2014 DNA Damage, Mutation and Cancer Gordon Research Conference

项目摘要/摘要 DNA损伤及其细胞加工到DNA突变的研究进展 复制是一个复杂的过程。取决于突变的性质和受影响的基因 进一步发展为肿瘤可能会更加复杂。最初的损坏可能发生在 难以修复的不寻常的DNA序列或结构，它可能嵌入染色质 结构限制对修复酶的访问，偶尔，主要原因事件可能是 被转录和/或复制错误处理的未损坏的DNA序列。这个 2014年关于DNA损伤、突变和癌症的戈登研究会议将集中讨论 哪些DNA损伤和异常DNA结构可以被细胞酶识别和处理 来调节它们的诱变效果。多个蛋白质可能识别相同的DNA改变和 影响其解决方案的路径选择。此外，修复途径中的每一步都会产生 另一种损伤，通常可从其他途径获得酶。竞争或竞争之间的串扰 DNA修复途径的协作将是本次会议的一个重要主题。我们还将探索 化疗干预以利用正常人之间潜在的基因差异 细胞和指定肿瘤中的细胞。综合致命性方法很重要，但还有其他方法 在正常细胞海洋中选择性灭活肿瘤细胞的方法。我们还将解决 DNA损伤在衰老中作用的证据，以及端粒处理在衰老和 癌症。 九个临时会议的标题是：突变致癌，揭示病因，并提供 治疗线索；感知环境基因组损伤，大海捞针；薄弱环节 在基因组中，复制和转录的内在挑战；在启动时的前沿 DNA修复；DNA氧化损伤和碱基切除修复，PARP的作用；错配修复和 对复制或转录受阻的反应；细胞周期检查点和链断裂修复； 根据癌症基因型别设计化疗方案；以及DNA损伤与癌症的关系 端粒的维持和老化。海报会议和开放的下午将提供充足的 各级调查人员之间接触的机会。 我们预计，这次会议期间的科学互动将影响到 建立富有成效的多学科研究合作的重要途径和结果。这个 2014 DNA损伤、突变与癌症戈登研究会议将在海滩举行 万豪酒店于3月16日至21日在加利福尼亚州文图拉举行，纪念据报道发现 切除修复和第一次DNA修复机制国际研讨会40周年。

Project Summary/Abstract The progression from damaged DNA and its cellular processing to mutagenesis during DNA replication is a complex process. Depending upon the nature of the mutations and the genes affected the further progression to a tumor can be even more complex. The initial damage may have occurred in unusual DNA sequences or structures that are refractory to repair, it may be embedded in chromatin structures that restrict access to repair enzymes and occasionally, the primary causal event may be an undamaged DNA sequence that has been processed incorrectly by transcription and/or replication. The 2014 Gordon Research Conference on DNA damage, mutation and cancer will focus on the manner in which DNA lesions and unusual DNA structures can be recognized and processed by cellular enzymes to modulate their mutagenic effects. Multiple proteins may recognize the same DNA alteration and impact the pathway choice for its resolution. Furthermore, each step in a repair pathway generates another lesion, often accessible to enzymes from other pathways. Crosstalk between competing or collaborating DNA repair pathways will be an important theme in this Conference. We will also explore chemotherapeutic interventions to take advantage of potential genotypic differences between normal cells and those in a designated tumor. The synthetic lethality approach is important, but there are other approaches to selectively inactivate tumor cells in the sea of normal cells. We will also address the evidence for the role of DNA damage in aging, and the importance of telomere processing in aging and cancer. The nine provisional sessions are titled: Mutations cause cancer, reveal etiology and provide clues for therapy; Sensing environmental genomic damage, finding needles in the haystack; Weak links in the genome, intrinsic challenges to replication and transcription; Cutting edges at the initiation of DNA repair; Oxidative DNA damage and base excision repair, roles of PARP; Mismatch repair and responses to arrested replication or transcription; Cell cycle checkpoints and strand-break repair; Designing chemotherapies based upon cancer genotypes; and Relationships of DNA damage to telomere maintenance and aging. Poster sessions and open afternoons will provide ample opportunities for engagement between investigators at all levels. We anticipate that scientific interactions during this conference will impact cancer research in significant ways and result in establishing productive multi-disciplinary research collaborations. The 2014 DNA Damage, Mutation & Cancer Gordon Research Conference will be held at the Beach Marriott, in Ventura, California March 16 - 21, on the 50th anniversary of the reported discovery of excision repair and the 40th anniversary of the first international workshop on DNA repair mechanisms.