with their US collaborators to test more than 2,000 chemicals, to find ones that might halt the disease. The best candidate blocked a protein also known to be targeted by the drug leflunomide, commonly used to treat arthritis.

The researchers showed that a combination of leflunomide and a promising experimental melanoma therapy called PLX4032 was particularly effective at blocking tumour growth over 12 days.

PLX4032 is currently being tested in clinical trials and is designed to block a protein called BRAF, which was shown by Cancer Research UK scientists to be overactive in around half of all melanomas.

Dr Wheeler, from the University of East Anglia's School of Biological Sciences, said: "This is a really exciting discovery - making use of an existing drug specifically to target melanoma.

"Deaths from melanoma skin cancer are increasing and there is a desperate need for new, more effective treatments. We are very optimistic that this research will lead to novel treatments for melanoma tumours which, working alongside other therapies, will help to stop them progressing."

But, Cancer Research UK-funded scientist Professor Richard Marais at The Institute of Cancer Research sounded a more cautious note. "This work represents a very interesting new experimental approach to melanoma, but obviously there's a long way to go before we can start using these sorts of combinations in patients. We need to do a lot more preclinical studies and a lot more studies in appropriate models."

Meanwhile, a second study in Nature, from the same US group that worked with the UEA team, has shed light on a molecule that appears to influence the growth of melanoma.

Again working with zebrafish, researchers led by Professor Leonard Zon, discovered that a histone-methylating enzyme called SETDB1 cooperates with BRAF faults in melanoma cells to significantly speed up the development of the disease.

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Cancer Research UK launches groundbreaking research centre in Oxford

Tuesday 15 March 2011

Cancer Research UK Press Release

A new centre launched today (Tuesday) will cement Oxford’s place at the forefront of cancer research, and form one of the final links in a unique chain of Cancer Research UK Centres across the country.

These new cancer centres will pull together world class laboratory research with medical expertise to provide the best possible results for cancer patients nationwide.

The Oxford Cancer Research Centre is a partnership between Cancer Research UK, the University of Oxford and the Oxford Radcliffe Hospitals NHS Trust.

It will help set the pace for national and international progress in the understanding and treatment of a variety of cancers, including breast, skin, urological and gastrointestinal.

Collaboration will be the key to the success of the centre, as it will bring together and build on Oxford’s existing world-class research in many areas of cancer medicine, from identifying the causes of cancer to improving diagnosis and treatment of the disease.

The centre will carry out research on the molecular basis of cancer, as well as work on understanding the genetic and lifestyle factors that can increase the risk of cancer.

Other research strengths will include new methods for improving cancer diagnosis, and finding new ‘biomarkers’ to predict the effect drugs have on patients.

The latest developments in radiotherapy and surgery will be brought together with clinical trials of new drugs, providing the best evidence to guide the treatment of cancer.

Professor Gillies McKenna, director of the Gray Institute for Radiation Oncology and Biology, and head of the Department of Oncology said: “With 2011 designated as the Year of Radiotherapy, there is increased recognition that greater access to this treatment is vital to improving cancer survival.

“Cancer Research UK has long been committed to improving radiotherapy through research, by supporting the Gray Institute in Oxford. The Institute has the world’s largest group of clinicians and scientists working in radiation oncology, and the Oxford Cancer Research Centre will help provide the vital infrastructure to help translate these discoveries into benefits for patients.”

Michael Kinane, 70, from Bicester, was diagnosed in September 2010 with bowel cancer which had spread to the liver.

He began his treatment with radiotherapy for the bowel tumour to relieve symptoms. He then received another form of radiotherapy in combination with chemotherapy to treat the spread of cancer to his liver.

He is being treated at the Oxford Cancer Research Centre, in one of the clinical trials developed by the Gray Institute for Radiation Oncology and Biology at the University of Oxford and supported by the Bobby Moore Fund for Cancer Research UK.

The trial – known as FOXFIRE - is testing a new treatment called radio-embolisation, a form of internal radiotherapy that uses the tumour’s blood supply to target multiple sites of disease within the liver.

Radiotherapy is already a well-established treatment in bowel cancer. This new way of administering high-dose radiation therapy directly into the blood supply of the cancer could be even more effective at treating bowel cancer which has spread to the liver, when combined with chemotherapy.

“Being part of the trial has been amazingly simple and I feel very fortunate to have had the opportunity of being given another treatment,” said Michael. “I hope that taking part in this trial will help more people like me in the future. I’ve been lucky to benefit from the excellent research which already takes place in Oxford and it’s good to know that this will become even better with the new Centre.”

Sir Jonathan Michael, chief executive of the Oxford Radcliffe Hospitals NHS Trust, said: “This is an exciting development for our cancer patients. Patients will benefit from the close working relationship between the Trust and the University. We want to ensure that research is translated into treatment for patients in order to prolong and improve their quality of life.”

The Oxford Cancer Research Centre is the 16th Cancer Research UK-funded centre and will be funded by Cancer Research UK to the tune of £2.8 million in the first year.

Professor Alastair Buchan, head of the medical science division at the University of Oxford, said: “The University of Oxford is delighted to join the Cancer Research UK Centre’s Initiative. The Centre will help bring together the extensive community of outstanding cancer researchers in Oxford, acting as a nucleus for researchers, doctors and patients to engage with each other. It will ensure optimal translation of fundamental research into patient benefit, and will train the next generation of world-leaders in cancer detection, treatment and prevention.”

Harpal Kumar, chief executive of Cancer Research UK, said: "Funding these centres of excellence is one of the charity's priorities and will enable us to work towards the goals we have set to improve the treatment and survival of cancer patients across all types of cancer.

“We continue to welcome the generous donations we receive from the public to ensure we can continue to build on what we have started today."

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AstraZeneca and Pfizer join Cancer Research UK's Stratified Medicine Programme

Tuesday 1 February 2011

Cancer Research UK Press Release

CANCER RESEARCH UK will be supported by AstraZeneca and Pfizer in a multimillion pound initiative to examine how genetic tests to improve cancer diagnosis can be best rolled out across the NHS.

Cancer Research UK’s pioneering Stratified Medicine Programme will also promote research into new targeted treatments by building a database of genetic information about tumours, treatments and survival rates that will enable researchers to design more effective cancer treatments in future.

Cancer Research UK will now select six hospitals and three labs to collect tumour samples from 9,000 cancer patients around the UK, and test them for a set of gene faults specifically linked to cancer – an approach called ‘molecular diagnosis’.

Molecular diagnosis of tumours is not yet available for all patients on the NHS and currently only possible using a single test for each mutation.

But the programme aims to develop a multi-gene panel that can test for genetic markers for drugs already used in the clinic - such as EGFR for gefitinib - as well as those for promising new drugs in late-stage trials.

So as and when new targeted cancer treatments become available, doctors will have access to the tests needed to help them match the right drug to the right patient.

