In the latest series on cancer and genetics, we look look at how breast cells produce new cells that are predisposed to become cancerous, unless they receive the protective action of the CHFR gene.

CHFR expression is missing in more than a third of breast cancers.  Is that significant or just an effect?  Scientists are currently paying this gene a significant amount of interest because it may also have a key role to play in colorectal, stomach, lung and other forms of cancer. 

Why do some women lack CHFR function or have low function in the first place? Currently, there’s no evidence that women inherit mutations that lead to low or absent CHFR protein.  It’s therefore likely that some other mechanism is shutting down the CHFR gene.


Images courtesy of University of Michigan.

A study from the University of Michigan reveals how and why new “daughter” cells, produced as cells in body tissues renew themselves, receive too few or too many chromosomes if expression of the CHFR gene is missing or low.  The loss of the CHFR gene can lead to the survival of genetically unstable cells loaded with too many chromosomes, which ultimately can lead to cancer.

The article appears online ahead of print in the journal Neoplasia.  If interested, you can access the abstract HERE or the full article as a PDF HERE.

Previously, the research team showed that loss of CHFR was associated with increased tumour size, and that normal breast epithelial cells would develop traits of cancer cells if CHFR was blocked.

So what do these findings mean?  Well, they could provide the scientific basis for diagnostic markers and identify which patients can benefit from specific types of cancer drugs.

For example, it has been shown that cancer cells cultured in the lab that have low or absent CHFR expression are more susceptible to treatment with a class of chemotherapy drugs called taxanes, such as paclitaxel (Taxol) and docetaxel (Taxotere).

These drugs are frequently used to treat breast cancer and other types of cancer and they work by targeting the structure used to separate chromosomes.  The new results offer further evidence of this relationship and begins to explain how the expression of CHFR alters the cell’s response to these kinds of drugs. 

It is possible that doctors may eventually decide which patients need different chemotherapy regimens based on the presence or absence of different types of genes.  We already know, for example, that women with breast cancer who over-express HER-2 will do better on Herceptin than those who do not.  Expanding this concept to chemotherapy allows patients to potentially receive personalised treatment with higher chances of success in stopping the cancer in its tracks.