title: Detection of E2A-PBX1 fusion transcripts in human non-small-cell lung cancer.
abstract: BACKGROUND
  E2A-PBX1 fusion gene caused by t(1;19)(q23;p13), has been well characterized in acute lymphoid leukemia (ALL). There is no report on E2A-PBX1 fusion transcripts in non-small-cell lung cancer (NSCLC).
  
  
  METHODS
  We used polymerase chain reaction (PCR) to detect E2A-PBX1 fusion transcripts in human NSCLC tissue specimens and cell lines. We analyzed correlation of E2A-PBX1 fusion transcripts with clinical outcomes in 76 patients with adenocarcinoma in situ (AIS) and other subgroups. We compared mutation status of k-ras, p53 and EGFR in 22 patients with E2A-PBX1 fusion transcripts.
  
  
  RESULTS
  We detected E2A-PBX1 transcripts in 23 of 184 (12.5%) NSCLC tissue specimens and 3 of 13 (23.1%) NSCLC cell lines. Presence of E2A-PBX1 fusion transcripts correlated with smoking status in female patients (P=0.048), AIS histology (P=0.006) and tumor size (P=0.026). The overall survival was associated with gender among AIS patients (P=0.0378) and AIS patients without E2A-PBX1 fusion transcripts (P=0.0345), but not among AIS patients with E2A-PBX1 fusion transcripts (P=0.6401). The overall survival was also associated with status of E2A-PBX1 fusion transcripts among AIS stage IA patients (P=0.0363) and AIS stage IA female patients (P=0.0174). In addition, among the 22 patients with E2A-PBX1 fusion transcripts, 12 (54.5%) patients including all four non-smokers, showed no common mutations in k-ras, p53 and EGFR.
  
  
  CONCLUSIONS
  E2A-PBX1 fusion gene caused by t(1;19)(q23;p13) may be a common genetic change in AIS and a survival determinant for female AIS patients at early stage.
authors.affiliation: School of Life Sciences, Tsinghua University, Beijing 10084, China.
authors.forename: Min-Li
authors.initials: ML
authors.lastname: Mo
authors.forename: Zhao
authors.initials: Z
authors.lastname: Chen
authors.forename: Hai-Meng
authors.initials: HM
authors.lastname: Zhou
authors.forename: Hui
authors.initials: H
authors.lastname: Li
authors.forename: Tomomi
authors.initials: T
authors.lastname: Hirata
authors.forename: David M
authors.initials: DM
authors.lastname: Jablons
authors.forename: Biao
authors.initials: B
authors.lastname: He
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001483:Base Sequence; D014408:Biomarkers, Tumor / Q000235:genetics; D002278:Carcinoma in Situ / Q000235:genetics; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics* / Q000401:mortality / Q000473:pathology; D045744:Cell Line, Tumor; D056905:Chromosome Breakpoints; D066246:ErbB Receptors / Q000235:genetics; D005260:Female; D018398:Homeodomain Proteins / Q000235:genetics*; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics* / Q000401:mortality / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009367:Neoplasm Staging; D015514:Oncogene Proteins, Fusion / Q000235:genetics*; D011379:Prognosis; D011518:Proto-Oncogene Proteins / Q000235:genetics; D016283:Proto-Oncogene Proteins p21(ras); D012307:Risk Factors; D012737:Sex Factors; D014158:Transcription, Genetic; D016159:Tumor Suppressor Protein p53 / Q000235:genetics; D018631:ras Proteins / Q000235:genetics
chemical_list: D014408:Biomarkers, Tumor; D018398:Homeodomain Proteins; C117307:KRAS protein, human; D015514:Oncogene Proteins, Fusion; D011518:Proto-Oncogene Proteins; D016159:Tumor Suppressor Protein p53; C089847:E2A-Pbx1 fusion protein; D066246:ErbB Receptors; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins