A number of these so-called targeted cancer drugs -- such as Roche's Tarceva and Novartis' Gleevec -- work by blocking the activity of various protein switches that tell the cell to grow. They are known as receptor tyrosine kinases or RTKs.
"They essentially allow the cell to communicate with the external world to sense growth factors that could maintain the survival of a cancer cell," said Dr. Ronald DePinho of the Dana-Farber Cancer Institute and Harvard Medical School, whose study appears in the journal Science.
These protein switches are on the surface of all cells, and they go haywire in a number of cancers.
Drugs that target a single switch have transformed the treatment of some patients with certain cancers -- for instance, Gleevec and chronic myelogenous leukemia.
But they only work in a small percentage of people. And certain tumors, including the aggressive brain cancer glioblastoma multiforme, respond poorly to such drugs.
DePinho and colleagues now believe they know why. His team studied 20 different batches of glioblastoma cells in the lab and found that many growth switches were flipped on at once.