Haritunians T, Mori A, O'Kelly J, Luong Q T, Giles F J, Koeffler H P
Division of Hematology/Oncology, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, CA 90048, USA.
Leukemia. 2007 Feb;21(2):333-9. doi: 10.1038/sj.leu.2404471. Epub 2006 Nov 30.
Mantle cell lymphoma (MCL) is an aggressive form of B-cell non-Hodgkin's lymphoma, with a mean survival of only 3-5 years and suboptimal therapeutic options. MCL is characterized by a balanced translocation t(11;14)(q13;q32), resulting in overexpression of cyclin D1, a G(1) cyclin regulated by the PI3K/Akt/mammalian target of rapamycin (mTOR) signaling pathway. As improved therapy for MCL is required and the mTOR pathway may be involved in its pathophysiology, the antiproliferative effects of RAD001 (everolimus), an mTOR inhibitor, against three MCL cell lines were investigated. As a single agent, RAD001 inhibited proliferation in MCL cell lines (Jeko1, SP49 and NCEB1) approximately 40-65% compared to diluent control cells. This was associated with G(1) cell-cycle arrest and reduced phosphorylation of the mTOR downstream target, 4E-BP1. Furthermore, combination drug studies revealed predominantly synergistic cytotoxicity with RAD001 and several secondary agents, including doxorubicin, vincristine or rituximab (components of the standard MCL regimen), as well as paclitaxel, vorinostat and bortezomib. These data indicate that single agent RAD001 is effective in inhibiting growth of MCL cells in vitro and combination studies with secondary agents further demonstrate synergistic cytotoxicity. Thus, these findings support future clinical studies of RAD001 in the treatment of MCL.
套细胞淋巴瘤(MCL)是一种侵袭性B细胞非霍奇金淋巴瘤,平均生存期仅3至5年,且治疗选择并不理想。MCL的特征是存在平衡易位t(11;14)(q13;q32),导致细胞周期蛋白D1过表达,细胞周期蛋白D1是一种受PI3K/Akt/雷帕霉素哺乳动物靶点(mTOR)信号通路调控的G(1)期细胞周期蛋白。由于需要改进MCL的治疗方法,且mTOR通路可能参与其病理生理过程,因此研究了mTOR抑制剂RAD001(依维莫司)对三种MCL细胞系的抗增殖作用。作为单一药物,与稀释剂对照细胞相比,RAD001抑制MCL细胞系(Jeko1、SP49和NCEB1)的增殖约40%至65%。这与G(1)期细胞周期阻滞以及mTOR下游靶点4E-BP1的磷酸化减少有关。此外,联合用药研究显示,RAD001与几种二线药物(包括阿霉素、长春新碱或利妥昔单抗(标准MCL治疗方案的组成部分)以及紫杉醇、伏立诺他和硼替佐米)主要表现出协同细胞毒性。这些数据表明,单一药物RAD001在体外有效抑制MCL细胞生长,与二线药物的联合研究进一步证明了协同细胞毒性。因此,这些发现支持RAD001治疗MCL的未来临床研究。