The programme will deliver a clear set of standards and processes for molecular diagnosis of NHS patients’ tumours, which can be scaled up to provide a national service.

This will help ensure that the hospitals and labs can deliver high quality, efficient molecular diagnosis of tumours, so all cancer patients across the NHS can get access to the tests that they need.

The £5.5m programme will be led by Cancer Research UK, with funding from AstraZeneca and Pfizer.

It is closely aligned with the Technology Strategy Board’s £5.6 million investment in tumour profiling and data capture to improve cancer care and the new cancer strategy recently launched by the coalition government.

Rob Day, Head of Pfizer Oncology, UK, said: “Pfizer is delighted to partner with Cancer Research UK on the Stratified Medicine programme to advance the role of genetic testing in cancer diagnosis and treatment selection. Personalised medicines are likely to transform the way cancer is treated in the future. As a company dedicated to advancing oncology research, Pfizer Oncology is focused on discovering gene-specific targeted medicines to improve outcomes for patients with cancer.”

Dr Susan Galbraith, Vice President and Head of Oncology, Innovative Medicines, at AstraZeneca, said: “We are delighted to be involved in this collaboration. AstraZeneca has spent over fifty years at the forefront of cancer research and it is our view that better understanding of which patients will benefit from treatment with currently available and new therapies is the way forward in fighting this disease.’

“This collaboration is particularly exciting as by building a database of tumour genetic information, treatments and outcomes, we can better understand which targets for new drugs occur in which patients. The information currently available on this is often incomplete. This kind of testing will mean better selection of patients for clinical trials with drugs which are more likely to make an impact on their disease. Ultimately this will help us develop drugs which improve the survival of patients with cancer.”

Paul Mason, Head of Development at the Technology Strategy Board, said: “We are delighted to be working with Cancer Research UK in this exciting area. The alignment of our activities to build a national programme, and their contribution to the Stratified Medicines Innovation Platform, will go a long way to help generate the critical mass the UK needs.”

James Peach, director of Cancer Research UK’s stratified medicine programme, said: “Cancer Research UK recognises the huge potential of personalised medicine to save lives from cancer. Such an ambitious vision could not be realised without partnership and we know that the support of AstraZeneca and Pfizer will be invaluable in facing the many challenges that lie ahead.”

“It’s important that NHS cancer patient have access to these kinds of tests to make sure they get the right treatment at the right time. And by acting now we can ensure patients benefit from personalised cancer medicines as soon as they become available.

“Cancer Research UK is proud to be leading this coordinated national effort – including the Government, NHS and pharmaceutical and diagnostic companies – that will bring us a step closer to tailored treatments becoming a routine part of NHS cancer care.”

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NICE issues new guidance on preventing skin cancer

Thursday 27 January 2011

The National Institute for Health and Clinical Excellence (NICE) has published new guidelines to help the NHS, local authorities and other organisations in their work to prevent skin cancer.

The guidelines say that some sun exposure is important, as it allows people to make vitamin D as well as providing an opportunity to be physically active.

But too much exposure to UV light is known to increase the risk of skin cancer.

Professor Mike Kelly, director of the institute's Centre for Public Health Excellence, revealed that about 100,000 people each year are diagnosed with non-melanoma skin cancer and over 10,000 with malignant melanoma, the most serious type of skin cancer.

He explained: "Through this guidance we hope to raise awareness of the risks of UV exposure and help people to protect themselves and others.

"Simple actions can greatly reduce the risk of developing skin cancer - opting to stay in the shade, wearing protective clothing in the sun, avoiding too much sun during the middle of the day and using sunscreen can all have an effect."

The guidance contains simple and practical recommendations for preventing over-exposure to the sun.

For instance, developers should attempt to create shaded areas around buildings, while schools should encourage children to use sunscreen and stay in the shade during breaks.

Sara Hiom, director of health information at Cancer Research UK, said that avoiding sunburn is one of the best ways to reduce the risk of skin cancer.

"Many of us like to make the most of the UK's rare sunny days and should be able to enjoy the sun safely.

"If we all make sure that our skin doesn't redden or burn in the sun, it could help to reduce the rocketing number of people who develop skin cancer every year. And that's the aim of Cancer Research UK's annual SunSmart campaign."

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Experimental melanoma drug shows promise in phase-III trial

Thursday 20 January 2011

Early results from a phase-III clinical trial of a new drug for advanced melanoma skin cancer indicate that it may help to improve survival.

Malignant melanoma is the most aggressive form of skin cancer and can be difficult to treat once it has spread.

RG7204 (also known as PLX4032) is a new, as-yet-unlicensed drug designed to target cancer cells with faults in a gene called BRAF. About half of all melanomas have these faults, which encourage the cancer cells to grow and spread. The drug blocks this process, helping to shrink the tumours.

A research team at the Royal Marsden NHS Foundation Trust have now completed a phase-III study comparing RG7204 with standard chemotherapy treatment. The early results show that patients treated with RG7204 survived for longer, and the new drug was better at slowing the growth of melanoma.

These results were so promising that all trial participants who were previously taking standard chemotherapy have now been offered treatment with the new pill instead.

However, the drug is not yet licensed and is currently only available to patients involved in clinical trials. Results from the trial will be presented at a major medical conference later this year.

Lead researcher Dr James Larkin, from the Royal Marsden, described the results as "an incredibly exciting breakthrough".

He said: "Malignant melanoma is a very difficult disease to treat and with a growing incidence in younger people the results of this phase-III trial are very encouraging."

Professor Richard Marais, whose work at The Institute of Cancer Research demonstrated the importance of BRAF in melanoma, added: "These results represent a paradigm shift in melanoma treatment and will change how we approach treatment of this disease."

Dr Lesley Walker, Cancer Research UK's director of cancer information, said: "There are very few options for patients with advanced melanoma, so these results are really encouraging. The drug is not yet licensed and unavailable to patients not on a clinical trial, but we hope that these results will change this situation very rapidly."

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Faulty gene behind skin cancer also triggers spread

Thursday 6 January 2011

Cancer Research UK Press Release

CANCER RESEARCH UK-funded scientists have discovered that skin cancer can spread to the lungs when a gene in an important cell communication pathway is blocked. The research is published in Cancer Cell.

Scientists from The Institute of Cancer Research (ICR) showed that in human cancer cells and mice, a gene called BRAF - which is damaged in about half of all skin cancer cases - triggers a cell signalling pathway that ultimately ‘blocks the instructions’ from a second gene called PDE5A.

In healthy cells PDE5A acts as a brake to stop cell movement. But in cancer cells, BRAF turns PDE5A’s signals off, removing its ability to block cancer spread.

By blocking the activity of PDE5A, BRAF drives skin cancer cells to invade new tissues and spread further around the body, converting skin cancer into a more aggressive disease.

