title: Pulmonary pleomorphic carcinoma: a clinicopathological study including EGFR mutation analysis.
abstract: BACKGROUND
  Pulmonary pleomorphic carcinoma is a rare epithelial tumor and has an aggressive clinical course. As few studies of pulmonary pleomorphic carcinoma have been described, the clinicopathological characteristics of the disease remain unclear. Especially, the information on the epidermal growth factor receptor (EGFR) mutation status of pulmonary pleomorphic carcinoma is sparse.
  
  
  METHODS
  We retrospectively examined 17 patients with pulmonary pleomorphic carcinoma. EGFR mutation and Ki-67 labeling index were investigated in these patients.
  
  
  RESULTS
  The median age of the patients was 72 years (range, 47-84 years). Thirteen patients were men and four were women. EGFR mutation was observed in 3 (18%) of 17 patients. The median value of Ki-67 labeling index was 62% (range, 20-87%). Positron emission tomography with 18-fluorodeoxy-glucose was performed in 16 patients, and the standardized uptake value tended to be high (median 19.3). The survival of patients without surgery demonstrated a significantly poor prognosis compared with those with surgery (P = 0.0096). Palliative chemotherapy was almost poor response in advanced pulmonary pleomorphic carcinoma. The response to gefitinib in a patient with EGFR mutation was small and transient.
  
  
  CONCLUSIONS
  EGFR mutation was recognized in approximately 20% of patients with pulmonary pleomorphic carcinoma. It is necessary to investigate whether the use of a molecular targeting drug improves outcome for pulmonary pleomorphic carcinoma.
authors.affiliation: Division of Thoracic Oncology, Shizuoka Cancer Center, Sunto-gun, Shizuoka, Japan. kkaira1970@yahoo.co.jp
authors.forename: Kyoichi
authors.initials: K
authors.lastname: Kaira
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Horie
authors.forename: Eriko
authors.initials: E
authors.lastname: Ayabe
authors.forename: Haruyasu
authors.initials: H
authors.lastname: Murakami
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Takahashi
authors.forename: Asuka
authors.initials: A
authors.lastname: Tsuya
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Nakamura
authors.forename: Tateaki
authors.initials: T
authors.lastname: Naito
authors.forename: Masahiro
authors.initials: M
authors.lastname: Endo
authors.forename: Haruhiko
authors.initials: H
authors.lastname: Kondo
authors.forename: Takashi
authors.initials: T
authors.lastname: Nakajima
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Yamamoto
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D002282:Adenocarcinoma, Bronchiolo-Alveolar / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D000368:Aged; D000369:Aged, 80 and over; D014408:Biomarkers, Tumor / Q000378:metabolism; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000235:genetics*; D005260:Female; D000077156:Gefitinib; D006801:Humans; D007124:Immunoenzyme Techniques; D019394:Ki-67 Antigen / Q000378:metabolism; D008175:Lung Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics*; D009367:Neoplasm Staging; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use; D011518:Proto-Oncogene Proteins / Q000235:genetics; D016283:Proto-Oncogene Proteins p21(ras); D011799:Quinazolines / Q000627:therapeutic use; D012189:Retrospective Studies; D015996:Survival Rate; D016896:Treatment Outcome; D018631:ras Proteins / Q000235:genetics
chemical_list: D014408:Biomarkers, Tumor; C117307:KRAS protein, human; D019394:Ki-67 Antigen; D047428:Protein Kinase Inhibitors; D011518:Proto-Oncogene Proteins; D011799:Quinazolines; C512478:EGFR protein, human; D066246:ErbB Receptors; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins; D000077156:Gefitinib