ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2016
[Clinical Analysis of 107 NSCLC Patients Harboring KRAS Mutation].
Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 2 citations in OpenAlex.
- Prognostic value ofOncology letters · 2019Article
- [Clinical Significance of Tumor Marker Detection in Patients with Advanced Squamous Cell Carcimoma of the Lung].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2016Article
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Authors and funding
11 authors at 1 institution in 1 country.
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Abstract
backgroundKirsten rat sarcoma viral oncogene (KRAS) mutation is one of the major driver genes of non-small cell lung cancer (NSCLC). KRAS is a resistant predictor of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), which raises controversy because of its role in chemotherapy sensitivity and prognosis. The aim of this study is to accumulate clinical experience in treating NSCLC patients harboring KRAS mutation.
methodsA total of 107 NSCLC patients harboring KRAS mutation were analyzed retrospectively. The efficacy was analyzed in terms of first-line chemotherapy or EGFR-TKIs therapy.
resultsThe objective response rate (ORR) to first-line chemotherapy of 52 patients with advanced disease harboring KRAS mutation was 9.6%. The disease control rate (DCR) was 53.8%, and the median progression-free survival (PFS) was 3 months. The ORR to EGFR-TKIs therapy in 21 patients harboring KRAS mutation and EGFR/KRAS co-mutation was 9.5%; the DCR was 23.8%, and the median PFS was 1 month. The ORR and DCR to EGFR-TKIs therapy of patients with EGFR/KRAS co-mutation were significantly higher than those of patients with KRAS mutation (50% vs 0, P=0.029; 75% vs 11.8%, P=0.043); the median PFS was also significantly longer (3 months vs 1 month, P=0.004).
conclusionsThe efficacy to first-line chemotherapy and EGFR-TKIs therapy in NSCLC patients harboring KRAS mutation was poor; thus, new drugs should be developed. Furthermore, the existence of EGFR/KRAS co-mutation was confirmed. Hence, EGFR-TKIs therapy should be administered to patients with EGFR/KRAS co-mutation.
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