GORDON RESEARCH CONFERENCE ON MUTAGENESIS, 2000

Gordon Research Conferences, East Greenwich RI

Investigators

Abstract

DESCRIPTION (Applicant's Description) Funds are requested to support travel and conference fees for scientists to attend the 12th bi-annual Gordon Research Conference on Mutagenesis, at Queen's College, Oxford, England, August 20-25, 2000. The selected speakers are experts in the field of mutagenesis, and the Conference will provide the opportunity to discuss their latest results and ideas. The meeting will serve as a forum for extensive interactions among all attending scientists through the Discussion Sessions and the Poster Presentations. Selected poster presenters, generally students and younger scientists, will be given the opportunity to introduce their research results for discussion in short presentations (five minutes with overheads but not slides). The Conference is usually heavily oversubscribed with attendance limited to 135 persons. Participants are selected from universities, government research laboratories, regulatory agencies, research institutes, and industrial laboratories world wide. Specific efforts are made and special consideration is given to encouraging attendance from minority groups, women, graduate students, and persons with disabilities. The 2000 Conference will extend our understanding of the mechanisms by which mutations occur and the strategies employed by organisms to control and modulate mutagenesis. Nine sessions will include topics on nucleotide and base-excision repair, standard and new DNA polymerases, mismatch repair and genetic instability, double-strand break repair, pathways of nucleotide metabolism, and mutagenesis in evolution an~ cancer. The Conference will examine mutagenesis from biochemical, molecular and genetic viewpoints. The field of mutagenesis is critical to human health because spontaneous and exogenously induced mutations can initiate and facilitate the progression of a multitude of human diseases, particularly cancer and neurodegenerative diseases, while accumulation of endogenous oxidative lesions is implicated in aging.