The drug vemurafenib has been successful in treating advanced melanomas with BRAF mutations, but was surprisingly unsuccessful in treating colon cancers with the same mutations, says Nature News' Heidi Ledford. A new study in Nature may shed some light on why colon cancer has resisted this drug, and may also offer answers as to how to get around that resistance. To examine the problem, researchers at the Netherlands Cancer Institute used an RNAi screen, and found that colon cells with BRAF mutations became sensitive to vemurafenib only after the expression of EGFR was knocked down, Ledford says. "In fact, treatment with vemurafenib activated EGFR in colon tumors, but not in melanoma, where EGFR is expressed only at low levels," she adds. This finding could mean that coupling EGFR inhibitors with vemurafenib may work to treat the 8 percent to 10 percent of colon cancers with a BRAF mutation.
Jan 31, 2012