PI 3-Kinase Signaling Pathways in Disease

描述（由申请人提供）：请求对由洛里弗里德曼、大卫A. Fruman和菲利普T.霍金斯会议将于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。PI 3 K-Akt-mTOR信号传导通路是响应于细胞内信号转导而控制细胞生长、存活和运动的主要机制之一。 信号和细胞外信号。导致该途径不适当激活的遗传事件在许多癌症中很常见，因此，是肿瘤学中基础癌症研究和药物发现工作的焦点。PI 3 K-Akt-mTOR网络还控制炎症和适应性免疫的各个方面。虽然最初被建模为独立的线性信号级联，但今天很明显，PI 3 K通路也作为与其他重要信号通路的垂直和相互反馈调节中的串扰的中心枢纽。如何调节代谢途径以满足肿瘤细胞和活化淋巴细胞的独特需求是一个富有成效的研究领域，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。该领域令人兴奋的进展之一是 新的抑制剂来对抗这种途径。然而，抑制PI 3 K/Akt/mTOR信号传导的单个或多个同种型的基本原理仍然是激烈争论的主题。本次Keystone研讨会旨在汇集来自学术界和工业界的科学家和临床医生，讨论靶向疾病中PI 3 K和相关通路的机会和责任，利用人类病理生理学和遗传学，临床前模型和PI 3 K通路抑制剂的临床数据。关于整合代谢和肿瘤生物学的联席会议将增加跨学科互动的机会。此外，与会者的融合 这两次会议的成果将有助于增加我们对PI 3 K通路在癌症背景下的理解，从而改善癌症患者的预后。

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.