ANN ARBOR, Mich. A University of Michigan study reveals in detail 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. Analysis of this gene is also a hot area of interest among researchers trying to explain colorectal, stomach, lung and other forms of cancer.
The new study 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 CHFR can lead to the survival of genetically unstable cells loaded with too many chromosomes, which can lead to cancer.
"Our findings show that loss of CHFR disrupts normal chromosome segregation in breast cells during cell division and creates genomic instability, which can drive genetic mechanisms that accelerate the development of cancer," says Elizabeth Petty, M.D., a U-M professor in the departments of human genetics and internal medicine and the senior author of the study. The article appears online ahead of print in the journal Neoplasia.
The new knowledge eventually could provide the scientific basis for diagnostic markers and identify which patients can benefit from specific types of cancer drugs.
"Our previous findings, and the work of others, have shown that cancer cells cultured in the lab that have low or absent CHFR expression are more susceptible to treatment with a class of drugs called taxanes, such as paclitaxel (Taxol) and docetaxel, that attack the dividing cells when they are trying to separate their chromosomes," says Lisa Privette, Ph.D., the study's first author, a recent U-M Medical School graduate and now a researcher at Cincinnati Children's Hospital.
"These drugs are frequently used to treat breast cancer and other types of cancer and they work by targ
|Contact: Anne Rueter|
University of Michigan Health System