Not Good News on Cancer
One of the first ideas people had when attempting to come up with a drug treatment for cancer was to discover what was different between a normal and a diseased cell. This seemingly smart idea was totally stymied because at the molecular level a cancer cell is bafflingly complex with scads of measurable differences compared to its healthy counterpart. The result is that most of the effective therapeutic agents are nonspecific toxins with lots of side effects.
The modern solution to this problem is to design drugs that ferret out the “critical lesion” among the many biochemical changes observed in a neoplastic cell. Hence, Gleevec, Erbitux, Herceptin and a few other new drugs that target essential growth pathways gone haywire in cancer. These can be very effective in patients whose cancer contains the altered target, but this is not all patients and even for the “lucky” ones, the specter of acquired drug resistance is ever present.
And now comes worse news. A large collaboration involving both American and European institutions examined whether individual cells inside the same tumor mass had different underlying biochemical changes. They measured DNA sequence differences at several locations within a person’s cancer and found that in every case examined there is not homogeneity of genetic alteration at different parts of the tumor. In some patients there is even the simultaneous presence of both “good” and “bad” prognostication for therapeutic response in a single tumor.
Why does this matter? Because any attempt to design a personalized therapy based on a single biopsy is likely to fail if other un-sampled areas of the tumor have a different drug response pattern. What is the solution? The authors remain silent, suggestive of a very hard problem.
Tom Tritton is President and CEO of CHF.