The team showed that when faulty BRAF blocked PDE5A, the skin cancer cells spread more easily to the lungs.

Lead study author, Professor Richard Marais, said: “This research further puts the focus on BRAF as an important target for therapy to prevent the spread of skin cancer.

“Our findings support recent studies into experimental BRAF-targeting drugs, which are showing great promise in patients with melanoma cells with a damaged BRAF gene, but not in patients whose melanomas do not have this alteration. This highlights the importance of personalising medicine to achieve effective treatments for cancer.”

Dr Lesley Walker, director of cancer information at Cancer Research UK, said: “These new findings reveal more of the complex web of signals that drive the development of tumours that have the ability to grow, survive and spread to new locations.

“Melanoma is the most dangerous form of skin cancer and more than 2,000 people die from the disease each year. Even more worrying is the fact that rates of melanoma are rising.

“There are definite signs when a mole is suspicious and should be seen by a doctor. If you have a mole that is getting bigger, changing shape or colour, is itchy or painful, bleeding or inflamed you should go to the doctor straight away.”

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Trial drug 'effective' against cancers with faulty BRAF gene

Thursday 26 August 2010

An experimental drug designed to treat cancers with a particular genetic fault has shown promising results in a small clinical trial.

The drug, PLX4032, is designed to block a protein produced by the faulty BRAF gene, which is overactive in more than half of all melanoma skin cancers.

Early stages of clinical testing, published in the New England Journal of Medicine, suggest that it may help to shrink advanced melanoma tumours with BRAF faults.

A new treatment for advanced melanoma would be an important advance, as it can be hard to treat once the original cancer has spread to other parts of the body.

Scientists at Massachusetts General Hospital (MGH) Cancer Centre and the Memorial Sloan-Kettering Cancer Centre in New York, along with colleagues in Australia, enrolled 55 patients for the first stage of their study.

Patients received doses of PLX4032 which were gradually increased until side effects became a problem, thus helping to determine an acceptable dose.

Of the 55 patients involved in this stage of the research, 16 had faulty BRAF genes and the tumours of 11 of these patients shrank.

In the second stage of the research, 32 patients with BRAF-mutated melanoma were given 960mg of PLX4032, twice a day for the duration of the trial.

In 26 out of 32 patients, tumours shrank by more than 30 per cent, and two of the patients saw their tumours completely disappear.

Lead study author Dr Keith Flaherty, director of developmental therapeutics at the MGH Cancer Centre, commented: "Until now, available therapies [for advanced melanoma] were few and unreliable.

"One of the things that makes these results truly remarkable is that this drug works so reliably."

However, the researchers observed that, after initially responding to treatment with PLX4032, patients did develop resistance to the drug after a time and their tumours started to grow again.

Dr Flaherty added: "Although we don't know how long response may last, the ability to beat this disease down in the short term will buy us time to strategise second-line therapies and design the next generation of trials."

Senior author Dr Paul Chapman, from the Melanoma and Sarcoma Service at Memorial Sloan-Kettering Cancer Centre, said, "We have seen many tumours shrink rapidly and, in some patients, quality of life improved dramatically.

"In the future, we hope to combine PLX4032 with other anti-melanoma drugs currently being developed."

Professor Richard Marais, Cancer Research UK's melanoma expert at The Institute of Cancer Research, said: "These results are extremely exciting. This is the first time in over 30 years that this level of response has been seen in melanoma patients in any clinical trial.

"While these results are very promising, there is still work to be done. Although patients initially respond they can often relapse during treatment, so now we need to learn how to get longer-lasting responses in these patients."

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DNA repair genes help predict impact of chemo for melanoma

Friday 13 August 2010

Cancer Research UK Press Release

A LINK between the level of active DNA repair genes in melanoma tumours and the effectiveness of chemotherapy for skin cancer patients has been established for the first time by a team of scientists.

The study, part-funded by Cancer Research UK and published in Clinical Cancer Research* today (Friday), found that higher levels of DNA repair genes in melanoma tumours were associated with a poorer response to chemotherapy.

It is the first time that genes involved in DNA repair have been identified as a possible predictive marker for a patient’s response to chemotherapy for melanoma.

The study looked at 502 cancer-related genes in the tumours of 472 patients – making it the largest piece of research to look at genes in melanoma.

The results could potentially help doctors decide the most effective treatment earlier on for a melanoma patient, increasing their chance of survival.

Professor Julia Newton-Bishop, lead author of the study who is based in the Cancer Research UK Centre at the University of Leeds, said: “This paper identifies so-called biomarkers - changes within the tumours themselves which predict how patients will respond to treatment.

“Our study found that the increased expression of DNA repair genes in melanomas predict poorer outcome overall and provide preliminary evidence that those patients whose tumours have lower levels of the genes may respond better to standard chemotherapy for melanoma.”

The research supports the theory that high levels of DNA repair genes in melanoma tumours constantly repair the damaging effects of chemotherapy to the DNA leading to further multiplication of cells.

This meant the treatment was inefficient at killing cancer cells and stopping tumour growth.

Sara Hiom, director of health information at Cancer Research UK, said: “Chemotherapy can be an unpleasant experience for some patients. This study shows that a genetic marker could help doctors assess whether a melanoma tumour will be resistant to chemotherapy and ensure that a patient receives a treatment that will be the most effective for them.

“The results showing the genetic link in melanoma tumours to chemotherapy were from a small sample. Scientists now need to test this finding with a larger number of melanoma tumours to see whether this genetic marker can actually be used by doctors to help treat patients.”

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Teenagers get sunburnt on purpose

Tuesday 6 July 2010

More than a quarter of teenagers will get sunburnt on purpose this summer in the belief that they will ultimately get a suntan, a survey has found.

The Teenage Cancer Trust discovered that 26 per cent of young people, aged 13 to 19, plan to get sunburnt on purpose this year.

Almost a third of respondents said they never used sun cream in the UK and 55 per cent wrongly thought the British sun was not as harmful as overseas.

More than one-fifth admitted they had been badly burnt after falling asleep in the sun and 74 per cent were under the impression that they would never get burnt on a cloudy day.

The shoulders are the most common area of skin to be burnt (47 per cent of teenagers), while the arms and nose are the next most frequently burned.

However, a fifth revealed that they put sun cream on to attract attention from the opposite sex and 16 per cent said they had asked someone to apply sun cream on hard-to-reach places as a chat-up line.

Simon Davies, chief executive of the Teenage Cancer Trust, said: "We've found that young people display a worrying lack of awareness when it comes to protecting their skin from the sun.

"We are trying to educate them to prevent the overexposure to sun whilst young, which can lead to problems with skin cancer later in life."

The charity has launched its sun safety campaign, Shunburn, which asks young people to 'love the sun, respect your skin'.

Mr Davies said: "If we can stop just one young person from developing skin cancer when they are older, then this year's Shunburn campaign will have been worth it."

