They found that many of the mutations were redundant, meaning that many of them affected components of the same pathway.
"The key to survival for cancer cells is redundancy: hit multiple pathways, mutate as much as you possibly can and then you can survive anything that comes at you," Borghaei explained.
The authors point out that this is one analysis from one patient. Other patients with lung cancer will have different mutational profiles, as will other tumor types.
And this particular tumor was smoking-related, with all of the damage conferred by cigarette carcinogens.
"In this particular case, it's smoking-related," Zhang said. "When you have a patient who has a long history of smoking, you can tell that most of the mutations are mediated by carcinogens, so we anticipate that we will observe a lot more mutations in such a [patient]."
The same is likely to be true of melanoma, because much of the damage here is caused by UV radiation, Zhang added, but the number of mutations in breast and prostate cancer, for instance, is likely to be much lower.
The U.S. National Cancer Institute has more on lung cancer.
SOURCES: Zemin Zhang, Ph.D., senior scientist, Genentech Inc., South San Francisco; Hossein Borghaei, D.O., director, Lung and Head and Neck Cancer Risk Assessment Program, and assistant professor, Fox Chase Cancer Center, Philadelphia; May 27, 2010, Nature
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