title: [Relationship between BIM gene polymorphism and therapeutic efficacy in the retreatment of advanced non-small cell lung cancer with tyrosine kinase inhibitor].
abstract: OBJECTIVE
  BIM gene is a member of the BCL-2 family, is involved in cell death. The aim of this study is to explore the relationship between BIM gene polymorphism and therapeutic efficacy in the retreatment advanced non-small cell lung cancer (NSCLC) with tyrosine kinase inhibitor (EGFR-TKI).
  
  
  METHODS
  In the study, there were 123 patients who were diagnosed with advanced NSCLC in Zhejiang Province Cancer Hospital between January 2009 to October 2012, all of who were received gefitinib and erlotinib therapy after failure to chemotherapy. We detected the genotype of peripheral blood leukocytes of patients with BIM gene polymorphism though polymerase chain reaction (PCR). Statistical analysis was performed by SPSS version 13.0.
  
  
  RESULTS
  On the disease control rates, BIM gene with no polymorphism type was slightly better trend than polymorphism types in disease control rate DCR (75.5% vs 57.1%, χ²=2.931, P=0.087). Univariate analysis the median PFS, women were longer than men (6.9 months vs 4.5 months, χ² =7.077, P=0.008). Non-smokers were longer than smokers (8.0 months vs 2.5 months, χ² =15.277, P<0.001). Adenocarcinoma were longer than others pathological type (7.0 months vs 2.0 months, χ² =14.978, P<0.001). The median PFS in BIM gene with no polymorphism type were longer than with polymorphism type (6.0 months vs 3.5 months, χ²=7.035, P=0.008). Multi-factor analysis showed that smoking, pathological type, the BIM gene polymorphism were the independent prognostic factors for PFS.
  
  
  CONCLUSIONS
  The patients with the BIM gene no polymorphism have longer the median progression-free time than the polymorphism types in retreatment advanced non-small cell lung cancer patients with tyrosine kinase inhibitor.
authors.affiliation: The Second Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou 310053, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Zheng
authors.forename: Baochai
authors.initials: B
authors.lastname: Lin
authors.forename: Zhengbo
authors.initials: Z
authors.lastname: Song
authors.forename: Fangjun
authors.initials: F
authors.lastname: Xie
authors.forename: Wei
authors.initials: W
authors.lastname: Hong
authors.forename: Jianguo
authors.initials: J
authors.lastname: Feng
authors.forename: Lan
authors.initials: L
authors.lastname: Shao
authors.forename: Yingping
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D051017:Apoptosis Regulatory Proteins / Q000235:genetics*; D000072224:Bcl-2-Like Protein 11; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy* / Q000235:genetics*; D066246:ErbB Receptors / Q000037:antagonists & inhibitors; D005260:Female; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000235:genetics*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D008875:Middle Aged; D015999:Multivariate Analysis; D011110:Polymorphism, Genetic; D047428:Protein Kinase Inhibitors / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016896:Treatment Outcome
chemical_list: D051017:Apoptosis Regulatory Proteins; C000606775:BCL2L11 protein, human; D000072224:Bcl-2-Like Protein 11; D008565:Membrane Proteins; D047428:Protein Kinase Inhibitors; D011518:Proto-Oncogene Proteins; D066246:ErbB Receptors