Cancer's "Genomic Landscapes"

This morning's issue of the journal Science (released about ten minutes ago) carries a paper ("The Genomic Landscapes of Human Breast and Colorectal Cancers") that I don't claim to even begin to understand... but which sounds tremendously promising. Emphasis added:

Human cancer is caused by the accumulation of mutations in oncogenes and tumor suppressor genes. To catalog the genetic changes that occur during tumorigenesis, we isolated DNA from 11 breast and 11 colorectal tumors and determined the sequences of the genes in the Reference Sequence database in these samples. Based on analysis of exons representing 20,857 transcripts from 18,191 genes, we conclude that the genomic landscapes of breast and colorectal cancers are composed of a handful of commonly mutated gene "mountains" and a much larger number of gene "hills" that are mutated at low frequency. We describe statistical and bioinformatic tools that may help identify mutations with a role in tumorigenesis. These results have implications for understanding the nature and heterogeneity of human cancers and for using personal genomics for tumor diagnosis and therapy.

One of the study's authors, Michail Shipitsin, is affiliated with the Department of Medical Oncology at Dana-Farber, as well as the Harvard Medical School. (That's him in the picture above). Go Michail!! Here's another article featuring his work--this one in terms more understandable to us laymen (emphasis added):

Doctors usually measure how well a cancer treatment works by how much tumor it destroys. The more cancer cells killed the better. The eradication of every last mutated cell is ideal, because nearly every tumor cell can regenerate the disease. Or so cancer biologists believed.

Treatments aimed at purported cancer stem cells may miss the deadly metastases that kill patients, suggests a new study...

A radically different idea is transforming cancer research. In this view, a relatively few dangerous cells fuel cancer growth. The implications are profound: find and kill this minority of crucial cells, and the rest of the tumor may languish or even self-destruct. This popular notion is called the cancer stem cell hypothesis.

A new study of human breast cancer tissue challenges this hypothesis in solid tumors. The presence of purported breast cancer stem cells in the primary tumors increased the risk of distant metastases, the researchers found, but the metastases were packed with more differentiated non-stem cancer cells. An experimental molecular therapy that shut down the “stem cells” in culture did not affect the more differentiated cells.

“Patients are killed by the metastases composed of cancer non-stem cells, even though it could have been the cancer stem cells that metastasized,” said senior author Kornelia Polyak, HMS associate professor of medicine at Dana–Farber Cancer Institute. Both groups of cancer cells are bad, she and her co-authors conclude in the March Cancer Cell, with distinct molecular pathways requiring differently targeted drugs.

Go Kornelia!! (That's her, in the picture above.)

Hey, if athletes, actors and musicians can be rock stars, why not cancer researchers too? :)

UPDATE: Turns out Kornelia (Nelly) Polyak was a DFMC teammate in 2006.