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PI 3-Kinase Signaling Pathways in Disease

PI 3-Kinase Signaling Pathways in Disease
疾病中的 PI 3 激酶信号通路
批准号:
8783453
负责人:
DAVID L. WOODLAND
金额:
$0.4万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2015
资助国家:
美国
项目状态:
已结题
起止时间:
2015-01-01 至 2015-12-31

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中文摘要
翻译
描述(由申请人提供):请求支持由Lori Friedman、David A.Fruman和Phillip T.Hawkins组织的题为PI 3-Kinase Signals Path in Disease的Keystone研讨会。会议将于2015年1月13日至18日在加拿大不列颠哥伦比亚省温哥华举行。PI3K-Akt-mTOR信号通路是控制细胞生长、存活和运动的主要机制之一 信号和细胞外信号。导致该通路不适当激活的遗传事件在许多癌症中很常见,因此,这是基础癌症研究和肿瘤学药物发现工作的重点。PI3K-Akt-mTOR网络还控制炎症和获得性免疫的各个方面。虽然最初被建模为独立和线性的信号级联,但今天很明显,PI3K通路也是垂直和相互反馈调节与其他重要信号通路的串扰的中心枢纽。如何调节代谢途径以满足肿瘤细胞和激活的淋巴细胞的独特需求是一个富有活力的研究领域,越来越多的证据表明,代谢调节与控制细胞生长和增殖的信号转导途径密切相关。该领域令人振奋的进展之一是发展 新的抑制剂对这一途径的影响。然而,抑制单个或多个PI3K/Akt/mTOR信号异构体的理论基础仍然是一个激烈争论的主题。本次Keystone研讨会旨在将来自学术界和工业界的科学家和临床医生聚集在一起,利用人类病理生理学和遗传学、临床前模型和PI3K途径抑制剂的临床数据,讨论针对PI3K及其相关疾病途径的机会和责任。关于整合新陈代谢和肿瘤生物学的联合会议将增加跨学科互动的机会。此外,参会人员的整合 这两次会议将有助于增加我们对癌症背景下PI3K途径的理解,从而改善癌症患者的预后。
英文摘要
DESCRIPTION (provided by applicant): Support is requested for a Keystone Symposia meeting entitled PI 3-Kinase Signaling Pathways in Disease, organized by Lori Friedman, David A. Fruman and Phillip T. Hawkins. The meeting will be held in Vancouver, British Columbia, Canada from January 13-18, 2015. The PI3K-Akt-mTOR signaling pathway is one of the primary mechanisms for controlling cell growth, survival, and motility in response to intracellular signaling and extracellular cues. Genetic events resulting in inappropriate activation of this pathway are common in many cancers and, as a result, are a focus of both basic cancer research and drug discovery efforts in oncology. The PI3K-Akt-mTOR network also controls diverse aspects of inflammation and adaptive immunity. Although originally modeled as an independent and linear signaling cascade, today it is evident that the PI3K pathway also functions as a central hub for cross-talk in both vertical as well as reciprocal feedback regulatio with other important signaling pathways. How metabolic pathways are regulated to meet the unique needs of tumor cells and activated lymphocytes is a fertile area of study, with mounting evidence that metabolic regulation is intimately linked with the signal transduction pathways that control cell growth and proliferation. One of the exciting advances in the field is the development of new inhibitors against this pathway. However, the rationale for inhibiting individual or multipl isoforms of PI3K/Akt/mTOR signaling remains a subject of intense debate. This Keystone Symposia meeting aims to bring together scientists and clinicians from academia and industry to discuss the opportunities and liabilities of targeting the PI3K- and related pathways in disease, drawing on human pathophysiology and genetics, preclinical models and clinical data with PI3K pathway inhibitors. A joint meeting on Integrating Metabolism and Tumor Biology will enhance opportunities for interdisciplinary interactions. In addition, the integration of attendees from both meetings will help increase our understanding of the PI3K pathway in the context of cancer, thereby improving outcomes for cancer patients.
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Stem Cells and Cancer
  • 批准号:
    8985625
  • 项目类别:
  • 资助金额:
    $0.5万
  • 财政年份:
    2016
  • 负责人:
    DAVID L. WOODLAND
  • 依托单位:
Fibrosis: From Basic Mechanisms to Targeted Therapies
  • 批准号:
    9039836
  • 项目类别:
  • 资助金额:
    $1.5万
  • 财政年份:
    2016
  • 负责人:
    DAVID L. WOODLAND
  • 依托单位:
Microglia in the Brain
  • 批准号:
    9125542
  • 项目类别:
  • 资助金额:
    $1.08万
  • 财政年份:
    2016
  • 负责人:
    DAVID L. WOODLAND
  • 依托单位:
Chromatin and Epigenetics
  • 批准号:
    9106870
  • 项目类别:
  • 资助金额:
    $0.4万
  • 财政年份:
    2016
  • 负责人:
    DAVID L. WOODLAND
  • 依托单位:
海外基金