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• W2999919299 abstract "ABSTRACT Background KRAS mutations are present in ∼30% of NSCLC patients and have been associated with upregulation of genes implicated in angiogenesis as vascular endothelial growth factor (VEGF). Bevacizumab (BVZ) is a recombinant monoclonal humanized antibody targeted against VEGF and added to carboplatin-paclitaxel chemotherapy has demonstrated to improve outcome in non-squamous NSCLC. The objective of this study was to analyze the impact of KRAS mutations in response rate (RR) and time to progression (TTP) in a cohort of patients homogeneously treated with BVZ in combination with platin-docetaxel compared with a control group of patients treated with same chemotherapy backbone. Methods EGFR wild-type patients treated with up to 6 cycles of carboplatin (AUC 5) or cisplatin (75mg/m2), docetaxel (75mg/m2) and BVZ (7.5mg/kg) on day 1, every 21 days. Patients with RR or stable disease continued maintenance BVZ (7.5 mg/kg) every 21 days until progression. Control group was treated with the same chemotherapy without BVZ. KRAS mutations at codons 12, 13 and 61 were analyzed by cobas KRAS Mutation Test (Roche) from DNA purified from diagnostic samples. Results 30 patients were enrolled in the BVZ group: 24 male, 6 female; median age: 62 years; ECOG 1/2: 22/8; 27 adenocarcinoma and 3 undifferentiated large cell carcinoma. From them, 7 (23.3%) patients were KRAS mutated. 16 patients were enrolled in the control group: 14 male, 2 female; median age 58; ECOG 1/2: 9/7; 13 adenocarcinomas and 3 undifferentiated large cell carcinoma. From control group, 3 (18.8%) were KRAS mutated. BVZ therapy showed a significant improved efficacy in KRAS wild-type compared to mutated patients (RR: 88.9% vs 14.3%, p = 0.045; and TTP: 9.4 months vs 7.5 months, p = 0.033), but did not impact on overall survival (12.4 months vs 11.1 months, p= 0.780). These differences were not observed in control group. Moreover, in KRAS wild-type patients, the BVZ addition to therapy showed a significant improved efficacy compared to control group (RR: 88.9% vs 20%; p = 0.001). Conclusions KRAS wild-type status in wild-type EGFR stage IV non-squamous NSCLC might be associated with enhanced RR and TTP in BVZ-platin-docetaxel treated patients, suggesting a potential role as a predictive biomarker in this population. Disclosure All authors have declared no conflicts of interest." @default.
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• W2999919299 date "2012-09-01" @default.
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• W2999919299 title "Kras Status as Predictive Marker of Response and Time to Progression in EGFR Wild-Type Stage IV Non-Squamous Non-Small Cell Lung Cancer (NSCLC) Patients Treated with Platin-Docetaxel-Bevacizumab" @default.
• W2999919299 doi "https://doi.org/10.1016/s0923-7534(20)32758-7" @default.
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