PI 3-Kinase Signaling Pathways in Disease

疾病中的 PI 3 激酶信号通路

基本信息

批准号：
8783453
负责人：
DAVID L. WOODLAND
金额：
$ 0.4万
依托单位：
KEYSTONE SYMPOSIA
依托单位国家：
美国
项目类别：
财政年份：
2015
资助国家：
美国
起止时间：
2015-01-01 至 2015-12-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8783453
关键词：
1-Phosphatidylinositol 3-Kinase Academia Activated Lymphocyte Antineoplastic Agents Area Autophagocytosis Basic Cancer Research Basic Science Beds Biological Markers Biology British Columbia Canada Cancer Patient Cell Proliferation Cell physiology Cells Clinic Clinical Clinical Data Collaborations Communication Cues Curiosities Development Disease Drug Combinations Educational workshop Event Feedback Friends Functional disorder Future Generations Genetic Growth Factor Growth Factor Receptors Human Individual Industry Inflammation Joints Knowledge Link Malignant Neoplasms Metabolic Metabolic Pathway Metabolism Methodology Modeling Nutrient Oncogenes Outcome PTEN gene Pathway interactions Pre-Clinical Model Protein Isoforms Receptor Signaling Regulation Research Research Personnel Role Scientist Signal Pathway Signal Transduction Signal Transduction Pathway Therapeutic Training Training Support Translational Research Tumor Biology Vesicle Work abstracting adaptive immunity analytical method cell growth cell motility clinical practice drug discovery extracellular human FRAP1 protein improved inhibitor/antagonist insight loris mTOR Signaling Pathway meetings neoplastic cell next generation novel oncology posters public health relevance receptor response skills structural biology symposium trafficking

项目摘要

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.

描述（由申请人提供）：请求支持由洛里·弗里德曼（Lori Friedman），戴维·A·弗鲁曼（David A.该会议将于2015年1月13日至18日在加拿大不列颠哥伦比亚省的温哥华举行。PI3K-AKT-MTOR信号通路是控制细胞内细胞生长，生存和运动的主要机制之一信号传导和细胞外提示。导致这种途径不当激活的遗传事件在许多癌症中很常见，因此，是基本癌症研究和药物发现工作的重点。 PI3K-AKT-MTOR网络还控制着炎症和适应性免疫的各个方面。尽管最初以独立和线性信号级联的形式建模，但如今，很明显，PI3K途径还可以作为垂直和其他重要信号通路的垂直和相互反馈调节的中心枢纽。如何调节代谢途径以满足肿瘤细胞的独特需求和活化的淋巴细胞是一个肥沃的研究领域，并有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。该领域令人兴奋的进步之一是发展针对这一途径的新抑制剂。但是，抑制PI3K/AKT/MTOR信号传导的个体或乘同工型的理由仍然是激烈争论的主题。这次Keystone研讨会会议旨在将来自学术界和行业的科学家和临床医生聚集在一起，讨论针对PI3K及相关途径的机会和责任，利用人类病理生理学和遗传学，临床前模型以及PI3K途径抑制剂。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，与会者的整合两次会议将有助于在癌症的情况下增加对PI3K途径的理解，从而改善癌症患者的结局。