title: [Cyclooxigenase-2 levels are increased in the lung tissue and bronchial tumors of patients with chronic obstructive pulmonary disease].
abstract: BACKGROUND
  The expression of cyclooxygenase 2 (COX-2) is usually increased in inflammation and cancer. This study examines the expression of COX-2 in the lung of chronic obstructive pulmonary disease (COPD) patients with lung cancer.
  
  
  METHODS
  We studied 44 male patients with bronchial cancer (27 squamous carcinoma and 17 adenocarcinoma). Samples were obtained from the pulmonary parenchyma, from the bronchial mucosa adjacent to the tumor and from the tumor itself. Lung tissue specimens from 14 patients with pneumothorax were used as control. The mRNA and the COX-1 and COX-2 proteins were assessed by RT-PCR and Western blot, respectively.
  
  
  RESULTS
  COX-1 and COX-2 mRNA levels were significantly higher in the lung parenchyma of COPD patients than in the control subjects. COX-2 mRNA levels were also higher in the lung parenchyma than in both tumor and airway tissue samples procured from COPD patients. There were no differences in the COX-2 mRNA levels between squamous carcinoma and adenocarcinoma. In contrast, COX-2 protein levels were significantly higher in tumors than in lung parenchyma and airways. COX-2 protein levels were higher in adenocarcinoma compared with squamous carcinoma.
  
  
  CONCLUSIONS
  This study shows that in COPD, the pathway of cyclooxygenase is activated and associated with an increase in the expression of COX-2 in lung tumors. These observations suggest that COX-2 is possibly involved in the association between COPD and cancer.
authors.affiliation: Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, España.
authors.forename: Jordi
authors.initials: J
authors.lastname: Roca-Ferrer
authors.forename: Laura
authors.initials: L
authors.lastname: Pujols
authors.forename: Carlos
authors.initials: C
authors.lastname: Agusti
authors.forename: Antoni
authors.initials: A
authors.lastname: Xaubet
authors.forename: Joaquim
authors.initials: J
authors.lastname: Mullol
authors.forename: Josep M
authors.initials: JM
authors.lastname: Gimferrer
authors.forename: César
authors.initials: C
authors.lastname: Picado
mesh_terms: D000230:Adenocarcinoma / Q000201:enzymology* / Q000209:etiology; D000368:Aged; D001984:Bronchial Neoplasms / Q000201:enzymology* / Q000209:etiology; D002294:Carcinoma, Squamous Cell / Q000201:enzymology* / Q000209:etiology; D003043:Cocarcinogenesis; D051545:Cyclooxygenase 1 / Q000032:analysis / Q000235:genetics; D051546:Cyclooxygenase 2 / Q000032:analysis* / Q000235:genetics; D015232:Dinoprostone / Q000378:metabolism; D004790:Enzyme Induction; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008168:Lung / Q000201:enzymology*; D008297:Male; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D009363:Neoplasm Proteins / Q000032:analysis* / Q000235:genetics; D011030:Pneumothorax / Q000201:enzymology; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications / Q000201:enzymology*; D012333:RNA, Messenger / Q000032:analysis; D012334:RNA, Neoplasm / Q000032:analysis; D012907:Smoking / Q000009:adverse effects
chemical_list: D009363:Neoplasm Proteins; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D015232:Dinoprostone