Younes Hashem, Leleu Xavier, Hatjiharissi Evdoxia, Moreau Anne-Sophie, Hideshima Teru, Richardson Paul, Anderson Kenneth C, Ghobrial Irene M
Department of Internal Medicine, Division of Hematology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Clin Cancer Res. 2007 Jul 1;13(13):3771-5. doi: 10.1158/1078-0432.CCR-06-2921.
Multiple myeloma is a plasma cell neoplasm with a median survival of 3 to 5 years. Recent advances have improved patient outlook, but the disease remains incurable. Therefore, continued efforts to develop new therapies that target aberrant signaling pathways are needed. The phosphatidylinositol 3-kinase pathway regulates apoptosis, cell cycle regulation, and tumor proliferation. This pathway is constitutively activated in multiple myeloma and its inhibition induces apoptosis. Advances in understanding the signaling cascades mediating proliferation and survival of multiple myeloma cells have markedly improved the treatment of this disease. In this article, we review the role of the phosphatidylinositol 3-kinase/Akt pathway in the pathogenesis of multiple myeloma and the potential therapeutic implications of targeting this pathway in the treatment of multiple myeloma.
多发性骨髓瘤是一种浆细胞肿瘤，中位生存期为3至5年。近期的进展改善了患者的预后，但该疾病仍无法治愈。因此，需要持续努力开发针对异常信号通路的新疗法。磷脂酰肌醇3-激酶通路调节细胞凋亡、细胞周期调控和肿瘤增殖。该通路在多发性骨髓瘤中持续激活，抑制它可诱导细胞凋亡。在理解介导多发性骨髓瘤细胞增殖和存活的信号级联方面取得的进展显著改善了该疾病的治疗。在本文中，我们综述了磷脂酰肌醇3-激酶/Akt通路在多发性骨髓瘤发病机制中的作用以及靶向该通路治疗多发性骨髓瘤的潜在治疗意义。
