|DNA Mutations Help Lung Cancer Drug Work|
By Kate Ruder
Posted: July 29, 2004
A small percentage of people with lung cancer improve dramatically while taking the drug Iressa, and these people have similar genetic mutations in their tumors, scientists reported a few months ago.
Now, a new study has found a connection between the gene mutations and the drug’s effects. According to the research, Iressa blocks a signal in tumor cells that is caused by the gene mutations, and tumors cannot live without the signal. So they end up dying.
“The burning question has been: What is it about the mutations that make the tumors more sensitive to this drug?” says Jeffrey Settleman of Massachusetts General Hospital Cancer Center and Harvard Medical School in Charlestown , who led the study.
Settleman and his colleagues were primarily interested in the gene mutations. These mutations, they found, turn on a strong survival signal that the tumor cells depend on. When a drug such as Iressa inhibits this specific signal, a tumor cell dies.
Drugs such as Iressa and Gleevac are part of a relatively new class of drugs that target a specific receptor in tumors called the epidermal growth factor receptor (EGFR). Some patients on these drugs can live months or years longer than expected.
“In a sense, the tumors become dependent or addicted to the signal from the gene mutations,” says Settleman. “Interfering with the signal with Iressa kills the cells rapidly.”
I. Bernard Weinstein of Columbia University in New York City agrees with the findings and says that they provide a clear example of how cancer cells become addicted to a specific signal they then depend on for their survival.
“The broader implication of this research is to then find other tumors and cancers that are also addicted to this pathway and responsive to this drug,” Weinstein says.
The study appears online today in Science.
See Related Article: Why a Lung Cancer Drug Works So Well in Some People