Subgroup analyses stratified by age group, performance status, histology/tumor grade, or stage/debulking status were also conducted. A total of 462 patients were enrolled in this study, with 276 evaluable for inclusion in the analysis (Figure 1). Patient characteristics are displayed in Table 1. The median age of

the study population was 61 years, and most patients had tumors that were classified as papillary serous (84%), poorly differentiated (83%), stage III (85%), and optimally debulked (72%) (Table 1). The majority (94%) completed 4-8 cycles of chemotherapy. The median follow-up period was 23 months (range, 12–37 months), and 193 (70%) patients experienced selleck chemicals disease progression within this time frame. The median PFS was estimated to be 15.9 months (95% confidence interval [CI], 14.3–17.1 months). Assay results for carboplatin were available for 231 patients, with 44 (19.1%) patients identified as resistant to this therapy in the chemoresponse assay. Assay data for paclitaxel were available for 226 patients, 49 (21.7%) of whom were classified as resistant. Assay resistance by age, performance status, histology/grade,

and stage/debulking status is summarized in Table 2. There is no evidence that assay result for either carboplatin or paclitaxel is correlated with patient characteristics. Assay result for carboplatin was significantly associated with clinical outcome (Figure 2). The median PFS was 16.6 and 11.8 months for assay Libraries nonresistant (sensitive + IS) and resistant tumors, respectively. Patients displaying assay resistance to find more carboplatin were at a higher risk of disease progression as compared to those who were nonresistant (HR, 1.87; 95% CI, 1.29–2.70; P < .001). These results were 17-DMAG (Alvespimycin) HCl consistent in multivariate analysis after controlling for clinical covariates (HR, 1.71; 95% CI, 1.12–2.62; P = .013) ( Table 3). Analysis of subgroups (age group, performance status, histology, stage/debulking status) was also conducted ( Figure 3), and the association between PFS and assay result for carboplatin was suggested across all subgroups.

The data also suggest that patients with assay resistance to paclitaxel would experience shortened PFS, but the association did not reach the level of statistical significance ( Table 3). Assay results for carboplatin and paclitaxel were highly correlated. For 220 patients with assay data available for both agents, 75.5% were nonresistant to both agents and 15.9% were resistant to both agents, while only 8.6% of patients were resistant to only 1 agent (5.9% to carboplatin and 2.7% to paclitaxel). Patients resistant to both agents experienced the worst outcomes (HR, 1.66; 95% CI, 1.10–2.52; P = .017, as compared to patients nonresistant to both agents). Multivariate analysis indicated the same tendency, although the association was not statistically significant ( Table 3).