274: Random evolution of drug resistance in cancer

Why Some Lung Cancers Stop Responding to Tarceva and Iressa | Science Blog:

The study involved six patients who had received treatment with gefitinib or erlotinib and who later developed acquired resistance. Researchers studied samples taken from the patients' tumors at different times before and during treatment. All of the tumors had the kinds of mutations in the EGFR gene that were previously associated with responsiveness to these drugs. But, in three of the six patients, they found that tumors that grew despite continued therapy had an additional mutation in the EGFR gene, strongly implying that the second mutation was the cause of drug resistance. Further biochemical studies showed that this second EGFR mutation, which was the same in all three tumors, could confer resistance to the EGFR mutants normally sensitive to these drugs.

It wasn't a supernatural "designer" who made these people's tumors resistant to drug therapy. There were random mutations in each cancer cell, and pretty soon one cell wasn't killed by the drugs. Soon, all the original cells were dead, and the cancer was drug resistant. Evolution.