Training Woes... and Light at the End of the Tunnel

I really can't complain, given the suffering that chemo patients go through--not even close--but for the past month or so, I've been in denial about a foot injury that's made my running increasingly painful and effectively brought to a halt my preparations for the Boston Marathon (in support of the Dana-Farber Cancer Institute). That's the bad news.

The good news is that, after a visit to the 'regular' doc (practically useless) a visit to the most amazing running doc on the planet (Tom Michaud, DP) who just happens to practice a mile from my house and just happens to treat many of the top runners in the world, two visits (and counting) with the amazing physical therapists at Boston Sports Medicine, plus some friendly and highly actionable advice from the non-running X-ray tech who suffers from the same condition (plantar fasciitis), I'm well on the road to recovery. (Funny how some of the most practical advice came from the lowest paid person in this entire circus.)

Just to be sure though, I'm taking a week off on the advice of DFMC team coach and 1976 Boston Marathon winner, Jack Fultz who knows a thing or two about running--as well as injury. In order to keep the withdrawal symptoms to a minimum, I hopped on my cobweb-covered CompuTrainer last night. Man, am I out of cycling shape! A long way from my last triathlon five and a half years ago at Ironman New Zealand.

Wise readers of this blog may wish to buy stock in Advil.

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.

Cancer Research Breakthrough - You Ain't Seen Nothin' Yet!

Check out this article on the front page of today's Boston Globe [emphasis added]:

An international team led by a Boston researcher yesterday unveiled the most detailed look ever at the genetic ravages inside a lung tumor, finding at least one target for drug research and laying the foundation for an ambitious - and controversial - federal effort to identify all the DNA damage that causes major cancers...

...the researchers - including scientists from the Dana-Farber Cancer Institute and the Broad Institute of Harvard and the Massachusetts Institute of Technology - said their study validates a new approach to fighting the nation's number two killer: systematically identifying genetic changes that turn healthy cells cancerous, in hopes of finding cancer's weaknesses. The study serves as a pilot project for the federal government's proposed 10-year, $1.5 billion research program to map the genetic blueprint of the 50 most lethal cancers.

"You ain't seen nothin' yet," said Dr. Matthew Meyerson of Dana-Farber and the Broad who is the lead author of the paper posted online yesterday by the science journal Nature. "The potential for finding things that will help cancer patients is so great. This absolutely gives me much more confidence that we should go forward" with similar research in other types of cancer.

Writes DFMC program head, Jan Ross: "Dr. Meyerson, is a Dana-Farber scientist and former Barr Investigator whose early research efforts in this area were funded by DFMC." Those of you who have contributed to DFMC in the past should take a moment to smile with great hope.

Want to fund the next Meyerson? Go here.