title: Analysis of BIM (BCL-2 like 11 gene) deletion polymorphism in Chinese non-small cell lung cancer patients.
abstract: BACKGROUND
  Drug resistance significantly weakens the efficacy of cancer treatment, and the BIM (also known as the BCL2L11 gene) deletion polymorphism has been identified as a potential biomarker for drug resistance. In this retrospective study, we included a total of 290 patients with advanced non-small cell lung cancer (NSCLC) who received treatment with epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) and chemotherapy.
  
  
  METHODS
  The BIM deletion polymorphism of each patient was detected by polymerase chain reaction. EGFR mutations were detected by denaturing high-performance liquid chromatography methods and the amplification refractory mutation system.
  
  
  RESULTS
  The BIM deletion polymorphism was detected in 45/290 (15.5%) Chinese NSCLC patients. No associations were observed between the BIM deletion and clinic-pathologic characteristics of patients. The BIM deletion polymorphism was predictive of shorter progression-free survival in Chinese patients with EGFR-mutant adenocarcinoma and who were treated with EGFR-TKIs (7.30 vs. 9.53 months, P = 0.034). Additionally, we found that the BIM deletion polymorphism was an effective predictor of short progression-free survival in individuals with EGFR-mutant NSCLC and treated with chemotherapy containing pemetrexed (3.32 vs. 5.30, P = 0.012) or second-/beyond-line chemotherapy containing taxanes (1.53 vs. 2.61 months, P = 0.025). The BIM deletion was not correlated with overall survival.
  
  
  CONCLUSIONS
  The BIM deletion polymorphism occurs in 15.5% of Chinese NSCLC patients, and is a biomarker for resistance to TKIs and chemotherapy. However, BIM deletion was not a decisive factor in overall survival.
authors.affiliation: Department of Thoracic Medical Oncology, Peking University Cancer Hospital & Institute Beijing, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Zhong
authors.affiliation: Department of Thoracic Medical Oncology, Peking University Cancer Hospital & Institute Beijing, China.
authors.forename: Zheng-Xiang
authors.initials: ZX
authors.lastname: Li
authors.affiliation: Department of Thoracic Medical Oncology, Peking University Cancer Hospital & Institute Beijing, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Zhao
authors.affiliation: Department of Thoracic Medical Oncology, Peking University Cancer Hospital & Institute Beijing, China.
authors.forename: Jian-Chun
authors.initials: JC
authors.lastname: Duan
authors.affiliation: Department of Thoracic Medical Oncology, Peking University Cancer Hospital & Institute Beijing, China.
authors.forename: Hua
authors.initials: H
authors.lastname: Bai
authors.affiliation: Department of Thoracic Medical Oncology, Peking University Cancer Hospital & Institute Beijing, China.
authors.forename: Tong-Tong
authors.initials: TT
authors.lastname: An
authors.affiliation: Department of Thoracic Medical Oncology, Peking University Cancer Hospital & Institute Beijing, China.
authors.forename: Xiao-Dan
authors.initials: XD
authors.lastname: Yang
authors.affiliation: Department of Thoracic Medical Oncology, Peking University Cancer Hospital & Institute Beijing, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Wang
keywords: Chemotherapy; EGFR tyrosine kinase inhibitor; non-small cell lung cancer; polymorphism