项目 2：识别错构瘤基因突变癌症的代谢脆弱性和目标-猫眼课题宝

项目 2：识别错构瘤基因突变癌症的代谢脆弱性和目标

批准号：

10221614

负责人：

DAVID J. KWIATKOWSKI

金额：

$54.42万

依托单位：

BRIGHAM AND WOMEN'S HOSPITAL

依托单位国家：

美国

项目类别：

财政年份：

2006

资助国家：

美国

项目状态：

已结题

起止时间：

2006-12-01 至 2023-07-31

来源：

https://reporter.nih.gov/project-details/10221614

关键词：

ATP Synthesis Pathway Acetyl-CoA Carboxylase Apoptosis Ascorbic Acid Biguanides Biochemical Cancer cell line Carboplatin Categories Cell Line Clinical Trials Clustered Regularly Interspaced Short Palindromic Repeats Combined Modality Therapy Data Defect Development Dissection Dose Drug Combinations Drug Targeting Enzymes FRAP1 gene Fatty Acids Funding Genes Genetic Genetic Predisposition to Disease Genetically Engineered Mouse Growth Hamartoma Homeostasis Human Immune Impairment In Vitro K-ras mouse model KRAS2 gene Laboratories MAP Kinase Gene Malignant Neoplasms Malignant neoplasm of lung Malignant neoplasm of pancreas Metabolic Metabolic Control Metabolism Modality Modeling Molecular Mus Mutation Non-Small-Cell Lung Carcinoma Normal Cell Oncogenes Oncology Oxidative Phosphorylation Oxygen PTEN gene Pancreas Pancreatic Ductal Adenocarcinoma Pathogenesis Pathway interactions Patients Pemetrexed Pharmaceutical Preparations Pharmacology Phenformin Play Pre-Clinical Model Principal Investigator Process Reporting Resistance Role STK11 gene Series Stress Syndrome TP53 gene TSC1 gene TSC2 gene Testing Therapeutic Tumor Burden Tumor Suppressor Genes Tumor Suppressor Proteins antitumor effect ascorbate base biomarker development biomarker-driven cancer cell cancer genetics docetaxel efficacy evaluation falls gain of function mutation in vivo inhibitor/antagonist loss of function mutation lung cancer cell metabolomics mutant novel patient population pre-clinical preclinical trial pressure programs rapid growth resistance mechanism response standard of care targeted agent tumor tumor metabolism

项目摘要

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中文摘要

翻译

项目主任/首席调查员(最后、第一、中间)：Kwiatkowski，David J.等人，项目2：坎特利和肖摘要在过去的五年里，很明显，许多肿瘤重新连接了它们的新陈代谢来支持快速生长，但是，每个肿瘤如何重新连接其新陈代谢的分子细节取决于独特的癌基因和主导新陈代谢的肿瘤抑制因子，包括所有错构瘤综合征基因，如 PI3K/mTOR/LKB1通路在正常细胞和癌细胞的代谢调控中起着重要作用。焦点这个项目的目的是更好地了解代谢脆弱性，并提供临床前数据，以支持生物标记物驱动的临床试验的发展，以评估具有生殖系或多个生殖系患者的此类药物含有错构瘤综合征基因(PTEN、LKB1、TSC1、TSC2)零星突变的肿瘤。

英文摘要

Program Director/Principal Investigator (Last, First, Middle):Kwiatkowski, David J. et al., Project 2: Cantley and Shaw Abstract Over the past five years it has become clear that many tumors rewire their metabolism to support rapid growth, but that the molecular details of how each tumor rewires its metabolism depends on the unique oncogenes and tumor suppressors that dominantly control metabolism, which include all of the hamartoma syndrome genes, as the PI3K/ mTOR/ LKB1 pathways play a major role in metabolic control in normal and cancer cells. The focus of this project is to better understand metabolic vulnerabilities and provide preclinical data that would support the development of biomarker driven clinical trials to evaluate such drugs in patients with germline or the many tumors containing sporadic mutations in hamartoma syndrome genes (PTEN, LKB1, TSC1, TSC2).

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