DNA Damage, Mutation & Cancer Gordon Research Conference

描述(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。细胞使用一个相互连接的通路网络来抑制突变和致癌。它们修复受损的DNA，并通过平衡效率和保真度的过程绕过阻止DNA复制的损伤。损伤触发的信号通路延缓了基因受损细胞的循环，并可能最终消除它们。2008年会议将高度重视对人类健康的影响。描述癌症“基因图景”的两个主旨演讲将为有关癌细胞的特定基因变化和散发性癌症的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引起的DNA损伤的反应，这种损伤可能会导致继发性癌症，并扩大对处理受损DNA对组织生长发育和衰老的影响的考虑。精选的演讲将强调新的模式系统--拟南芥和斑马鱼--对DNA修复和突变社区的价值。更关注损伤处理的分子起点的会议将侧重于结构生物学和DNA损伤识别的理论，并扩大损伤的定义，以包括无损伤DNA中的新结构和序列上下文效应。核心会议将旨在通过生化手段了解易出错与高保真响应之间的平衡，从而阻止复制堡垒。其中一个将描述由特定DNA损伤启动的通路中的连续步骤。

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.