NCI Cancer Bulletin: A Trusted Source for Cancer Research NewsNCI Cancer Bulletin: A Trusted Source for Cancer Research News
October 4, 2005 • Volume 2 / Number 38 E-Mail This Document  |  Download PDF  |  Bulletin Archive/Search  |  Subscribe

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A Conversation with Dr. Robert Weinberg

Dr. Robert Weinberg Dr. Robert Weinberg is a founding member of the Whitehead Institute for Biomedical Research at the Massachusetts Institute of Technology. His lab has pioneered discoveries in cancer biology since the late 1970s, including the first human oncogene and the first tumor suppressor gene. He was awarded the National Medal of Science in 1997. On September 28, he discussed "Mechanisms Leading to the Formation of Human Malignancies" in the Stars in Nutrition and Cancer lecture series at NIH.

What is your lab's current model of cancer formation and metastasis?
This is the last frontier of cancer research, but we have a good rough map of the territory. Earlier work with the telomerase gene allowed Vogelstein in 1989 to diagram the five signaling pathways normal human cells must navigate to become tumorigenic. Along the way, they accumulate gene mutations in a process that is very much driven by Darwinian evolution, played out in the microcosm of the body's tissue.

Metastasis is a critical issue in cancer because 9 of 10 cancer deaths are due to distant metastases, not to the primary tumor. Once a small cluster of cells has reached a distant site, the transition from microscopic to macroscopic metastasis occurs very inefficiently. Perhaps only one in a million cancer cells will be the progenitor of an ultimate, possibly life-threatening, macro-metastasis. We are studying four different transcription factors that we believe can program the invasiveness of primary tumor cells that allows them to metastasize: Twist, Slug, Mesenchyme Forkhead, and Goosecoid. Each of these, which is normally active during early embryonic development, has the ability to force cells to become invasive and metastatic.

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What role do you see for nutrition in cancer prevention?
It is clear that far more people could avoid cancer by following the precepts developed here at the Division of Cancer Prevention than could ever be saved by even the most successful therapies. I find it quite remarkable that body mass index has such a high positive correlation with the incidence of many types of cancer. The American Cancer Society estimates that 90,000 cancer deaths a year are attributable to obesity. I think it's plausible that insulin-like growth factors present in elevated concentrations in the blood of the obese perturb the biology of cells throughout the body and inhibit their natural death. This could lead in turn to their developing into cancer cells.

What does the future look like for cancer biology?
We know that each of the 110 major types of human cancer has its own genetic biography, its sequences of accumulated genetic changes. The question is whether certain laws will emerge that enable us to rationalize why these changes occur in all of these types of cancer cells. I do expect that the molecular and genetic mechanisms that we and others are uncovering will eventually coalesce into a set of rules that explain how all types of cancer arise. This holds the prospect of making cancer research into a logical, rigorous science rather than just a collection of diverse phenomena that are only described without being understood.