Ed Yong, head of health information at Cancer Research UK, said: "It's worrying that so many teenagers are prepared to go through the pain and discomfort of sunburn for the sake of a tan.

"Sunburn is basically a radiation burn. It means that the DNA in your skin has been damaged by the sun's ultraviolet radiation. Even after the sunburn fades, this damage can remain and greatly increase the risk of skin cancer later on in life. People with fair skin who burn easily but tan with difficulty should take particular care to avoid sunburn."

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Scientists identify melanoma stem cells

Friday 2 July 2010

Researchers at Stanford University School of Medicine in the US have discovered that rogue stem cells appear to be capable of kick-starting the development of melanoma skin cancer in humans.

Many researchers think that tumour growth is fuelled by a subset of 'immortal' cancer stem cells. When they multiply, they produce 'bulk' tumour cells, as well as more stem cells.

Cancer stem cells may explain why cancer can return in patients who first appear to have been successfully treated. Although treatments such as chemotherapy and radiotherapy are effective against bulk tumour cells, they don't appear to target cancer stem cells.

Cancer stem cells have been identified in a number of different types of cancer, but until now, they have not been discovered in melanoma.

The researchers analysed protein molecules on the surface of cells from melanoma samples that had been taken from patients at the Stanford Cancer Centre. They found that between 2.5 and 41 per cent of cells had a protein called CD271 on their surface.

The researchers then transplanted human melanoma cells into mice, some of which received cells with CD271 on their surface while others received cells which lacked CD271.

Cells with CD271 were much more likely to grow into tumours than cells without the protein, suggesting they may have stem cell-like properties.

All but one of the new tumours arising from CD271 cells contained a mixture of CD271-positive and CD271-negative melanoma cells.

This shows that the stem cells could produce bulk tumour cells as well as new stem cells - a classic hallmark of stem cell behaviour.

The team also found that melanoma stem cells lack proteins that are targeted by immunotherapy - a treatment that harnesses the patient's immune system to destroy cancer cells. This helps to explain why some melanomas don't respond to immunotherapy, and could shape the design of future therapies for the disease.

Commenting on the discovery, which is published in the journal Nature, lead researcher Dr Alexander Boiko, a post-doctoral fellow at Stanford, revealed: "These cells lack the traditional melanoma cell surface markers targeted by these treatments. Without wiping out the cells at the root of the cancer, the treatment will fail.

"This could be the reason why we often see melanoma patients relapsing and coming back to the clinic. Our research indicates that it may be more appropriate to also target cells expressing CD271."

Dr Kat Arney, science information manager at Cancer Research UK, said: "Researchers are finding cancer stem cells in many different types of tumour, and many scientists believe they are at the heart of a wide range of cancers.

"Understanding these elusive 'immortal' cells will be the key to developing more effective treatments for cancer in the future, so this research is an important step towards beating melanoma."

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NICE updates skin cancer guidance

Wednesday 2 June 2010

The National Institute for Health and Clinical Excellence (NICE) has updated its recommendations on the diagnosis and treatment of 'low risk' basal cell carcinomas (BCCs).

GPs had raised concerns about the implementation of the institute's previous guidance in relation to the removal of 'low risk' tumours and the commissioning of services for skin cancer patients.

NICE announced a formal review of the recommendations in July 2009. The results of this review, by an expert group, mean that small skin cancers that are unlikely to spread can be removed by a GP rather than a specialist skin cancer surgeon, as long as the doctor has received appropriate and up-to-date training.

The institute's updated recommendation emphasises that primary care trusts (PCTs) or local health boards (LHBs) should ensure that all GPs who diagnose, manage and remove low-risk BCCs are fully accredited to do so.

GPs who treat BCCs must undergo continuous training in the diagnosis and management of skin lesions to maintain their accreditation, which should be performed locally by PCTs or LHBs.

Dr Fergus Macbeth, director of the NICE Centre for Clinical Practice, said that the institute had responded to doctors' concerns.

"BCC is the most common type of cancer in the UK, with an average of 48,000 new cases registered each year. However, because it is not fatal, its importance can be underappreciated," he claimed.

"It is vital that patients are accurately diagnosed, receive appropriate treatment and avoid unnecessary or incomplete surgery. We hope this updated guidance will ensure that patients get the care they need in the most appropriate setting."

Professor Steve Field, chair of the Royal College of General Practitioners, described the updated guidance as a "major step forward" for patients with skin cancer.

"Many patients will prefer to have minor surgery at their GP practice rather than going to hospital and the guidance acknowledges the important role of GPs in carrying out this treatment. But GPs are not expected to have expertise in this area so it is vital that we have a defined and consistent framework for referral when necessary," he explained.

"We are pleased that NICE has listened to the concerns of GPs and made the necessary adjustments that should now enable all healthcare professionals involved in the diagnosis and treatment of skin cancers to deliver a better deal for patients."

Hilary Tovey, Cancer Research UK's policy manager, said: "Cancer Research UK welcomes this update from NICE. In particular we welcome the emphasis in this guidance on ensuring that GPs performing this type of minor surgery are appropriately accredited and trained to do so.

"It will also be important to ensure that these doctors feel adequately equipped and supported to perform these procedures, and that patients are aware of their rights if they have questions or concerns about the treatment that is being offered to them."

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Men's skin cancer death rates double in last 30 years

Monday 31 May 2010

Cancer Research UK Press Release

The rates of men dying from malignant melanoma – the deadliest form of skin cancer – have doubled in the last 30 years, according to the latest Cancer Research UK figures published today.

In the late 70s fewer than 400 (1.5 per 100,000) men died from melanoma but now more than 1100 (3.1 per 100,000) men are dying from the disease1.

Experts are concerned because this sharp rise in death rates from malignant melanoma is due to so many more men developing what is largely a preventable disease.

The figures also reveal that death rates in men over 65 have risen shockingly from 4.5 per 100,000 to 15.2 per 100,000 since the late 70s.

More women are diagnosed2 with malignant melanoma but more men are dying from it and in comparison death rates for women have risen more slowly from 1.5 per 100,000 to 2.2 per 100,000 since the late 1970s.

Male malignant melanoma incidence rates are now more than 5 times higher than they were 30 years ago – rising from 2.7 per 100,000 to 14.6 per 100,0003.

Cancer Research UK’s SunSmart programme provides evidence-based information about skin cancer and sun protection to help people enjoy the sun safely and avoid sunburn.

Caroline Cerny, Cancer Research UK’s SunSmart manager, said: "These figures show that a worryingly high number of men are dying unnecessarily from malignant melanoma because of the rapidly rising numbers diagnosed with the disease. Preventing the disease developing in the first place will help stop this trend and save lives

"To curb this huge rise in deaths from malignant melanoma it's more important than ever that people are aware of the dangers of too much sun. Too often men leave it up to their partners or mothers to remind them to use sunscreen or cover up with a shirt and hat and even to visit the doctor about a worrying mole.

