6th EU-US Conference on Repair of Endogenous DNA Damage
第六届欧盟-美国内源性DNA损伤修复会议
基本信息
- 批准号:9329792
- 负责人:
- 金额:$ 0.5万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2017
- 资助国家:美国
- 起止时间:2017-09-01 至 2018-08-31
- 项目状态:已结题
- 来源:
- 关键词:Abnormal DNA RepairAddressAffectAgingAlkylating AgentsAppearanceAreaBasic ScienceCell physiologyCollaborationsComplexDNADNA DamageDNA Modification ProcessDNA RepairDNA Repair PathwayDNA lesionDefectDevelopmentDiseaseEnsureEnvironmentEnvironmental ExposureEnvironmental PollutionEpigenetic ProcessEtiologyEuropeEuropean UnionExplosionExposure toFosteringGenomeGenome StabilityGenomic InstabilityGenomicsGoalsHealthHumanInborn Genetic DiseasesInflammationInheritedInternationalInterventionInvestigationItalyKnowledgeLinkLocationMaintenanceMalignant NeoplasmsMetabolicMutagensNerve DegenerationNeurologic DeficitOralParticipantPathologicPathway interactionsPhysiologicalPostdoctoral FellowPredispositionPremature aging syndromeRNAReactionReactive Oxygen SpeciesRepair ComplexResearchResearch PersonnelRoleScientistSeriesSiteSourceStudentsTechniquesTechnologyTimeTranslational ResearchTranslationsUnited StatesUniversitiesUracilcancer genomecancer therapycareercollaborative environmentgenome editinghuman diseaseimprovedindividualized preventioninsightinterestknowledge translationmeetingsnervous system disordernew technologynew therapeutic targetnext generationnoveloxidative DNA damagepersonalized approachplanetary Atmospherepostersprogramsrepairedresearch and developmentresponsesymposiumtherapy developmenttreatment strategy
项目摘要
Project Summary / Abstract
The 6th US-EU Conference on Repair of Endogenous DNA Damage will be held September 24-28, 2017 in
Udine, Italy. The uniqueness of this series of meetings is its focus on the cellular responses to naturally formed
genomic damage, and the relationship of defects in these responses to genetically inherited disorders associated
with cancer predisposition, neurological deficits and premature aging. Understanding the contributions of
endogenous DNA damage to human disease, in particular cancer, and the pathological changes associated with
aging is indeed the major theme of this conference. Recently, there has been an explosion-like increase of
information on cancer genomes; the development of novel technologies for genome editing; visualizing DNA
repair complexes; the role for RNA in genome stability; novel mechanisms of DNA repair and epigenetics; and the
role of aging and environmental exposures in genome stability. A major goal of this meeting is to foster
collaborative research on the cellular processes that affect genomic instability in cancer. The role of endogenous
DNA damage, in particular oxidative DNA damage, as a driver of normal and accelerated aging and the study of
premature aging syndromes remain important areas of interest. Insights from rare inherited human diseases with
defects in the DNA damage response continue to illuminate links between endogenous DNA damage and cancer,
aging and neurologic disease. To promote the translation of knowledge about the sources and repair of
endogenous DNA lesions into interventions that improve global human health, this meeting will stimulate
collaborative translational research focused on the identification of new therapeutic targets and the development
of treatment strategies that either regulate DNA repair pathways in order to enhance cancer treatment, or delay
neurodegeneration, or reduce the pathological changes associated with aging. A key objective of the 2017
meeting is to provide an environment for both early career and senior investigators of diverse backgrounds to
communicate their latest results on relevant scientific topics and establish interactions that will not only strengthen
the numerous basic science and translational research efforts in this arena, but also enhance the development of
the next generation of researchers. The meeting will be held at the University of Udine, a venue chosen because
it offers a unique informal interactive environment in the center of Europe. This location will maximize interactions
amongst participants, ensuring that the goal of promoting productive interactions between scientists in the US and
the European Union (EU) is achieved.
项目摘要 /摘要
第六届美国欧盟内源性DNA损害修复会议将于2017年9月24日至28日在
意大利Udine。这一系列会议的独特性是它的重点是对天然形成的细胞反应
基因组损害以及这些对遗传遗传疾病相关的疾病的缺陷的关系
癌症易感性,神经系统缺陷和过早衰老。了解
内源性DNA对人类疾病的损害,尤其是癌症,以及与
衰老确实是这次会议的主要主题。最近,爆炸状的增加
有关癌症基因组的信息;用于基因组编辑的新技术的发展;可视化DNA
修复复合物; RNA在基因组稳定性中的作用; DNA修复和表观遗传学的新型机制;和
衰老和环境暴露在基因组稳定性中的作用。这次会议的主要目标是培养
关于影响癌症基因组不稳定性的细胞过程的协作研究。内源性的作用
DNA损伤,特别是氧化DNA损伤,是正常和加速衰老的驱动器
过早衰老综合症仍然是重要的感兴趣领域。从罕见的遗传性人类疾病中的见解
DNA损伤反应中的缺陷继续照亮内源性DNA损伤与癌症之间的联系,
衰老和神经疾病。促进有关来源和维修知识的翻译
内源性DNA病变成改善全球人类健康的干预措施,这次会议将刺激
协作转化研究的重点是识别新的治疗靶标和发展
调节DNA修复途径以增强癌症治疗或延迟的治疗策略
神经变性,或减少与衰老相关的病理变化。 2017年的关键目标
会议是为早期职业和不同背景的高级调查员提供环境
传达有关相关科学主题的最新结果,并建立互动,不仅会加强
该领域的众多基础科学和翻译研究工作,但也增强了
下一代研究人员。会议将在乌代大学举行,因为
它在欧洲中心提供了独特的非正式互动环境。此位置将最大化互动
在参与者中,确保促进美国科学家与
实现了欧盟(EU)。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Robert W Sobol其他文献
Robert W Sobol的其他文献
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{{ truncateString('Robert W Sobol', 18)}}的其他基金
Measuring genomic DNA damage and DNA repair capacity in longitudinal population samples - a step towards precision prevention
测量纵向群体样本中的基因组 DNA 损伤和 DNA 修复能力——迈向精准预防的一步
- 批准号:
9767787 - 财政年份:2018
- 资助金额:
$ 0.5万 - 项目类别:
Measuring genomic DNA damage and DNA repair capacity in longitudinal population samples - a step towards precision prevention
测量纵向群体样本中的基因组 DNA 损伤和 DNA 修复能力——迈向精准预防的一步
- 批准号:
10817292 - 财政年份:2018
- 资助金额:
$ 0.5万 - 项目类别:
Measuring genomic DNA damage and DNA repair capacity in longitudinal population samples - a step towards precision prevention
测量纵向群体样本中的基因组 DNA 损伤和 DNA 修复能力——迈向精准预防的一步
- 批准号:
10202602 - 财政年份:2018
- 资助金额:
$ 0.5万 - 项目类别:
Measuring genomic DNA damage and DNA repair capacity in longitudinal population samples - a step towards precision prevention
测量纵向群体样本中的基因组 DNA 损伤和 DNA 修复能力——迈向精准预防的一步
- 批准号:
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Transcriptional Signatures of Homologous Recombination Deficiency for Targeted Ch
目标 Ch 同源重组缺陷的转录特征
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8424340 - 财政年份:2012
- 资助金额:
$ 0.5万 - 项目类别:
Transcriptional Signatures of Homologous Recombination Deficiency for Targeted Ch
目标 Ch 同源重组缺陷的转录特征
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8582064 - 财政年份:2012
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Novel approaches to enhance tumor cell cytotoxicity of alkylating agents
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