Molecular Pathogenesis of the Hamartoma Syndromes

错构瘤综合征的分子发病机制

• 批准号: 10715598
• 负责人: DAVID J. KWIATKOWSKI
• 金额: $ 216.84万
• 依托单位: BRIGHAM AND WOMEN'S HOSPITAL
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-04-24 至 2028-07-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10715598
• 关键词: Adult; Alleles; Automobile Driving; Bannayan Syndrome; Cell Line; Cell division; Cells; Critical Pathways; Dependence; Development; Drosophila genus; Event; Frequencies; Genes; Genetic; Genetic Transcription; Germ-Line Mutation; Goals; Growth; Hamartoma; Human; Individual; Kidney; Malignant Neoplasms; Metabolic; Modeling; Molecular; Multiple Hamartoma Syndrome; Mutation; Oncogenic; Organoids; PTEN gene; Pathogenesis; Pathway interactions; Peutz-Jeghers Syndrome; Phosphotransferases; Program Research Project Grants; Regulation; Renal Angiomyolipoma; Ruvalcaba syndrome; STK11 gene; Secondary to; Signal Pathway; Signal Transduction; Substrate Interaction; Syndrome; TFE3 gene; TSC1 gene; TSC2 gene; Technology; The Cancer Genome Atlas; Tissues; Tuberous Sclerosis; Tumor Suppressor Genes; Tumor Suppressor Proteins; United States National Institutes of Health; cell preparation; clinical care; gene function; inhibitor; jun Oncogene; loss of function mutation; mTOR Inhibitor; mTOR Signaling Pathway; novel; novel therapeutic intervention; novel therapeutics; programs; response; stem cells; transcription factor; tumor

Overall - Project Summary/Abstract Please see each project/core for individual Project Summary/Abstract

总体-项目摘要/摘要 有关个别项目摘要/摘要，请参阅每个项目/核心

项目成果

PARK2 Depletion Connects Energy and Oxidative Stress to PI3K/Akt Activation via PTEN S-Nitrosylation.

• DOI: 10.1016/j.molcel.2017.02.019
• 发表时间: 2017-03-16
• 期刊: Molecular cell
• 影响因子: 16
• 作者: Gupta A;Anjomani-Virmouni S;Koundouros N;Dimitriadi M;Choo-Wing R;Valle A;Zheng Y;Chiu YH;Agnihotri S;Zadeh G;Asara JM;Anastasiou D;Arends MJ;Cantley LC;Poulogiannis G
• 通讯作者: Poulogiannis G

Signaling events downstream of mammalian target of rapamycin complex 2 are attenuated in cells and tumors deficient for the tuberous sclerosis complex tumor suppressors.

• DOI: 10.1158/0008-5472.can-09-0975
• 发表时间: 2009-08-01
• 期刊: Cancer research
• 影响因子: 11.2
• 作者: Huang J;Wu S;Wu CL;Manning BD
• 通讯作者: Manning BD

Equivalent benefit of rapamycin and a potent mTOR ATP-competitive inhibitor, MLN0128 (INK128), in a mouse model of tuberous sclerosis.

• DOI: 10.1158/1541-7786.mcr-12-0605
• 发表时间: 2013-05
• 期刊: Molecular cancer research : MCR
• 作者: Guo Y;Kwiatkowski DJ
• 通讯作者: Kwiatkowski DJ

Sequential Response to FGFR3 Inhibition With Subsequent Exceptional Response to Atezolizumab in a Patient With FGFR3-TACC3 Fusion-Positive Metastatic Urothelial Carcinoma.

FGFR3-TACC3 融合阳性转移性尿路上皮癌患者对 FGFR3 抑制的连续反应以及随后对 Atezolizumab 的异常反应。

• DOI: 10.1200/po.18.00117
• 发表时间: 2018
• 期刊: JCO precision oncology
• 影响因子: 4.6
• 作者: Nassar,AminH;Lundgren,Kevin;Kim,Jaegil;Choueiri,ToniK;Sonpavde,GuruP;Kwiatkowski,DavidJ;Bellmunt,Joaquim
• 通讯作者: Bellmunt,Joaquim

LKB1: cancer, polarity, metabolism, and now fertility.

LKB1：癌症、极性、新陈代谢，现在是生育能力。

• DOI: 10.1042/bj20082023
• 发表时间: 2008
• 期刊: The Biochemical journal
• 作者: Shaw,ReubenJ