“And even though more women are diagnosed with the disease, more men die from it. This suggests that men are either not aware of skin cancer symptoms or are ignoring them and putting off going to see their GP. It’s crucial that people go to their doctor as soon as they notice any unusual changes to their skin or moles – the earlier the cancer is diagnosed the easier it will be to treat.”

Care Services Minister, Paul Burstow said: "The rise in skin cancer deaths among men is worrying and highlights how important it is for everyone to protect themselves from overexposure to sun. Seeing many people with sunburn from the recent sunny weather is a reminder of how easy it is to damage your skin.

"We should all keep a careful eye on our skin. Shrugging off any changes in a mole’s appearance could put your life at risk. Always see your GP as soon as possible if you have concerns. When skin cancer is caught early treatment is more likely to be successful, and fast action could stop the significant rise we've seen in the number of deaths."

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Deadly skin cancer rates soar for generation of baby boomers

Thursday 1 April 2010

Cancer Research UK Press Release

People in their 60s and 70s are now over five times more likely to be diagnosed with malignant melanoma – the deadliest type of skin cancer – than their parents would have been 30 years ago, reveal new Cancer Research UK statistics1 to launch the 2010 SunSmart campaign today (Thursday).

Of all ages, this generation has seen the biggest increase in incidence rates of melanoma, rising from seven cases per 100,000 people in the mid 1970s2 to 36 cases per 100,000 today3.

The stark rise shows the impact that a shift in tanning behaviour has had on a whole generation of men and women who would have been in their 20s and 30s during the dawn of cheap package holidays in the 1970s – when sunburn before suntan was a common ritual – and sunbeds arrived in the UK4.

For men in their 60s and 70s the rates of melanoma have risen most dramatically – they are now over seven times more likely to be diagnosed with the disease than in the 1970s.

Sue Deans, a 64 year old grandmother from Dorset, was diagnosed with malignant melanoma after discovering a lump in her lymph nodes. She had a mole removed a few years earlier but was shocked to be diagnosed with skin cancer. She had an operation to remove the tumour.

“I was famous for getting brown. When I was younger having a tan was seen to be very attractive and I would spend hours in the sun without any protection. My skin would burn and peel and I would pick off the skin after it had blistered. And then when I was in my early 20s I began going abroad on holiday and would spend most of my time sunbathing.

“I truly believe my skin cancer diagnosis was due to the sunburn I suffered as a child and teenager. If only we’d known at the time how dangerous getting burnt was and the effect it would have 30 to 40 years later. But we just weren’t aware of the risks and how important it was to be safe in the sun and not get burnt.

“There’s nothing clever about having a tan. I am now always careful not to burn by wearing sun screen and sitting in the shade. And my young grandson has very fair skin so I worry about him and make sure he is protected.”

The worrying rise in incidence rates is expected to continue. By 2024 rates in people aged 60-79 are predicted to increase by a third from where they are today 5.

For men and women of all ages melanoma incidence rates have quadrupled since the 1970s.

Caroline Cerny, SunSmart manager at Cancer Research UK, said: “A change in the culture of tanning including the explosion of cheap package holidays and the introduction of sunbeds in the seventies means we’re now seeing alarming rates of melanoma for an entire age group.

“The battle against melanoma is far from won. Today the problem threatens to get worse as teenagers continue to crave a tan on the beach and top it up cheaply on sunbeds. Already skin cancer is predicted to become the fourth most common cancer for men and for women in the UK by 2024. We must continue to try and stop this pattern of behaviour or melanoma rates in future generations will hit an all time high.

“Melanoma is largely preventable. Burning is not only painful and unsightly; it’s a clear sign that UV rays from the sun have damaged the DNA in your skin cells. This significantly increases the chance of developing skin cancer and makes skin look older. People with fair skin, freckles and lots of moles should take extra care in the sun. But everyone should avoid the temptation to redden or burn in order to get a tan.”

There has also been a large increase in the overall death rates. Over a similar period they have more than doubled from 1.2 per 100,000 in 1971 to 2.6 per 100,000 in the UK in 2007.

If melanoma death rates had stayed the same as they were in 1973, around 19,000 fewer people would have died from melanoma6.

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Surprising discovery could help scientists refine treatment for advanced melanoma

Monday 1 February 2010

Cancer Research UK Press Release

A team of UK scientists has made the unexpected discovery that drugs which target a well known fault in a protein called BRAF could actually fuel the progression of cancer in some cases. The findings of this study, which was jointly funded by Cancer Research UK, The Institute of Cancer Research (ICR) and the Wellcome Trust are published in Cell.

Malignant melanoma is the most deadly form of skin cancer and is difficult to treat successfully once it has spread to other organs. The BRAF gene is faulty in about half of malignant melanomas and many other cancers, making it a suitable drug target. Drugs that block BRAF function in cells are already showing positive results in early clinical trials in melanoma patients in the US.

About half of the melanomas that do not have faults in BRAF have errors in a different protein called RAS. In this study, scientists examined the effect of drugs that block BRAF function on the melanomas with faulty RAS. They found that the drugs caused an unexpected activation of the processes that drive cancer cell growth. So one of the consequences of giving these drugs to patients with a faulty RAS gene is that the drug could encourage the melanoma to grow, rather than slow down.

Lead author Professor Richard Marais, a Cancer Research UK-funded scientist from The Institute of Cancer Research, said: “These unexpected findings give us much more insight into how BRAF drugs will behave in humans. These are preliminary laboratory findings, but they strongly suggest that BRAF drugs should not be given to patients who have faults in the RAS gene, because long-term use could accelerate tumour growth.

“This study highlights the importance of understanding the genetics of cancer to achieve therapeutic benefit. It will enable clinicians to select which patients they administer these drugs to, allowing them to personalise treatment for each patient. This research also provides the springboard for developing drugs that will work in patients whose tumours carry a faulty RAS gene.”

Dr Lesley Walker, director of cancer information at Cancer Research UK, said: “These findings provide an important insight into the genetic mechanisms of human cancer. They show how basic scientific research is vital to clinical care and emphasise the importance of understanding the makeup of individual cancers when using new targeted treatments of this type.

“The impact of this research will enable doctors’ testing BRAF inhibitors in the clinic to target the treatments more precisely to patients who will definitely benefit, and avoid treating those who won’t.”

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Scientists complete "groundbreaking" analyses of lung cancer and melanoma genomes

Thursday 17 December 2009

The Wellcome Trust Sanger Institute has announced the first comprehensive analyses of the genomes of lung cancer and melanoma skin cancer.

Published in Nature, the studies reveal all of the mutations that are present in the genomes of these two cancers.

The researchers analysed tissue samples taken from a lung cancer patient and a malignant melanoma patient using powerful new DNA sequencing technologies.

