If you want cancer cells to respond to internal signals telling them to die like they're supposed to die, you have to blunt the signals they're receiving telling them to proliferate, according to research from Stanford University.
This is the formula behind therapies that are successful at targeting cancer-causing genes—they do not induce cell death; rather, they slow the rate of tumor cell division.
Stanford University associate professor of medicine and of pathology Dean Felsher calls it "just advanced high-school-level math" and says that they are able to use it to determine "when a cancer is addicted to a particular cancer gene and will respond to therapy targeting that gene."
The research was published in the most recent issue of the journal Science Translational Medicine. In it Felsher and colleague David Palk explore what they call "oncogene addiction", a situation in which a cancer becomes dependent on the activity of a single cancer-causing gene.
The act of blocking the activity of that oncogene can cause tumors to regress and by using their computational biology approach, they can "quickly predict whether the tumor is oncogene-addicted and likely to be treated successfully by targeted therapies."
Source: Medical News Today
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