The research showed treatments that disable cancer-promoting genes called oncogenes are much more successful in eradicating tumors in the presence of a signaling molecule secreted by kind of immune cell called a T helper cell.
The finding is important because many drugs now in use in humans are often tested in lab animals with weakened immune systems and many human cancer therapies actually compromise a patient's immune system.
"We may be biasing ourselves by expecting these drugs to work on their own, without factoring in the effect of the immune system," said Dean Felsher, MD, PhD, associate professor of medicine and of pathology and the leader of the Stanford Molecular Therapeutics Program. "We're looking for efficacy while ignoring a whole part of biology. What we're choosing as the best candidates may not in fact be the best drugs for patients."
Felsher, who is also a member of the Stanford Cancer Center, is the senior author of the research, which will be published online Oct. 28 in Cancer Cell.
Oncogenes are genes that, when mutated, contribute to the development of many cancers including leukemias and lymphomas. Although cancers are by nature quite complex, some types of tumors rely so completely on the activity of the mutated genes that researchers have coined the term "oncogene addiction." Blocking the effect of these oncogenes -- the focus of several current cancer therapies -- can cause the tumors to shrink. For instance, the drug imatinib, marketed as Gleevec, targets a key oncogene in chronic myelogenous leukemia and gastrointestinal stromal tumors.
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