Westin Jason R
Division of Cancer Medicine, Department of Lymphoma and Myeloma, University of Texas M.D. Anderson Cancer Center, Houston, TX.
Clin Lymphoma Myeloma Leuk. 2014 Oct;14(5):335-42. doi: 10.1016/j.clml.2014.01.007. Epub 2014 Feb 7.
The phosphatidylinositol-3-kinase (PI3K) pathway is well known to regulate a wide variety of essential cellular functions, including glucose metabolism, translational regulation of protein synthesis, cell proliferation, apoptosis, and survival. Aberrations in the PI3K pathway are among the most frequently observed in cancer, and include amplifications, rearrangements, mutations, and loss of regulators. As a net result of these anomalies, the PI3K pathway is activated in many malignancies, including in Hodgkin and non-Hodgkin lymphomas, and yields a competitive growth and survival advantage, increased metastatic ability, and resistance to conventional therapy. Numerous inhibitors targeting various nodes in the PI3K pathway are undergoing clinical development, and their current status in lymphoma will be the focus of this review.
磷脂酰肌醇-3-激酶（PI3K）信号通路因调节多种重要细胞功能而广为人知，这些功能包括葡萄糖代谢、蛋白质合成的翻译调控、细胞增殖、凋亡和存活。PI3K信号通路异常是癌症中最常见的异常之一，包括扩增、重排、突变以及调节因子缺失。这些异常的最终结果是，PI3K信号通路在许多恶性肿瘤中被激活，包括霍奇金淋巴瘤和非霍奇金淋巴瘤，从而产生竞争性生长和生存优势、增强转移能力以及对传统疗法的耐药性。许多针对PI3K信号通路不同节点的抑制剂正在进行临床开发，它们在淋巴瘤中的当前研究状况将是本综述的重点。
