Aspen Cancer Conference: Mechanisms of toxicity, carcinogenesis, and cancer prevention
โ Scribed by Miriam Sander; Benjamin F. Trump; Curtis C. Harris; Raymond W. Tennant
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 139 KB
- Volume
- 30
- Category
- Article
- ISSN
- 0899-1987
No coin nor oath required. For personal study only.
โฆ Synopsis
The 15th Aspen Cancer Conference was held July 16ยฑ18, 2000 in Aspen, Colorado. The program of the conference was organized by a Scientiยฎc Advisory Committee Cochaired by Benjamin Trump (AMC Cancer Center) and Curtis C. Harris (National Cancer Institute, NIH). The tradition of the Aspen Cancer Conference is to provide a forum for discussion of recent advances in the understanding of fundamental mechanisms of toxicity and carcinogenesis. This understanding can then be applied to the challenges of identifying carcinogenic risk, assessing the public-health impact of such risk, and diagnosing, preventing, and treating neoplastic disease. The Aspen Cancer Conference fosters intensive interaction and discussion among participants, which leads to new insights and understanding. The conference also focuses on new concepts and technologies. The 15th Aspen Cancer Conference was organized into 10 sessions. As a facet of the organizational strategy of this series of conferences, the Scientiยฎc Advisory Board will select seven to eight topics from sessions for an expanded in-depth analysis in the program for the 16th Aspen Cancer Conference in 2001. This meeting summary concisely describes the content of each session of this year's conference. MOLECULAR CARCINOGENESIS 30:14ยฑ25 (2001) Published 2001 WILEY-LISS, INC. y This article is a US Government work and, as such, is in the public domain in the United States of America.
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repair; 3MeA, 3methyladenine; O 6 -MeG, O 6 -methylguanine; MGMT, O 6 -methylguanine DNA methyltransferase; OGA, oncogene-generated activity; NSAID, nonsteroidal anti-inflammatory drug; COX, cyclooxygenase; PCR, polymerase chain reaction; PPARฮฑ, peroxisome proliferatoractivated receptor ฮฑ; PKC, prot