Interactions between inflammatory and oncogenic signaling pathways in GBM

GBM 炎症和致癌信号通路之间的相互作用

基本信息

  • 批准号:
    9339563
  • 负责人:
  • 金额:
    --
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2014
  • 资助国家:
    美国
  • 起止时间:
    2014-07-01 至 2018-06-30
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (provided by applicant): Project Summary Glioblastoma (GBM) is the most common primary malignant brain tumor in veterans. The prognosis for GBM is dismal and there is an urgent need for novel treatments. The receptor interacting protein (RIP1, RIPK1) has emerged as a central regulator of cell death in cell stress, inflammation, and development. Depending on the cellular context, RIP1 is known to either activate the transcription factor NF-�B and promote cell survival, or induce apoptotic or necrotic cell death in response to a number of stressful stimuli. Recent studies have shown that activation of NF-�B plays an important role in the pathogenesis of GBM. In this proposal, we propose to examine the role of RIP1 as a cell life death/switch in glioblastoma (GBM). A characteristic histopathological feature of GBMs is the presence of necrosis within the tumors. We have previously shown that RIP1 is expressed in GBM and confers a worse prognosis. In this proposal we examine the hypothesis that the RIP1 switch in GBM is regulated by EGFR signaling. The experimental goals of this project are to examine whether RIP1 is essential for tumor formation in an experimental model of GBM, and to investigate whether RIP1 regulates the induction of necrotic cell death in GBM. We aim to elucidate the mechanisms used by a mutant EGFRvIII to activate the oncogenic potential of RIP1 and the mechanism used the EGFR wild type (EGFRwt) to switch RIP1 to a cell death mode using an experimental intracranial mouse model of GBM. Additionally, we investigate RIP1 as a target for treatment in GBM using two alternative hypothesis. Hypothesis A: RIP1 silencing will result in inhibition of tumor growth in GBM. Hypothesis B: Activation of the cell death function of RIP1 using the EGFR network will eliminate GBM cells in vivo. Thus, RIP1 studies in GBM have the potential to significantly impact understanding of GBM and improve its treatment.
描述(由申请人提供):

项目成果

期刊论文数量(0)
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AMYN HABIB其他文献

AMYN HABIB的其他文献

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{{ truncateString('AMYN HABIB', 18)}}的其他基金

Bimodal EGFR signaling in glioblastoma
胶质母细胞瘤中的双峰 EGFR 信号转导
  • 批准号:
    10363582
  • 财政年份:
    2022
  • 资助金额:
    --
  • 项目类别:
Bimodal EGFR signaling in glioblastoma
胶质母细胞瘤中的双峰 EGFR 信号转导
  • 批准号:
    10544555
  • 财政年份:
    2022
  • 资助金额:
    --
  • 项目类别:
The role of Nrf2 in mediating resistance to EGFR inhibition in glioblastoma
Nrf2 在介导胶质母细胞瘤对 EGFR 抑制的抵抗中的作用
  • 批准号:
    10404075
  • 财政年份:
    2020
  • 资助金额:
    --
  • 项目类别:
The role of Nrf2 in mediating resistance to EGFR inhibition in glioblastoma
Nrf2 在介导胶质母细胞瘤对 EGFR 抑制的抵抗中的作用
  • 批准号:
    10615766
  • 财政年份:
    2020
  • 资助金额:
    --
  • 项目类别:
Interactions between inflammatory and oncogenic signaling pathways in GBM
GBM 炎症和致癌信号通路之间的相互作用
  • 批准号:
    8735239
  • 财政年份:
    2014
  • 资助金额:
    --
  • 项目类别:
Interactions between inflammatory and oncogenic signaling pathways in GBM
GBM 炎症和致癌信号通路之间的相互作用
  • 批准号:
    10266003
  • 财政年份:
    2014
  • 资助金额:
    --
  • 项目类别:
A Role for RIP1 in Gliomagenesis
RIP1 在神经胶质瘤发生中的作用
  • 批准号:
    8147853
  • 财政年份:
    2009
  • 资助金额:
    --
  • 项目类别:
A Role for RIP1 in Gliomagenesis
RIP1 在神经胶质瘤发生中的作用
  • 批准号:
    8308027
  • 财政年份:
    2009
  • 资助金额:
    --
  • 项目类别:
A Role for RIP1 in Gliomagenesis
RIP1 在神经胶质瘤发生中的作用
  • 批准号:
    7785369
  • 财政年份:
    2009
  • 资助金额:
    --
  • 项目类别:
EGFR MEDIATED APOPTOSIS IN GLIOMAS
EGFR 介导的胶质瘤细胞凋亡
  • 批准号:
    6633249
  • 财政年份:
    1999
  • 资助金额:
    --
  • 项目类别:

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