News

The discovery of a key molecule linked to the immortalization of human tumor cells provides an important new target for anti-cancer drug design. Researchers led by Dr. Robert A. Weinberg of the Whitehead Institute for Biomedical Research have isolated and cloned the gene for the long-sought catalytic subunit of human telomerase, a molecule believed to play a major role in the transition from normal to cancerous growth.

The National Academy of Sciences today announced that two faculty of the Whitehead Institute for Biomedical Research, Dr. Peter S. Kim and Dr. Eric S. Lander, have been elected to membership in the National Academy of Sciences (NAS). Dr. Kim, who is also Associate Investigator of the Howard Hughes Medical Institute (HHMI), recently discovered a structure on the surface of HIV that could lead to a new strategy for designing AIDS drugs. Dr. Lander, a pioneer in gene mapping and sequencing, is director of the Whitehead/MIT Center for Genome Research. Both are also professors of biology at the Massachusetts Institute of Technology

A new study has found that Deleted in Colorectal Cancer (DCC), a gene thought to play a role in human colorectal cancer, does not play a role in the development of mouse colon cancer. Instead, the mouse version of the DCC gene, called Dcc, functions as a receptor involved in the wiring of the brain and the spinal cord. DCC was first identified in 1990 as a candidate "tumor suppressor" gene that acts as a brake during normal growth of colonic cells but is missing in most colon cancer cells. The new mouse study, led by Dr. Amin Fazeli in the laboratory of Dr. Robert Weinberg at the Whitehead Institute for Biomedical Research, weakens the candidacy of DCC as a cancer gene and sho;ws that the gene helps establish connections in the developing nervous system.

For the first time scientists have a high-resolution picture of the protein fragment that enables HIV (the AIDS virus) to invade human cells—work that has immediate implications for new drug design. In the April 18 issue of Cell magazine, Dr. Peter S. Kim and his colleagues at the Whitehead Institute for Biomedical Research and the Howard Hughes Medical Institute present the crystal structure of a key fragment of the HIV envelope protein.

Using a method of surveying an entire mammalian genome, scientists have discovered that an immune system protein may play a previously unsuspected role in quelling the spread of tuberculosis infection. The finding has implications for devising new therapies for tuberculosis (TB), especially for the drug resistant strains that now affect some 50 million people world wide. The study, reported in the June 10 issue of the Proceedings of the National Academy of Sciences, was led by Dr. Richard Young at the Whitehead Institute for Biomedical Research. "We believe this is the first time that scientists have used a survey of the entire genome to identify genes turned on by infectious agents. We suspect that this method (strategy) will become a powerful new weapon in the war against other microbes, including HIV," says Dr. Young.

An international consortium of genome laboratories from North America, Europe, and Japan has created a unified gene map that establishes the location of more than 16,000 human genes. The unified gene map represents the first edition of the quintessential goal of the Human Genome Project—a catalog of all the genes that make up a human being—and provides the location of one in five of all human genes.

Keynote speaker Dr. Harold E. Varmus, director of the National Institutes of Health (NIH), President Charles M. Vest of the Massachusetts Institute of Technology (MIT), and Senator Paul E. Tsongas, Chairman of the Board of the Whitehead Institute for Biomedical Research, joined more than 300 business leaders, educators, and scientists in dedication ceremonies for the Whitehead Institute's new research wing.

Non-insulin dependent diabetes mellitus (NIDDM) affects more than 100 million people worldwide. Screening more than 4,000 individuals from an isolated region in Finland, an international research group has located a gene, called NIDDM2, that may be involved in a significant fraction of adult-onset diabetes tied to low insulin secretion. The strategy used to find this gene has important implications for genetic analysis of other complex diseases (caused by the interaction of multiple genes and the environment), as well as our understanding of the causes of human diabetes.

For decades the human Y chromosome, the male sex chromosome, has been the Rodney Dangerfield of human genetics: "it don't get no respect." For long, the Y was considered to be little more than a smaller, less stable version of the X. Now, new evidence from Dr. Page and his collaborators at the Whitehead Institute, the Massachusetts Institute of Technology, and the University of Washington reveals that the Y chromosome has led an independent existence after all.

Familial hypercholesterolemia, a genetic disease characterized by high levels of cholesterol and early mortality, is caused by defects in the receptor for the low-density lipoprotein (LDL)—the bad cholesterol. Now, Boston area scientists have found that this occurs because mutations in the LDL receptor prevent the protein from folding into its normal shape. This in turn impedes the receptor's ability to bind bad cholesterol and remove it from the bloodstream, causing the hypercholesterolemia.