EGFR 家族和整合素串扰在乳腺癌进展中的作用-猫眼课题宝

EGFR 家族和整合素串扰在乳腺癌进展中的作用

批准号：

8381358

负责人：

William Muller

金额：

$19.16万

依托单位：

UNIVERSITY OF TX MD ANDERSON CAN CTR

依托单位国家：

美国

项目类别：

财政年份：

资助国家：

美国

项目状态：

未结题

起止时间：

至

来源：

https://reporter.nih.gov/project-details/8381358

关键词：

1-Phosphatidylinositol 3-Kinase 8p11 AKT1 gene AKT2 gene Acceleration Address Alleles Anchorage-Independent Growth Binding Sites Bypass C-terminal Cell Culture System Cell Proliferation Clinical Trials Collaborations Complement Coupled Coupling Data Set Development Dominant-Negative Mutation Embryo Ensure Epidermal Growth Factor Receptor Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Epithelial Epithelial Cells Event Exhibits Family Family member Funding Gefitinib Gene Expression Genes Genetic Germ Lines Growth Factor Receptors Human Instruction Integrin Signaling Pathway Integrins Internal Ribosome Entry Site Knock-in Mouse Knock-out Laboratories Link Malignant - descriptor Mammary Neoplasms Mammary Tumorigenesis Mammary gland Measurement Mediating Metabolic Metastatic to Modeling Molecular Mouse Mammary Tumor Virus Mouse Strains Mus Mutate Neoplasm Metastasis Oncogenes PTEN gene Pathway interactions Penetrance Phenotype Phenylalanine Play Property Protein Tyrosine Kinase Proteins Proto-Oncogene Proteins c-akt RNA Interference Recruitment Activity Regulation Relative (related person)Role Signal Pathway Signal Transduction Signaling Molecule Testing Transcriptional Regulation Transgenic Mice Transgenic Organisms Treatment Efficacy Tumor Suppressor Genes Tumor Suppressor Proteins Up-Regulation adapter protein base comparative cytosolic receptor in vivo inhibitor/antagonist insight lapatinib malignant breast neoplasm malignant phenotype mammary epithelium mouse model mutant novel promoter protein function recombinase synergism therapeutic target tumor tumor growth tumor initiation tumor progression vector

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项目成果

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中文摘要

翻译

项目SuIVIMARY(请参阅说明)：原代乳腺上皮细胞向恶性表型的进展被认为涉及多种遗传事件，包括显性作用癌基因的激活和特异性肿瘤的丧失抑制基因。与这一提议相关的是观察到某些酪氨酸激酶的激活与相当大比例的人类乳腺癌的恶性进展有关。许多实验室的研究表明，PI-3K信号级联的激活在乳腺肿瘤进展。这项建议的主要目的是阐明相对贡献 EGFR家族在PI-3K信号通路激活中的作用。为达致这个目标，我们计划建立两种在转录水平下表达ErbB2的转基因小鼠模型 MMTV启动子的控制(NDL)或其自身的转录控制(ErbB2KI)。特别是，我们计划为了评估ERBBS及其耦合的下游信号分子(包括PI-3K)的相对贡献， Akt1和Akt2。最后，我们还将研究Rab25及其效应器Rab偶联蛋白在体内的作用 (RCP)在ErbB2乳腺肿瘤进展中的作用

英文摘要

PROJECT SUIVIMARY (See Instructions): The progression of a primary mammary epithelial cell to the malignant phenotype is thought to involve multiple genetic events including the activation of dominant acting oncogenes and the loss of specific tumor suppressor genes. Of relevance to this proposal is the observation that activation of certain tyrosine kinases has been implicated in the malignant progression of a significant proportion of human breast cancers. Studies by many laboratories suggest that activation ofthe PI-3K signaling cascade plays a critical role in mammary tumor progression. The principle objective of this proposal is to elucidate the relative contribution of the EGFR family in activation of the PI-3K signaling cascade. To accomplish this objective, we plan to exploit two well characterized transgenic mouse models expressing either ErbB2 under the transcriptional control of the MMTV promoter (NDL) or under its own transcriptional control (ErbB2KI). In particular we plan to assess the relative contribution of ErbBS and its coupled downstream signaling molecules including PI-3K, Aktl and Akt2. Finally, we also will examine the in vivo role of Rab25 and its effector Rab coupling protein (RCP) in ErbB2 mammary tumor progression

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