Herceptin 'may target breast cancer stem cells'
New US research has suggested that the effectiveness of new 'targeted' breast cancer drugs, such as Tyverb (lapatinib) and Herceptin (trastuzamab), may be due to their ability to target a small group of cells known as cancer stem cells.
Many scientists think that tumours originate from a small number of these cancer stem cells - which represent fewer than five per cent of cells in a typical tumour - and that the cells are responsible for fuelling a tumour's growth.
Researchers at the University of Michigan Comprehensive Cancer Centre have now found that the HER2 gene, which is highly active in around a fifth of breast cancers, causes cancer stem cells to multiply and spread.
The discovery sheds light on why HER2-positive breast cancers tend to be more aggressive than other forms of breast cancer, and why they are often able to spread to other parts of the body.
However, several new targeted therapies have been designed to target cancer cells with high levels of HER2, so one reason for their success might be that they seek out and destroy cancer stem cells directly.
Study author Dr Max Wicha, professor of oncology and director of the University of Michigan Comprehensive Cancer Centre, commented: "This work suggests that the reason drugs that target HER2, such as herceptin and lapatanib, are so effective in breast cancer is that they target the cancer stem cell population.
"This finding provides further evidence for the cancer stem cell hypothesis."
The study, which is published in the journal Oncogene, revealed that breast cancer cells which over-express HER2 contain between four and five times more cancer stem cells than HER2-negative cancer, indicating that the gene causes them to multiply.
In HER2-positive cancers, cancer stem cells also tend to invade surrounding tissue, suggesting that the gene is involved in driving the spread of cancer.
However, laboratory tests on breast cancer cells revealed that in HER2-positive cells treated with herceptin, the number of cancer stem cells fell by 80 per cent to the levels found in HER2-negative breast cancer cells. The drug had no noticeable effect in HER2-negative cells.
Co-author Dr Hasan Korkaya, a research fellow in internal medicine at the University of Michigan, revealed that the team is now looking more closely at what happens with HER2 is over-expressed.
"Our hope is that we could develop inhibitors of these pathways that might be effective in targeting cancer stem cells in women whose tumours do not over-express HER2 or those who are resistant to herceptin," he added.