For Release on June l, l998

For Further Information Contact:

Johanna Spangenberg (703) 527-7424
or Donna Krupa at (703) 527-7357

ADVANCES IN DETERMINING CAUSES OF CANCER: UPDATE PRESENTED AT GENERAL MOTORS CANCER RESEARCH FOUNDATION'S 20th ANNUAL CONFERENCE

Two-day session at the National Institutes of Health offers research findings which demonstrate why developmental biology can help stop the growth of cancers of embryonic-type cells

More than 300 of the world's leading cancer research scientists will be attending the General Motors Cancer Research Foundation Annual Conference, "Developmental Biology and Cancer," to be held June 9-10, 1998, at the Jack Masur Auditorium, National Institutes of Health, Bethesda, MD.

Attendees will hear internationally renowned physicians and scientists offer the latest findings in cancer research as applied to developmental biology, which is concerned with describing and understanding how a fertilized egg, spore, or bud turns into an adult organism. In addition, lectures will be given by the recipients of the 1998 General Motors Cancer Research Foundation Awards.

This year marks the 20th anniversary of the General Motors Cancer Research Foundation, formed to recognize individual excellence in cancer research. After twenty years cancer research remains a key philanthropic priority for GM as it annually honors basic and clinical scientists throughout the world for demonstrated achievements in research on the causes, prevention, and treatment of cancer.

The Program Medical and Scientific Presentations: Over the two-day conference, four scientific sessions featuring 17 research presentations are scheduled. The dates and agenda of each follow:

Tuesday, June 9, l998

Session I

Pax Genes (8:40 -10:00 am):
Differences in gene expression and development is brought about by the interplay of tissue specific and general transcription factors. This session examines the role of paired, box- containing (Pax) transcription factors in the early development of a variety of neoplasms.

Three presentations will be made during this session; representative of the research is The Role of Chimeric Paired Box Transcription Factors in The Pathogenesis of Pediatric Rhabdomyosarcoma, authored by Frederic G. Barr, MD, Ph.D., from the University of Pennsylvania School of Medicine, Philadelphia, PA. Dr. Barr conducted cytogenetic studies of alveolar rhabdomyosarcoma, a malignant pediatric soft tissue tumor derived from striated (skeletal) muscle. Using gene mapping and cloning strategies, Dr. Barr examined how different Pax genes can create significant differences in the tumor subtype and therefore affect disease severity and patient survival rates.

Session II

Embryonal Tumors (10:30-11:50 am):
Three research presentations will address how cancerous tumors originate and grow during embryonic development. Of particular note is a study by Brenda Gaille, MD, Professor and Director of Cancer and Blood Research, University of Toronto, Toronto, Canada.

Dr. Gaille's research effort, Developmental Basis of Retinal-Specific Induction of Cancer by RBI Mutation, examines the role of the retinoblastoma gene in the causation of cancer. Heretofore, this gene was perceived as a tumor suppressor gene because a germline mutation almost always results in a malignant ocular tumor during infancy. This study suggests that a mutation of the gene that affects programmed cell death may constitute a major factor in tumor development.

Session III

Embryonal Tumors and Breast Cancer (1:00-3:20 pm):
Certain endocrine risk factors for breast cancer are related to normal developmental events such as the time of the first menstrual cycle, menopause, and age at first full-term pregnancy. This is a contention made by Lewis A. Chodosh, MD, from the University of Pennsylvania School of Medicine, and author of Mammary Gland Development and Carcinogenesis: Molecules at the Crossroads, one of five research studies being presented during this session. Dr. Chodosh examines a widely-held observation that women who undergo pregnancy at an early age have a reduced risk for breast cancer, suggesting that giving birth, and not other extrinsic factors, produces a protective effect. His study attempts to understand how a woman's reproductive history affects breast cancer risk by identifying molecular biomarkers occurring during these changes, and the roles played by tumor suppressor genes in altering the degree of cancer risk. Separately, David Livingston, MD, Professor of Medicine and Genetics at the Dana-Farber Cancer Institute, Harvard Medical School, will talk about results from his recent research.

Wednesday, June 10, l998

Sessions IV

Leukemia and Developmental Genes (8:30-11:50 am):
Almost 40 years ago, medical researchers could differentiate between the types of leukemia by chromosomal rearrangement. By the 1980s, new advances in molecular biology allowed scientists to examine the uniqueness of these arrangements and how they contribute to causing this disease. This half-day session addresses these issues with six research presentations.

Stuart Orkin, MD, Leland Fikes Professor of Pediatric Medicine at Harvard Medical School, asserts that certain genes involved in a leukemic development may have a role in normal cell hematopoiesis, the process by which mature blood cells are generated from rare stem cells residing in the bone marrow of an adult. His study, Intersection Between Leukemia Genes and Normal Blood Cell Development, examines whether the loss of these cells can represent a "second hit" in the progression of certain types of the disease.

General Motors Cancer Research Foundation Awards

For the last 20 years, the General Motors Cancer Research Foundation has presented annual awards honoring basic and clinical scientists throughout the world for demonstrated achievements in research on the causes, prevention, and treatment of cancer. To ensure recognition across the broad field of cancer research, three different prize categories have been established. The selections are made by an Awards Assembly composed of internationally prominent basic scientists and clinical scientists. The prizes and 1998 recipients are:

The Charles F. Kettering Prize recognizes the most outstanding recent contribution to the diagnosis or treatment of cancer. The 1998 recipient is H. Rodney Withers M.BBS, Ph.D., D.Sc., of the University of California-Los Angeles, for his work in demonstrating that proliferating cells, compared to nonproliferating cells, are less able to repair themselves following radiation injury.

The Charles S. Mott Prize is for the most outstanding recent contribution related to the causes or ultimate prevention of cancer and is shared this year by Suzanne Cory, Ph.D., and Stanley J. Korsmeyer, MD, respectively from the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, and the Washington University School of Medicine, St. Louis Missouri. Both researchers discovered that the Bcl gene codes for a protein which exerts its oncogenic effects through suppression of programmed cell death rather than increased cell division.

The Alfred P. Sloan, Jr. Prize honors the year's most outstanding recent basic science contribution to cancer research. H. Robert Horvitz, Ph.D., of the Massachusetts Institute of Technology and Howard Hughes Medical Institute, is the 1998 recipient for his work that demonstrated that programmed cell death is active biological process that is genetically determined.

The award recipients will be honored at a dinner on June 10 at the Library of Congress. Health and Human Services Secretary Donna E. Shalala, Ph.D., will open the evening with remarks. Additional speakers include Jack Smith, Chairman of the Board, General Motors Corporation, and Samuel A. Wells, MD, President of the General Motors Cancer Research Foundation. Sam Donaldson, White House correspondent for ABC's "World News Tonight," will emcee.

(Editor's Note: A newsroom will be open during the conference. Contact Johanna Spangenberg (703) 527-7424 or Donna Krupa (703) 527-7357 for additional information or to arrange interviews with presenters or award recipients.)

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