2014 DNA Damage, Mutation and Cancer Gordon Research Conference

项目总结/摘要 从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。根据突变的性质和受影响的基因 进一步发展为肿瘤可能更加复杂。最初的损坏可能发生在 不寻常的DNA序列或结构难以修复，它可能嵌入染色质中 限制修复酶进入的结构，偶尔，主要的因果事件可能是 未受损的DNA序列已被转录和/或复制不正确地处理。的 2014年戈登研究会议上DNA损伤，突变和癌症将集中在方式， 哪些DNA损伤和不寻常的DNA结构可以被细胞酶识别和处理 来调节它们的诱变效应多种蛋白质可以识别相同的DNA改变， 影响其解决途径的选择。此外，修复途径中的每一步都会产生 另一个病变，通常可以从其他途径获得酶。竞争或 合作DNA修复途径将是本次会议的一个重要主题。我们还将探索 化疗干预，以利用正常人之间的潜在基因型差异， 细胞和指定肿瘤中的细胞。合成杀伤力方法很重要，但还有其他方法。 在正常细胞的海洋中选择性地包裹肿瘤细胞的方法。我们还将讨论 DNA损伤在衰老中作用的证据，以及端粒加工在衰老中的重要性， 癌 九个临时会议的标题是：突变导致癌症，揭示病因，并提供 治疗的线索;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; DNA修复;氧化性DNA损伤和碱基切除修复，PARP的作用;错配修复， 细胞周期检查点和链断裂修复; 根据癌症基因型设计化疗; DNA损伤与癌症的关系 端粒维持和老化。海报会议和开放的下午将提供充足的 各级调查人员之间的接触机会。 我们预计，这次会议期间的科学互动将影响癌症研究， 建立多学科研究合作的重要途径和结果。的 2014年DNA损伤、突变与癌症戈登研究会议将在海滩举行 3月16日至21日，在加州文图拉的万豪酒店，据报道， 切除修复和第一届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.