GENETIC DISSECTION OF INSULIN RESISTANCE IN CANCER AND METABOLIC FUNCTION

癌症中胰岛素抵抗和代谢功能的基因剖析

• 批准号: 7601000
• 负责人: Courtney Montgomery
• 金额: $ 0.51万
• 依托单位: CASE WESTERN RESERVE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-08-01 至 2008-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7601000
• 关键词: Adult; Attention; Cancer Survivorship; Candidate Disease Gene; Child; Complex; Computer Retrieval of Information on Scientific Projects Database; Development; Disease; Dissection; Epidemic; Fasting; Functional disorder; Funding; Genetic; Genetic Variation; Genome; Genotype; Glucose; Grant; Institution; Insulin; Insulin Resistance; Insulin-Like Growth Factor I; Localized; Malignant Neoplasms; Metabolic; Metabolic Pathway; Molecular; Morbidity - disease rate; Obesity; Pathway interactions; Predisposition; Prevention intervention; Research; Research Personnel; Resources; Risk Factors; Source; United States National Institutes of Health; genetic linkage analysis; indexing; mortality; tool; trait

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The genetic study of complex diseases like cancer has gained increased attention over the past several years and has become more and more important as we discover likely common metabolic pathways for several common traits. The primary tool for such studies, to this point, has been linkage analysis. However, the ability of linkage analysis to localize a locus potentially segregating for susceptibility/protective genotypes is limited to, at best, a region of 5-10 centimorgans (cM). In parallel with the development of more sophisticated molecular tools to investigate the genome, increasing evidence has been collected on risk factors leading to the development and decreased survivorship of cancer. Obesity and metabolic dysfunction have been at the top of this list. In fact, the epidemic increase in obesity and metabolic dysfunction over the last 30 years (doubling in adults and tripling in children) portend a substantial increase in cancer morbidity and mortality. It is important, therefore, to identify sources of genetic variation for these traits comorbid with cancer, to elucidate important pathophysiological pathways and pave the way for targeted intervention and prevention. This study assesses the relationship between indices of metabolic pathways implicated in cancer, including insulin resistance (fasting and post glucose load insulin and glucose levels) and the candidate gene region for insulin-like growth factor 1 (IGF1).

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 在过去的几年里，像癌症这样的复杂疾病的遗传学研究越来越受到关注，并且随着我们发现几种常见特征的可能共同代谢途径而变得越来越重要。 到目前为止，这类研究的主要工具是联系分析。 然而，连锁分析定位可能分离易感性/保护性基因型的基因座的能力最多限于5-10厘摩（cM）的区域。 在开发更复杂的分子工具来研究基因组的同时，越来越多的证据已经收集到导致癌症发展和生存率下降的风险因素。 肥胖和代谢功能障碍一直在这个列表的顶部。 事实上，过去30年来肥胖症和代谢功能障碍的普遍增加（成人增加一倍，儿童增加两倍）预示着癌症发病率和死亡率的大幅增加。 因此，重要的是要确定这些性状与癌症共病的遗传变异来源，阐明重要的病理生理学途径，并为有针对性的干预和预防铺平道路。 这项研究评估了与癌症有关的代谢途径指标之间的关系，包括胰岛素抵抗（空腹和葡萄糖负荷后的胰岛素和葡萄糖水平）和胰岛素样生长因子1（IGF 1）的候选基因区域。