report of BCRF symposium 2004

At BCRF's 2004 Symposium on October 13th, five leading scientists reported on breakthroughs that are pointing the way toward a revolution in breast cancer treatment and prevention. Eminent oncologist Larry Norton, M.D., chair of BCRF's Medical Advisory Board and scientific director, moderated the discussion.

2004 Jill Rose Award co-recipients, Michael Bishop, MD, (pictured left) chancellor of the University of California, San Francisco, and Harold Varmus, MD, president of Memorial Sloan-Kettering Cancer Center, (pictured second left) who shared the 1989 Nobel Prize in medicine for their insights into cancer-promoting genes known as oncogenes, spoke about new findings. Described as "jammed accelerators" inside the cell, oncogenes are damaged versions of genes that normally play essential roles in regulating cell growth. "Our cells contain hundreds, if not thousands of potential oncogenes," explained Dr. Bishop.

Dr. Varmus's comments focused on another set of genes, the tumor suppressors, which usually help guard against cancer. If oncogenes are the accelerators of cell growth, noted Dr. Varmus, tumor suppressor genes are the brakes. When mutations disrupt their function, though, the so-called tumor suppressor genes can contribute to the uncontrolled proliferation of cancer cells. A prime example is the BRCA1 gene, which is often abnormal in breast cancer patients.

Michael Wigler, PhD, of Cold Spring Harbor Laboratory, a grantee since 1999, described how his research group is scrutinizing human genetic blueprints for changes that increase cancer susceptibility. Some of these changes are tiny DNA "point mutations," while others are large genetic additions or deletions. By correlating genetic changes with cancer development, Dr. Wigler's work will aid in optimizing treatments and, eventually, in designing novel interventions.

Cancer cells possess the dangerous ability to divide indefinitely. According to Titia de Lange, PhD, of The Rockefeller University, the reason may be found by studying their telomeres, or chromosome ends. In most human cells, the telomeres erode each time the cell divides, and when the chromosomes become too short, the cell dies. Many cancer cells have learned to activate a telomere-maintaining enzyme, thereby achieving a sort of cellular immortality. Because this enzyme has no role in most human cells, it offers an attractive target for cancer treatment.

Other promising strategies focus on genes and proteins involved in tumor cell metastasis, which accounts for virtually all breast cancer deaths, said Robert Weinberg, PhD, of the Whitehead Institute for Biomedical Research. Cancer cells use a variety of "biological gymnastics" to invade surrounding tissue, travel through the bloodstream, and seed tumor colonies at distant sites in the body. Long considered a process too complicated to understand, metastasis is finally yielding its molecular secrets.

Much of the research described at this year's Symposium has broad implications. As Dr. Norton noted in his concluding remarks, "by unraveling the mysteries of breast cancer, we are casting light on many other cancers as well."