BioOncology Watch

Timely Information for Practicing Physicians

 

July 2002

 

 Radioimmunotherapy

90Y ibritumomab tiuxetan vs. rituximab. 90Y ibritumomab tiuxetan (Zevalin®, IDEC Pharmaceuticals) is made up of ibritumomab, the parent anti-CD20 antibody of rituximab, and tiuxetan, a high-affinity chelation site for the pure beta emitter 90Y. Thomas Witzig and colleagues conducted a phase III study in which patients with relapsed or refractory low-grade, follicular, or transformed CD20+ NHL were randomized to receive either radioimmunotherapy with 90Y ibritumomab tiuxetan as a single dose (0.4 mCi/kg) or rituximab 375 mg/m2 IV weekly for 4 doses. Patients in the radioimmunotherapy group were also pretreated with 2 doses of rituximab (250 mg/m2) to improve biodistribution and one dose of indium-111 ibritumomab tiuxetan for imaging and dosimetry. The overall response rate for the radioimmunotherapy patients was 80% compared to 56% for the rituximab patients (p=0.002). Also, the complete remission (CR) rates were 30% and 16% for the radioimmunotherapy and rituximab groups, respectively (p=0.04). Median durations of response and median times to progression were similar for the 2 treatment groups. Reversible myelosuppression was the most common adverse event associated with 90Y ibritumomab tiuxetan treatments. This trial demonstrated that 90Y ibritumomab tiuxetan is well tolerated and produces higher remission rates than rituximab alone in patients with relapsed or refractory low-grade CD20+ NHL. (Witzig TE, et al. J Clin Oncol 2002; 20:2453-2463)

 

131I tositumomab treatment of mantle cell lymphoma (MCL). MCL is an aggressive lymphoma associated with short remission durations following either conventional-dose chemotherapy or high-dose therapy (HDT) supported by autologous stem cell transplantation (ASCT). Ajay Gopal et al. treated 16 consecutive patients with relapsed or refractory MCL with an infusion of 131I tositumomab, a radiolabeled anti-CD20 monoclonal antibody, followed by HDT  (etoposide and cyclophosphamide) and ASCT. The antibody dose was 1.7 mg/kg and the amount of 131I was calibrated to deliver 20 to 25 Gy to normal organs. Among 11 evaluable patients, the complete and overall response rates were 91% and 100%, respectively. Twelve patients have not developed disease progression 6 to 57 months after ASCT and the 3-year survival rate is estimated to be 93%. There were no treatment-related deaths reported. The addition of 131I tositumomab to HDT may provide durable remissions for patients with relapsed or refractory MCL. (Gopal AK, et al. Blood 2002;99:3158-3162)

 

Waldenstrom’s Macroglobulinemia (WM)

Rituximab treatment. In a phase II study, Meletios Dimopoulos and associates investigated the use of rituximab in the treatment of WM, a hematologic malignancy characterized by CD20+ lymphoplasmacytic cells. Twenty-seven patients were treated with rituximab 375 mg/m2 IV weekly for 4 weeks. Patients who had not developed disease progression within 3 months after the completion of rituximab therapy received a second 4-week cycle of study treatment. Partial responses were achieved in 6 (40%) of 15 previously untreated patients and in 6 (50%) of 12 previously treated patients. With a median follow-up of 15.7 months, the median time to progression was 16 months and 9 of 12 responding patients remained progression-free. Approximately 25% of patients experienced mild infusion-related toxicities. These results show that rituximab therapy is well tolerated by WM patients and that rituximab is active against WM. (Dimopoulos MA, et al. J Clin Oncol 2002;20:2327-2333)

 

Chronic Lymphocytic Leukemia (CLL)

Campath-1H after fludarabine failure. B-cell CLL is the most common adult leukemia in Western nations. Although a patient with CLL may have a long clinical course, the median survival is only 8 months after fludarabine treatment has failed. Michael Keating and colleagues conducted a multicenter phase II study in which 93 previously treated (exposed to alkylating agents and failed fludarabine) patients with B-cell CLL received Campath-1H (alemtuzumab), an anti-CD52 monoclonal antibody. Thirty-three percent of patients achieved a response (2% CR) and the median time to progression for responders was 9.5 months. The median survival time was 16 months (95% CI: 11.8-21.9) overall and 32 months for responders. Thirty percent of patients became neutropenic and grade 3 or 4 infections were reported in 25 (26.9%) patients. However, only 3 (9.7%) responders developed grade 3 or 4 infection. This phase II study demonstrated that Campath-1H has activity in a high-risk group of patients with B-cell CLL with acceptable toxicity. (Keating MJ, et al. Blood 2002;99:3554-3561)

 

Multiple Myeloma

Nuclear factor (NF)-kB blockade. The transcription factor NF-kB has been found to be important for the survival of activated B cells. In addition, it is constitutively active in several malignancies. Thus, Nicholas Mitsiades and colleagues investigated the role of NF-kB activity in multiple myeloma. A specific inhibitor of NF-kB, SN50, was utilized in their experiments. SN50 induced apoptosis in multiple myeloma cells (cell lines as well as patient myeloma cells) and it activated caspase-9 and caspase-3. Moreover, the expression of inhibitors of apoptosis (XIAP, cIAP-1, cIAP-2, and survivin) was down regulated. SN50 pretreatment also sensitized myeloma cells to TNF-a-induced apoptosis and inhibited the expression of intracellular adhesion molecule-1. These studies indicate that NF-kB activity may be important for the proliferation of malignant myeloma cells and therefore is a target for novel therapies against multiple myeloma. (Mitsiades N, et al. Blood 2002;99:4079-4086)

 

Phase I Studies of New Therapies

Oncolytic virus. PV701 is an attenuated strain of Newcastle disease virus, an avian paramyxovirus. This virus strain has been found to directly lyse human cancer cells in vitro, to activate T-cell specific antitumor immunity, and to activate tumoricidal macrophages. In a phase I study of 79 patients with advanced solid tumors, a 100-fold dose intensification was achieved and the maximum-tolerated dose was identified. Objective responses were also observed and progression-free survival ranged from 4 to 31 months. Further investigation is warranted. (Pecora AL, et al. Blood 2002;99:2251-2266)

 

Farnesyl transferase inhibitor. A phase I study (n=28) of R115777, a farnesyl transferase inhibitor, has recently been completed. Myelosuppression was found to be the dose-limiting toxicity. However, continuous dosing of R115777 was well tolerated at a dose of 300 mg bid. Antitumor activity (1 partial response, 1 minimal response, 3 with stable disease) was detected in this refractory patient population. Further clinical testing is warranted. (Crul M, et al. J Clin Oncol 2002;20:2726-2735)

 

Cancer vaccine. Keith Knutson and colleagues administered 6 monthly vaccinations with HER-2/neu-derived HLA-A2 peptide (p369-377) (500 ug) admixed with GM-CSF (100 ug) to 6 HLA-A2 patients with HER-2/neu-overexpressing malignancies (breast and ovarian cancers). They found that the vaccination induced HER-2/neu peptide specific IFN-g-producing CD8+ T cells. However, the responses were short-lived and were of a small magnitude. CD4+ T-cell activity may be required for lasting immunity to this epitope. (Knutson KL, et al. Clin Cancer Res 2002;8:1014-1018)

 

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