They then compared these genome sequences with those obtained by analysing each patient's normal tissue, enabling them to identify any changes that were specific to the cancer.

More than 23,000 mutations were found in the lung cancer genome - approximately one mutation for every 15 cigarettes smoked, according to the researchers - while the melanoma genome had more than 33,000 mutations.

Professor Mike Stratton, from the Cancer Genome Project at the Wellcome Trust Sanger Institute, pointed out that lung cancer and melanoma skin cancer are two cancers for which the main risk factors are known - smoking in the case of lung cancer and exposure to UV radiation for skin cancer.

"With these genome sequences, we have been able to explore deep into the past of each tumour, uncovering with remarkable clarity the imprints of these environmental mutagens on DNA, which occurred years before the tumour became apparent," he revealed.

"We can also see the desperate attempts of our genome to defend itself against the damage wreaked by the chemicals in cigarette smoke or the damage from ultraviolet radiation," he continued.

"Our cells fight back furiously to repair the damage, but frequently lose that fight."

The next step will be to find out which of the mutations actually cause cancer.

It may also be possible to produce a complete genome catalogue for individual patients which would inform treatment decisions.

As Dr Peter Campbell from the Wellcome Trust Sanger Institute explained, "The knowledge we extract over the next few years will have major implications for treatment.

"By identifying all the cancer genes, we will be able to develop new drugs that target the specific mutated genes and work out which patients will benefit from these novel treatments."

Professor Carlos Caldas, a cancer genomics expert from Cancer Research UK's Cambridge Research Institute, said the research was groundbreaking.

"Like molecular archaeologists, these researchers have dug through layers of genetic information to uncover the history of these patients' disease. What's so new in this study is the researchers have been able to link particular mutations to their cause.

"By repeating and refining this technique with other forms of cancer, and comparing the results to data from the Human Genome Project, the hope and excitement for the future is that we'll eventually have a detailed picture of how different cancers develop, and ultimately how better to treat and prevent them."

Harpal Kumar, Cancer Research UK's chief executive, added: "This fascinating work shows that great progress is being made to understand a lot more about how cancer develops. It shows in precise detail, and for the first time, the huge impact that smoking has in triggering the development of lung cancer, as well as the extent of the damage caused by UV radiation in relation to melanoma.

"The next step will be to find out which of these thousands of mutations are just 'collateral damage' and which actually drive these cancers. Only then can we begin to find ways to correct or prevent them.

"Cancer Research UK is extremely encouraged by this fast-emerging area of research. Never before has the potential of genomics to bring benefits to patients been so apparent, and we are already planning major new investments to add further depth to this cutting-edge work."

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Scientists find 'sibling' cancer genes work together to fight skin cancer

Monday 16 November 2009

Cancer Research UK Press Release

CANCER RESEARCH UK scientists have shown, for the first time, how two genes from the same ‘family’ can interact with each other to stop cancer in its tracks - according to new findings published in Molecular Cell*.

The team of scientists from Cancer Research UK’s Cambridge Research Institute made the unexpected discovery that BRAF, which is linked to around 70 per cent of melanomas and seven per cent of all cancers, is in fact controlled by a gene from the same RAF family called CRAF - which has also been linked to the disease.

It is hoped this surprising finding may help scientists improve a new generation of genetically targeted treatments for cancers including melanoma.

Faults in the BRAF gene can promote the growth of cancer cells via a pathway called the MAPK. This disruption causes cells to replicate uncontrollably, leading to tumours forming.

This study looked at a drug which represents an early version of a targeted treatment for malignant melanoma, the most dangerous form of skin cancer in patients. This drug - which targeted CRAF and to a lesser extent BRAF - wasn’t successful in patients with melanoma, despite its early promise in laboratory studies.

By showing that CRAF can interact with and prevent the activation of BRAF in melanoma cell lines, the scientists think they may have explained the disappointing results which came from the clinical trial and suggest that future treatments should selectively target the BRAF protein - leaving the CRAF to help fight cancer.

Lead author, Dr David Tuveson, head of experimental medicine laboratory at Cancer Research UK’s Cambridge Research Institute, said: “Previous studies on CRAF suggested it can cause cancerous changes to develop, so drugs were developed to tackle this. To our surprise, we can now see that CRAF actually helps control cancer in some situations, such as when the BRAF gene is mutated in melanoma. Strangely, in this case, two ‘wrongs’ make a ‘right’.

“We have learnt something very important about the interplay between these two genes. The first generation of BRAF inhibitors targeted both RAF genes, but the new generation, which are now being developed, should switch off BRAF and leave CRAF alone. If our hypothesis is correct, these drugs will have more success in controlling the cancer. But this avenue will need further investigation before we can be sure this is the case.”

Dr Lesley Walker, Cancer Research UK’s director of cancer information, said: “Drugs which target the genetic faults driving cancer are extremely exciting and it is important that their potential is fulfilled. This area or research is particularly important for malignant melanoma because it can be difficult to control effectively with current treatments.

“But as this study shows, targeting these genes is extremely complicated as they interact with each other in intricate ways. An increased understanding of this process will help to improve the next generation of treatments, enabling them to work more effectively.”

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More than 250,000 children sizzle on sunbeds risking skin cancer in later life

Friday 13 November 2009

Cancer Research UK Press Release

More than one quarter of a million children aged 11-17 are risking their health by seeking a tan from sunbeds - warn Cancer Research UK researchers in a letter published today in the British Medical Journal.

In England, on average, six per cent of 11-17 year olds use sunbeds. But in Liverpool and Sunderland a shocking 50 per cent of 15-17 year-old girls aim to tan on sunbeds, and more than two in five use them at least once a week.

Experts agree that using sunbeds increases the risk of developing malignant melanoma, the most dangerous and potentially fatal form of skin cancer.

Cancer Research UK data showed that children from lower socio-economic backgrounds used sunbeds more than their better-off counterparts. Researchers found that nationally of those who used a sunbed almost 27 per cent did so at least once a month in England, and almost one quarter (23.2 per cent) did so at home.

And when it came to visiting a tanning salon only just over 11 per cent of children who used sunbeds were actually shown how they worked and warned of any potential harm.

Justine Sheils, a 37-year-old administrator from Liverpool, began using sunbeds when she was 15 so she could get a base tan before summer holidays and then top the tan up when she came home. Five years ago she was diagnosed with malignant melanoma and has since had two major operations to remove cancerous tumours from her chest and the top of her head.

"The tanning salon was near my school and I used to go in for sunbed sessions on my way home," said Justine. "There was always an occasion like a party or an outing when I had the excuse to top up my tan. Now I see girls of 14 or 15 in their school uniforms going into that same salon I used to use and they come out looking like lobsters so the results of this survey are shocking but not surprising.”

