Melanoma mutation rewires cell metabolism
A mutation found in most melanomas rewires cancer cells’ metabolism, making them dependent on a ketogenesis enzyme, researchers at Winship Cancer Institute of Emory University have discovered.
The finding points to possible strategies for countering resistance to existing drugs that target the B-raf V600E mutation, or alternatives to those drugs. It may also explain why the V600E mutation in particular is so common in melanomas.
The growth-promoting V600E mutation in the gene B-raf is present in most melanomas, and also in some cases of colon and thyroid cancer. Drugs such as vemurafenib are available that target this mutation, but in clinical trials, after a period of apparent remission, cancers carrying the V600E mutation invariably develop drug resistance
Researchers led by Jing Chen, PhD and Sumin Kang, PhD found that the B-raf V600E mutation stimulates cancer cells to produce more of the enzyme HMG-CoA lyase, and that melanoma cells with the V600E mutation are dependent on that enzyme, while other melanoma cells are not.
Click here to view the full story in the Emory News Center. The story was also featured on the Science 2.0 blog.