DNA Damage, Mutation & Cancer Gordon Research Conference

描述（由申请人提供）：GRC系列的一个主要前提是，许多与环境诱导和内源性DNA损伤相关的癌症与损伤诱导的突变有关。细胞利用相互连接的通路网络来抑制突变和癌变。它们通过平衡效率和保真度的过程修复受损的DNA并绕过DNA复制阻断病变。损伤触发的信号通路延迟了基因受损细胞的循环，并可能最终消灭它们。2008年会议将着重强调对人类健康的影响。两场描述癌症“遗传景观”的主题演讲将为有关癌细胞中特定遗传变异和散发性癌症遗传流行病学的会议奠定基础。其他与健康相关的会议侧重于细胞对化疗诱导的可能诱发继发性癌症的DNA损伤的反应，并扩大对受损DNA处理对组织生长发育和衰老的影响的考虑。选定的会谈将强调新的模型系统——拟南芥和斑马鱼——对DNA修复和诱变界的价值。更关注损伤处理的分子起点的会议将集中在结构生物学和DNA损伤识别理论上，并扩展损伤的定义，包括无损伤DNA和序列上下文效应中的新结构。核心课程将旨在从生化角度理解易出错与高保真反应之间的平衡。其中一个将描述由特定DNA损伤启动的途径的连续步骤。

DESCRIPTION (provided by applicant): A major premise of the GRC series has been that much of the cancer associated with environmentally-induced and endogenous DNA damage is linked to damage-induced mutagenesis. Cells use a network of interconnected pathways to suppress mutagenesis and carcinogenesis. They repair damaged DNA and bypass DNA-replication-blocking lesions by processes that balance efficiency and fidelity. Damage-triggered signaling pathways delay cycling of genetically-compromised cells and may eventually eliminate them. The 2008 conference will place a strong emphasis on consequences for human health. A pair of keynote talks that describe the "genetic landscapes" of cancer will set the stage for sessions concerned with specific genetic alternations in cancer cells and on the genetic epidemiology of sporadic cancer. Other health-related sessions focus on cellular responses to chemotherapy-induced DNA damage that may induce secondary cancers and expand consideration of consequences of processing of damaged DNA to tissue growth and development and aging. Selected talks will emphasize the value of new model systems - Arabidopsis and Zebrafish - to the DNA repair and mutagenesis community. Sessions more concerned with the molecular starting points of damage-processing will focus on the structural biology and theory of DNA-damage recognition and expand the definitions of damage to include novel structures in lesion-free DNA and sequence context effects. Core sessions will aim at biochemical understanding of the balance between error-prone vs. high-fidelity responses blocked replication forts. One will describe successive steps in pathways initiated by specific DNA lesions.