Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, Darwin 3, Madrid 28049, Spain
University of Wisconsin School of Medicine and Public Health, 1300 University Avenue, Madison, WI 53706-1532, USA.
J Cell Sci. 2019 Jan 2;132(1):jcs228395. doi: 10.1242/jcs.228395.
The different mechanisms of phosphoinositide 3-kinase (PI3K) activation in cancer as well as the events that result in PI3K pathway reactivation after patient treatment with PI3K inhibitors was discussed on October 15-17th, 2018, in the medieval town of Baeza (Universidad Internacional de Andalucía, Spain) at the workshop entitled 'The cell biology behind the oncogenic PIP3 lipids'. These topics and the data presented regarding cellular functions altered by PI3K deregulation, the cooperation of PI3K/PTEN mutations with other tumor drivers, and the lessons learned for PI3K-targeted therapy, are discussed below.
2018 年 10 月 15 日至 17 日，在西班牙安达卢西亚国际大学位于巴埃萨（Baeza）的中世纪小镇举行了题为“致癌 PIP3 脂质背后的细胞生物学”的研讨会，会上讨论了癌症中磷酸肌醇 3-激酶（PI3K）激活的不同机制，以及患者接受 PI3K 抑制剂治疗后导致 PI3K 途径重新激活的事件。下面讨论了这些主题以及有关 PI3K 失调改变细胞功能、PI3K/PTEN 突变与其他肿瘤驱动因素的合作，以及 PI3K 靶向治疗经验教训的相关数据。
