Department of Internal Medicine, Division of Hematology & Oncology, Ohio State University, Columbus, Ohio 43210, USA.
MAbs. 2009 Jan-Feb;1(1):31-40. doi: 10.4161/mabs.1.1.7472.
Mantle cell lymphoma (MCL) is a distinct histologic subtype of B cell non-Hodgkins lymphoma (NHL) associated with an aggressive clinical course. Inhibition of the ubiquitin-proteasome pathway modulates survival and proliferation signals in MCL and has shown clinical benefit in this disease. This has provided rationale for exploring combination regimens with B-cell selective immunotherapies such as rituximab. In this study, we examined the effects of combined treatment with bortezomib and rituximab on patient-derived MCL cell lines (Jeko, Mino, SP53) and tumor samples from patients with MCL where we validate reversible proteasome inhibition concurrent with cell cycle arrest and additive induction of apoptosis. When MCL cells were exposed to single agent bortezomib or combination bortezomib/rituximab, caspase dependent and independent apoptosis was observed. Single agent bortezomib or rituximab treatment of Mino and Jeko cell lines and patient samples resulted in decreased levels of nuclear NFkappaB complex(es) capable of binding p65 consensus oligonucleotides, and this decrease was enhanced by the combination. Constitutive activation of the Akt pathway was also diminished with bortezomib alone or in combination with rituximab. On the basis of in vitro data demonstrating additive apoptosis and enhanced NFkappaB and phosphorylated Akt depletion in MCL with combination bortezomib plus rituximab, a phase II trial of bortezomib-rituximab in patients with relapsed/refractory MCL is underway.
套细胞淋巴瘤(MCL)是一种独特的 B 细胞非霍奇金淋巴瘤(NHL)组织学亚型,与侵袭性临床病程相关。抑制泛素-蛋白酶体途径可调节 MCL 中的生存和增殖信号,并已在该疾病中显示出临床益处。这为探索与 B 细胞选择性免疫疗法(如利妥昔单抗)联合的联合方案提供了依据。在这项研究中,我们研究了硼替佐米联合利妥昔单抗对源自患者的 MCL 细胞系(Jeko、Mino、SP53)和 MCL 患者肿瘤样本的治疗效果,验证了可逆蛋白酶体抑制与细胞周期阻滞和凋亡的相加诱导同时发生。当 MCL 细胞暴露于单药硼替佐米或硼替佐米联合利妥昔单抗时,观察到半胱天冬酶依赖性和非依赖性凋亡。单药硼替佐米或利妥昔单抗治疗 Mino 和 Jeko 细胞系和患者样本导致能够结合 p65 共识寡核苷酸的核 NFkappaB 复合物(es)水平降低,并且这种降低通过联合增强。Akt 通路的组成性激活也随着硼替佐米单独或与利妥昔单抗联合而减弱。基于体外数据表明硼替佐米联合利妥昔单抗在 MCL 中具有相加的凋亡作用和增强的 NFkappaB 和磷酸化 Akt 耗竭,目前正在进行硼替佐米-利妥昔单抗治疗复发性/难治性 MCL 的 II 期试验。