British scientists are developing a new drug that could stop the spread of breast cancer in a fifth of sufferers, reported the Daily Express . It said that the drug is based on a genetic ‘breakthrough’ that identified how cells break away from highly aggressive HER2 breast cancers.
This news story was based on laboratory research looking at the role of a gene called C35 in breast cancer cells. The researchers were interested in C35 as 40-50% of breast tumours produce excess amounts of C35 protein. They found that cells producing excess amount of C35 in the laboratory take on the characteristics of cancerous cells, e.g. being able to spread. The study carried out preliminary tests that found certain chemicals could stop C35 causing some of these changes occurring in laboratory-grown cells. Much more research will be needed to determine whether these chemicals might be safe and effective for testing in humans.
This research contributes to our knowledge of which genes play a role in the development of breast cancer. Such advances are important for identifying possible targets for new drug development. However, it is unfortunately much too early to say that we have a new drug for stopping the spread of breast cancer.
Where did the story come from?
The study was carried out by researchers from the University of Edinburgh and other research centres in the UK and US. It was funded by the Scottish Funding Council and Breakthrough Breast Cancer. Two of the authors work for a company called Vaccinex Inc, which discovered that C35 was a biomarker for breast cancer. The study was published in the peer-reviewed British Journal of Cancer.
The Daily Express, Daily Telegraph , and BBC News covered this story. The Express and Telegraph headlines highlight the possibility of a new drug, with the Express headline implying that the drug already exists. This claim is not supported by the current research, which investigated the role of a gene called C35 in breast cancer cells in the laboratory. This did involve looking at certain chemicals that could interfere with the effects of C35 on cells in the laboratory, but it is much too soon to suggest that a ‘new drug’ has been developed that ‘stops’ the spread of breast cancer. The BBC News headline better reflected the findings of the research, noting that a gene involved in the spread of cancer has been found.
What kind of research was this?
This laboratory study investigated the role of a gene called C35 in breast cancer. In about a fifth of breast cancers the tumour cells have undergone a genetic mutation. This results in the cell carrying multiple copies of a piece of DNA, which carries the HER2 gene as well as other genes, including C35. Tumours carrying this mutation (called HER2 positive tumours) tend to be more aggressive than those that do not. This is at least in part because the cells are producing too much HER2, but could also be due to them producing more of the proteins encoded by other copied genes such as C35. The researchers wanted to investigate whether this was the case, particularly as about 40-50% of breast cancers are reported to produce excess amounts of the C35 protein.
Laboratory research is essential to furthering our knowledge of how cells become cancerous. Such knowledge can help to identify targets for new drug treatments.
What did the research involve?
The researchers used tissue samples from 122 primary breast cancers and examined whether the cells producing excess HER2 protein also produced excess C35 protein. They also took some normal breast tissue cells and genetically engineered them to produce excess C35 protein to see what happened. Finally, they looked at whether a protein called Syk, which they thought might be involved, was needed for C35 to have an effect. They did this by looking at whether blocking Syk with two chemicals, called BAY61-3606 and piceatannol, stopped C35 from having an effect on the genetically engineered cells.
What were the basic results?
The researchers found that breast cancer tissue that produced excess HER2 protein also tended to produce more C35 protein.
Normal breast tissue cells that were genetically engineered to produce excess amounts of C35 protein took on some of the characteristics of cancer cells. This included forming clumps of ‘colonies’ when grown in a soft gel in the laboratory, and spreading through such gels. The cells also lost their typical characteristics and took on the characteristics of less specialised, more immature cells, another characteristic typical of cancer cells. Further investigation showed a protein called Syk was involved in allowing C35 to have these effects. Blocking the action of Syk using the chemicals BAY61-3606 or piceatannol also blocked some of the effects of C35.
How did the researchers interpret the results?
The researchers conclude that ‘amplifying’ the C35 gene can promote a normal cell to develop the characteristics of a cancer cell (that it, it acts as an ‘oncogene’) in breast cells grown in the laboratory. They suggest that drugs targeting C35 or Syk “might be helpful in treating a subset of patients with HER2-amplified breast cancers”.
This research contributes to our knowledge of which genes play a role in the development of cancer. Such advances are important for identifying possible targets for new drug development. Although the researchers did illustrate that chemicals known to inhibit the activity of Syk can reduce the effect of C35, much more research will be needed to determine whether these chemicals might be appropriate for use in humans.
The path to developing a new drug for use in humans is a long one and designed to be as certain as possible that the drug will be effective and safe. Therefore, even if these chemicals are successful in the laboratory, they will also have to be tested on animals before they can be tested on humans. It is much too early for newspapers to report of a new drug that stops the spread of breast cancer, but research such as this will hopefully yield new treatments in the long term.