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DNA Damage & Cancer Susceptibility Syndromes

November 6–9, 2003

Chaired By

 Alan D'andrea, MD of Dana-Farber Cancer Research Institute
 Jan Hoeijmakers of Erasmus University

Meeting Description

Sessions:

  1. DNA Repair I
  2. Damage Response & Checkpoints
  3. DNA Repair II
  4. Chromosome Instability

The important role that DNA damage plays in cancer development is illustrated by the clear connections between exposures to certain types of DNA damaging agents in the environment and the development of cancer, such as the links between cigarette smoking and lung cancer or sunlight exposure and skin cancer. In addition, the majority of inherited syndromes characterized to date that lead to increased cancer development in families result from inherited mutations in genes that are important for DNA damage responses. For example, inherited mutations in either the Brca1 or p53 genes results in a very high risk of developing breast cancer and both of these gene products are important for helping cells respond to various types of DNA damage. The genes mutated in certain rare diseases that affect children, such as Fanconi's Anemia, Ataxia-telangiectasia, and Xeroderma Pigmentosum, all play roles in cellular responses to DNA damage and children with these diseases have very high incidences of certain cancers. Studies of the genes mutated in these diseases have led to a much better understanding of how all cells respond to DNA damage and even more importantly to insights about how cancers develop. In addition, since radiation therapy and most chemotherapy used to treat cancer actually cause DNA damage, understanding how these gene products operate provides new ways to approach the treatment of cancer. The discussions at the forum will focus on how these gene products function, contribute to cancer and can be manipulated to improve cancer therapies."

Meeting Summary

The important role that DNA damage plays in cancer development is illustrated by the clear connections between exposures to certain types of DNA damaging agents in the environment and the development of cancer, such as the links between cigarette smoking and lung cancer or sunlight exposure and skin cancer. In addition, the majority of inherited syndromes characterized to date that lead to increased cancer development in families result from inherited mutations in genes that are important for DNA damage responses. For example, inherited mutations in either the Brca1 or p53 genes results in a very high risk of developing breast cancer and both of these gene products are important for helping cells respond to various types of DNA damage. The genes mutated in certain rare diseases that affect children, such as Fanconi’s Anemia, Ataxia-telangiectasia, and Xeroderma Pigmentosum, all play roles in cellular responses to DNA damage and children with these diseases have very high incidences of certain cancers. Studies of the genes mutated in these diseases have led to a much better understanding of how all cells respond to DNA damage and even more importantly to insights about how cancers develop. In addition, since radiation therapy and most chemotherapy used to treat cancer actually cause DNA damage, understanding how these gene products operate provides new ways to approach the treatment of cancer. The discussions at the forum will focus on how these gene products function, how they contribute to cancer development, and how they can be manipulated to improve cancer therapies.

Quotes from Participants “It was very useful and stimulating and the responses I had from various participants were uniformly positive and enthusiastic.” - Prof. Jan Hoeijmakers

“The field of DNA damage and repair has developed so remarkably in the 40 years since I entered the field and co-discovered the process of excision repair of DNA. It is timely that you are sponsoring this forum on DNA damage and cancer susceptibility syndrome.” - Philip C. Hanawalt

“I came away with many new ideas, renewed inspiration, and ideas for some new contacts and collaborations.” - Richard Wood, Ph.D., F.R.S.

“Thanks again for organizing the 2003 Forbeck Forum and for providing the right environment for an open exchange of scientific ideas. It was truly an enlightening experience for us all. Not only that, we came away with a whole bunch of new friends!” - Stephen C. West, Ph.D.

“I and the other participants were unanimous in our view that it ranked among the best conferences that we had ever attended. The format is excellent and I would encourage you to continue with such an innovative and productive format.” - Ian Hickson, Ph.D.

“In addition to receiving an enormous number of new insights into the field of DNA repair, the meeting has paved the way for new collaborations between my research group and those of several other attendees. Moreover, the Forum strongly reinforced my conviction that the DNA damage and repair field has the potential to lead to better treatments for cancer. A prime goal for my career is to help realize this potential.” - Steve Jackson, Ph.D.

“It was a truly wonderful and unique experience that is already having immediate impact on my further research.” - Hans Joenje, Ph.D."

Forum Participants

James Amatruda, MD, PhD
UT Southwestern Medical Center
 Forbeck Scholar

Christopher Bakkenist, PhD
University of Pittsburgh
 Forbeck Scholar

Alan D'Andrea, MD
Dana-Farber Cancer Institute

Elsa Flores, PhD
MD Anderson Cancer Center
 Forbeck Scholar

Philip C. Hanawalt
Stanford University

Ian Hickson, PhD
Oxford Cancer Centre

Jan Hoeijmakers
Erasmus University

Steve Jackson, PhD
University of Cambridge

Hans Joenje, PhD
VU University Medical Centre

Michael Kastan, MD, PhD
St. Jude Children's Research Hospital

Richard D. Kolodner, PhD
University of California San Diego

Tom A. Kunkel
National Institutes of Health

John H. J. Petrini, PhD
Memorial Sloan Kettering Cancer Center

Norman Sharpless, MD
University of North Carolina
 Forbeck Scholar

Gregory L. Verdine
Harvard Medical School

Jean Y. Wang, PhD
University of California San Diego

Stephen West, PhD
Barts Centre - Cancer Research UK

Sam Wilson
National Institutes of Health

Richard D. Wood, PhD, FRS
University of Pittsburgh

Michael B. Yaffe, MD, PhD
Massachusetts Institute of Technology