title: Clinical and molecular analysis of synchronous double lung cancers.
abstract: BACKGROUND
  Since multiple lung cancer treatment strategies differ, it is essential for clinicians to be able to distinguish between separate primary lesions and metastasis. In the present study, we used array comparative genomic hybridization (aCGH) and somatic mutation (epidermal growth factor receptor: EGFR) to analyze genomic alteration profiles in lung cancer patients. To validate the consistency among the pathological assessments and clarify the clinical differences between double primary lesions and metastasis, we also examined synchronous double lung cancer clinical data.
  
  
  METHODS
  Between January 1970 and March 2010, 2215 patients with lung cancer underwent surgical resection at Nagasaki University Hospital. We performed molecular analysis of 12 synchronous double lung cancer patients without lymph node metastasis (intrapulmonary metastasis in the same lobe (pm1): n=6, primary: n=6). We then evaluated the clinical outcomes of patients with pathologically diagnosed synchronous double lung cancers (intrapulmonary metastasis (pm): n=80, primary: n=39) and other T3 tumors (n=230).
  
  
  RESULTS
  Examination of the concordance rate (CR) of the copy number changes (CNCs) for paired tumors showed that the metastasis group was larger than the primary group (55.5% vs. 19.6%, p=0.04). Pathological diagnosis and molecular classification were the same in 10 out of 12 cases (83%). As compared to the primary group, there tended to be an inferior 5-year survival curve for the pm group. However, in N0 patients, the survival curve for the pm group overlapped the primary group, while the survival rate of the pm1 group was much higher than that of other T3 group (p<0.01).
  
  
  CONCLUSIONS
  Both pathological and molecular assessment using aCGH adapted in the current study appeared to have a consistency. Pathological pm1(T3)N0 patients may have a better prognosis than other T3N0 patients.
authors.affiliation: Division of Surgical Oncology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki, Nagasaki 852-8501, Japan.
authors.forename: Junichi
authors.initials: J
authors.lastname: Arai
authors.forename: Tomoshi
authors.initials: T
authors.lastname: Tsuchiya
authors.forename: Masahiro
authors.initials: M
authors.lastname: Oikawa
authors.forename: Koji
authors.initials: K
authors.lastname: Mochinaga
authors.forename: Tomayoshi
authors.initials: T
authors.lastname: Hayashi
authors.forename: Koh-Ichiro
authors.initials: K
authors.lastname: Yoshiura
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Tsukamoto
authors.forename: Naoya
authors.initials: N
authors.lastname: Yamasaki
authors.forename: Keitaro
authors.initials: K
authors.lastname: Matsumoto
authors.forename: Takuro
authors.initials: T
authors.lastname: Miyazaki
authors.forename: Takeshi
authors.initials: T
authors.lastname: Nagayasu
mesh_terms: D000328:Adult; D000368:Aged; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics* / Q000401:mortality / Q000473:pathology / Q000556:secondary*; D055028:Comparative Genomic Hybridization; D066246:ErbB Receptors / Q000235:genetics; D005260:Female; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics* / Q000401:mortality / Q000473:pathology / Q000556:secondary*; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009367:Neoplasm Staging; D016609:Neoplasms, Second Primary / Q000235:genetics* / Q000401:mortality / Q000473:pathology; D016019:Survival Analysis
chemical_list: D066246:ErbB Receptors