Cancer Research UK commissioned two surveys*, funded by the National Cancer Action Team and supported by the department of health, to assess just how many children use sunbeds, and where. The first survey questioned 3,100 children from all over England about their tanning habits.

The second survey questioned 6,200 children across six different cities.** Researchers found that the English average of six per cent almost doubled to 11 per cent in 11-17 year olds questioned in the north of the country.

Sara Hiom, Cancer Research UK’s director of health information, said: “Allowing children to be regularly exposed to harmful radiation from sunbeds is irresponsible. The COMARE*** report recommended that the Government take strong action to protect young people from the dangers of using sunbeds. This included stopping under 18s from using sunbeds, closing down unmanned, coin-operated salons and ensuring that local enforcement officers have powers to inspect salons and check that minimum standards are being met.

“Numerous other countries, including Scotland, have introduced legislation to protect children from sunbeds; we are calling on the Government to introduce legislation as a matter of urgency.”

Children who used sunbeds were also invited to focus groups to see what they knew about health risks associated with sunbeds and to find out more about how and why they chose to use them.

Sunbed users said there was peer pressure to get a tan and that sunbeds were an easy, quick and cheap way to do that. They knew of health risks but rationalised their use by arguing that many friends used sunbeds more often than they did.

Catherine Thomson, lead author of the report and Cancer Research UK’s head of statistics, said: “The International Agency for Research into Cancer (IARC) reclassified UV radiation exposure as “carcinogenic to humans” – and this includes radiation from sunbeds and tanning beds.

“We know that rates of malignant melanoma are rising faster than any other cancer in the UK and causing more than 2000 deaths a year.”

More than 10,400 cases of malignant melanoma were recorded in the UK in 2006, with ten per cent of cases being diagnosed in the under 35s and 30 per cent in the under 50s. Incidence rates of this form of skin cancer have quadrupled since the 1970.

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Hollyoaks star bares all under the spotlight to highlight dangers of sunbeds

Tuesday 10 November 2009

Cancer Research UK Press Release

Soap Star Gemma Merna has got up-close-and-personal with her skin to highlight the dangers of sunbeds for Cancer Research UK’s SunSmart campaign.

The actress, who plays Carmel Valentine in Channel 4’s Hollyoaks, is known for her looks and year round tan. But, in these exclusive images, she has removed all traces of make-up and gone under the camera to highlight the hidden damage that sunbeds and overexposure to UV light can cause.

The specialist cameras show all the unseen damage that has been caused to the skin by overexposure to UV, given off by sunbeds and the sun. The damage that the cameras can show ranges from age and liver spots to wrinkles, dehydration and areas of damage linked to sunburn.

Gemma, 25, started using sunbeds from the age of 15. She has naturally pale skin, a type very sensitive to sun damage, and would use them once or twice a week with her friends. Gemma remembers burning quite regularly as she tried to get the tan she aspired to. Once she realised the damage she was doing to her skin, she switched to using fake tan to get her year-round glow instead. Now, Gemma wants to raise awareness of how using sunbeds can have far-reaching repercussions – not just on your looks but on your health as well.

Gemma said: “When I was younger, I didn’t realise the damage I was doing to my skin by using sunbeds. I just wanted to look tanned and to fit in with everyone and didn’t give any thought to the risks I was taking or the fact that it would actually make my skin look worse as I got older. When I realised how dangerous sunbeds were, I stopped using them and started using fake tan instead. Looking at these photos, I can see there are already signs of sun damage and I’m only 25! It’s quite shocking. You only get one skin so you really need to look after it. These pictures have convinced me for sure that I’ll never use a sunbed again.”

Jane Lewis, skin specialist, adds: “The pictures of Gemma show that she has signs of sun damage. This is particularly evident in the number of freckles she has on her forehead and across her cheeks, which are not apparent to the naked eye. It’s likely that this damage happened during her childhood and when she used sunbeds. It’s great to hear she has realised the danger she was putting herself in, and now has a really positive approach to protecting her skin.”

This time of year is a key time for sunbed use in the UK, as large numbers of people turn to sunbeds to top up their holiday tans, putting themselves at increased risk of developing skin cancer. Research shows that the intensity of some UV rays from sunbeds can be 10 - 15 times stronger than the midday sun and using a sunbed just once a month can increase the risk of developing melanoma skin cancer by more than half.

Katy Scammell, SunSmart campaign manager at Cancer Research UK, said: “By showing these shocking pictures, we’re hoping that people will see that by using sunbeds they really are storing up problems for the future. Not only do sunbeds increase the risk of developing melanoma, the most serious type of skin cancer, but they also cause irreversible damage to your skin, making it leathery, wrinkly and old before its time.”

Melanoma is now the most common form of cancer for women in their 20s, with almost one woman aged 20 to 29 being diagnosed each day. And with the total number of people developing the disease have recently crashed through the 10,000 barrier each year, it pays to look after your skin.

For more information on SunSmart please visit www.sunsmart.org.uk

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Experimental melanoma drug shows promise in early trials

Thursday 24 September 2009

Scientists have presented early clinical trial results for a new drug for melanoma - the most dangerous form of skin cancer. The findings were presented at the European cancer congress ECCO 15 - ESMO 34.

Researchers at Memorial Sloan-Kettering Cancer Centre in the US carried out a small-scale study involving a new compound, called PLX4032, that blocks the activity of a faulty protein in cancer cells.

Faults in this protein, called BRAF, are believed to be involved in around half of melanomas and five per cent of bowel cancers.Scientists recruited 31 melanoma patients, all of whom had the BRAF fault. Researchers found that, of the 22 patients who had been assessed so far, 20 had responded to the drug. Around two thirds of them showed at least 30 per cent tumour shrinkage for at least a month.

Co-lead researcher Dr Paul Chapman commented: "We are very excited about these results. Of the 22 patients we have been able to evaluate so far, 20 have had some objective tumour shrinkage. This is impressive as they all had metastatic disease and most of them had failed several prior therapies.

"A lot of these patients were pretty sick but many of them had a significant and rapid improvement in the way they function. We've had patients come off oxygen and we've got several patients who have been able to come off narcotic pain medication soon after starting treatment."

Dr Chapman explained that the experimental treatment attacks a faulty signal inside cells, whereas most chemotherapy drugs interfere with DNA replication.

"PLX4032 is different because it attacks the genetic programme that is causing the cells to divide uncontrollably, and we think the BRAF mutation is driving that programme," he revealed.

"The drug is blocking the genetics of the tumour, rather than trying to interfere with the proliferation of the cells and, as a result, there are fewer side-effects."

A further small-scale trial of PLX4032 involving 90 patients is expected to start later this year, followed by a larger phase III trial in North America, Europe and Australia.

Dr Chapman emphasised that it is too early to think of PLX4032 as a cure for advanced melanoma, but described the results as a "huge step forward".

