Biweekly PLD and L-OHP combination has high activity, with less than anticipated adverse toxicity, for treatment of platinum-resistant ovarian cancer. A comparison of the doublet PLD/L-OHP with single-agent treatment is warranted.

The influence of rituximab therapy on prognosis and hepatic toxicity (HT) in patients with hepatitis C virus (HCV)-positive diffuse large B-cell lymphoma (DLBCL) is unclear. Thus, we assessed HT and clinical outcome in patients with DLBCL and HCV infection who received rituximab-containing immunochemotherapy. We carried out a prospective analysis on a total of 280 HCV-positive patients with DLBCL, 200 of whom received chemotherapy plus rituximab (R-CHT), 80 received chemotherapy (CHT)-only. Survival outcomes and HT were compared according to rituximab administration. The median follow-up was 41 months. Addition of rituximab did not significantly affect prognosis (median progression-free survival, 40 vs 35 months, P = 0.26; median overall survival, 51 vs 43 months P = 0.09). Of 200 patients who received rituximab, 53 (26.5 %) had severe HT (grade 3-4), compared with 11 of 80 (13.75 %) patients who received rituximab-free regimens (P = 0.033). Among patients treated with rituximab, 50 patients (25 %) did not complete planned course of therapy, 14 patients because of hepatic toxicity and 36 patients because of progressive disease. Pretreatment liver function impairment was predictive of severe HT. These results raise concerns regarding the routine use of rituximab with chemotherapy in individuals with HCV-positive DLBCL. However, more studies are warranted before a definitive conclusion can be made.

A phase II study was conducted to assess the efficacy and toxicity of combination therapy with capecitabine and cisplatin in patients with de-novo advanced gastric cancer, and in patients with refractory/recurrent gastric cancer after previous nonplatinum-based therapy. Sixty-four patients were enrolled in the study. Of these, 50 patients had untreated gastric cancer, and 14 had received previous therapy with nonplatinum-based therapy. All patients received oral capecitabine 1250 mg/m2 twice daily, days 1-14, and intravenous cisplatin 60 mg/m2 on day 1. This cycle was repeated every 3 weeks. Among the 50 previously untreated patients, three achieved complete response, and 19 had partial response, giving a response rate of 44% in the intention-to-treat population. The median time to progression and median overall survival were 6 months [95% confidence interval (CI): 1.4-10.6] and 9 months (95% CI: 5.7-12.3), respectively. In patients who had received previous therapy, clinical usefulness was evaluated resulting in response rate of 14%, disease control rate of 28.5%, and median overall survival of 4 months (95% CI: 3.1-4.9). The principal grade 3/4 adverse events were neutropenia (20%), anemia (14%). No neutropenic fever or treatment-related deaths. Capecitabine in combination with cisplatin is effective and well tolerated as first-line treatment in patients with advanced gastric cancer. Unfortunately, we could not positively suggest the usefulness of the same combination regimen as salvage therapy in patients with progressive or recurrent disease after nonplatinum-based therapy.

Clinical risk classification is inaccurate in predicting outcome in adult patients with acute lymphoblastic leukemia (ALL), sometimes resulting in patients receiving inappropriate chemotherapy or stem cell transplantation. To identify complementary markers suitable for further treatment stratification in patients with standard-risk (SR)/philadelphia-negative (Ph-negative) precursor B-ALL, we evaluated the predictive value of minimal residual disease (MRD) after induction and consolidation chemotherapy in strictly defined SR/Ph-negative precursor B-ALL patients who were treated with a standard protocol using quantitative real-time polymerase chain reaction with the rearranged immunoglobulin heavy chain gene as a molecular marker. The cytologic complete response (CR) rate was 92.3 % after induction. At this time point, the molecular CR rate was 73.9%. Patients with molecular CR (MolCR) after induction had a significantly higher probability of disease-free survival (DFS; 78.8 vs 30.8%; P = .001) and of overall survival (OS; 82.4 vs 41.7%; P < .0001) compared to patients with molecular failure (MolFail). MRD at end consolidation had the same significance. Quantitative MRD assessment identified patients with MolFail after induction and/or consolidation as a high-risk group, with 3-year DFS and OS rates of 28.6 and 35.7%, respectively. Patients with MolCR after induction and consolidation were classified as low-risk and had 3-year DFS rate of 89.7% and OS rate of 93.3%. Thus, MRD quantification during treatment identified prognostic subgroups within the otherwise homogeneous SR/Ph-negative precursor B-ALL population who may benefit from individualized treatment.

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