Dr Kat Arney, Cancer Research UK's senior science information officer, commented: "Cancer Research UK and others have been investigating drugs that can block faulty BRAF, so it is interesting to see the results from a small-scale trial of such a drug.

"Melanoma is a very difficult cancer to treat and the results of this early-stage trial are promising, but larger trials need to be done before we know for sure how effective this treatment is."

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Half of sunburn cases happen at home in the UK

Monday 31 August 2009

Cancer Research UK Press Release

More than 50 per cent of people who suffered sunburn last summer were burnt while at home in the UK, according to a Cancer Research UK survey released today as Bank Holiday temperatures are expected to soar.

In a survey of nearly 4,000 people around one in five people were burnt during the summer.

And almost 10 per cent of people who got sunburnt, were burnt both in the UK and abroad.

Sara Hiom, director of health information at Cancer Research UK, said: "Sun exposure leading to sunburn is the major cause of melanoma - a potentially fatal form of skin cancer - so it's extremely worrying to see that so many people are getting burnt at home in the UK.

"The British weather causes a problem in this country. For a lot of the time we see no sun and when it does come out people want to make the most of it and may not take as much care to avoid burning as they should.

"Even though the sun's rays are more intense the closer you get to the equator we still need to take care in the UK. UV rays are invisible and can't be felt on the skin but can damage skin cells leading to sunburn and an increased risk of skin cancer. So even if it's a breezy summer day when it may not feel as warm - the potential for sunburn is still there.

"Importantly people need to know their skin. This means understanding your own skin type and knowing how likely you are to burn. Everyone is different and you're most at risk from melanoma if you have fair skin, red hair, lots of freckles, moles or a family history of the disease.

"But people do need to spend some time in the sun as vitamin D is important for good health. Everyone can make enough vitamin D from short periods of exposure to the summer sun - and this is always less than the time it takes to burn."

The survey also reported that 70 per cent of people said that using sunbeds is not safer than sun tanning.

Sarah Woolnough, head of policy at Cancer Research UK, said: "It's encouraging to see that the majority of people understand that using a sunbed is not a safer way to tan. The intensity of some UV rays from sunbeds can be 10-15 times higher than the midday sun. Too much UV can damage the DNA in our skin cells. This can mean cells start growing out of control which, over time, can lead to skin cancer.

"Cancer Research UK is calling to ban under 18s using sunbeds, close salons that aren't supervised by trained staff and ensure information about the risks of using sunbeds is given to all customers."

ENDS

For media enquiries please contact the press office on 020 7061 8300 or, out-of-hours, the duty press officer on 07050 264 059.

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Cricketers in England to get skin cancer tests

Monday 18 May 2009

First class cricketers in England are to receive skin cancer tests after figures showed that many are at risk of melanoma - the deadliest form of the disease.

A number of Australian players have had melanomas removed in recent years. Now, new statistics show that one in seven English county players who had check-ups were referred to a specialist after being found to have potential signs of the disease.

All members of the Professional Cricketers Association (PCA) will now undergo screening with private specialist clinics in a bid to detect any signs of skin cancer.

In a statement on its website, the PCA said that it takes the disease "very seriously" and is working "to raise awareness of the dangers, screening players and umpires to ensure that any signs are detected and treated early".

The organisation is also extending its skin cancer awareness campaign to supporters at cricket matches, with staff from skin clinics set to attend and inform people about the need for sunscreen and hats.

Jason Ratcliffe, assistant chief executive of the PCA, told Sky News: "Every first class player will get a 20-minute check from a visiting nurse."

Mr Ratcliffe pointed out that the length of the game and the time spent in foreign countries puts cricketers at a greater risk of skin cancer than other sportspeople.

"As such, we feel it's our duty of care to them to provide this service," he added.

Worcestershire player Kabir Ali welcomed the move, telling the news provider: "Most cricketers wouldn't notice or know what to do if they saw something on their skin. These tests are very useful for us."

Hazel Nunn, health information manager at Cancer Research UK, said: "Too much exposure to UV radiation from the sun is the main cause of skin cancer.

"People, like cricketers, who spend a lot of time outside in the middle of the day need to be especially aware of the risks and protect themselves with hats, clothing and at least factor 15 sunscreen when in strong sunlight."

Ms Nunn noted that skin cancer is much easier to treat - and the chances of survival greatly improved - if it is caught early.

She advised: "If you notice a change in size, shape or colour of a mole, freckle or other patch of skin you should get this checked out by your GP without delay."

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Molecular superfamily causes melanoma spread

Wednesday 13 May 2009

Cancer Research UK Press Release

A superfamily of molecules holds the secret to the development and spread of melanoma - the deadliest form of skin cancer, revealed a study published in the British Journal of Cancer* today (Wednesday).

Scientists based at the University of Nebraska Medical Centre investigated the roles of a superfamily of molecules called 'chemokines' and their receptor 'partner molecules' in melanoma development. The scientists ‘turned up’ the normal activity of two receptor molecules called CXCR1 and CXCR2 inside human melanoma cell lines and studied the effect on tumour growth in mice.

Their results suggested that CXCR1 and CXCR2 play key roles in the development and spread of melanoma. The scientists found that the molecules helped tumour cells to grow. And when they ‘turned up’ the activity of CXCR1 and CXCR2 in healthy cells it triggered tumour formation.

'Chemokines' together with their receptor 'partner molecules' control the movement of many types of cells in the body. Scientists already knew that some molecules from this superfamily regulated the movement of certain types of healthy cells in the body's lymphoid system and thought that chemokines might also control the migration of tumour cells in the body. Several studies have implicated CXCR1 and CXCR2 as important players in tumour progression.**

Malignant melanoma*** incidence rates in Britain have quadrupled since the 1970s killing more than 1,800 each year.It is a malignant tumour that originates in melanocytes, the cells which produce the pigment melanin that colours our skin, hair, and eyes and is the most serious form of skin cancer. If detected and treated early, it is easy to treat. But if it is ignored the cancer can advance and spread to other parts of the body, where it becomes hard to treat and can be fatal.

Professor Rakesh Singh, lead author, said: "These results suggest that a superfamily of molecules controls whether a melanoma advances and spreads to other parts of the body - when it becomes difficult to treat. There is a possibility these molecules could be used in future therapy for melanoma - something that doesn’t exist at the moment."

Dr Lesley Walker, director of cancer information at Cancer Research UK, said: "This important research helps us understand how malignant melanoma progresses and spreads.

"Malignant melanoma is the most deadly form of skin cancer and a life threatening disease which could be prevented if people protect themselves in the sun with at least factor 15 sun cream, covering up, wearing sunglasses and staying in the shade between 11 and three when the sun is hottest. Sun beds are just as dangerous as staying out too long in the sun."

ENDS

For media enquiries please contact the pres office on 020 7061 8300 or, out-of-hours, the duty press officer on 07050 264 059.

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