Summary:Background: Tumors arising in the lungs are in over 90% bronchogenic carcinomas that have been attributed predominantly to tobacco smoking, asbestos or air pollution but little is known about endogenous factors that could facilitate their development and invasiveness. The lungs originate embriologically from the same endoderm cells which form the epithelia lining the digestive tract, where gastrin is the major proliferative stimulus. Aims: Since lung cancer patients were recruited mostly among smokers, who also have been found to exhibit significantly higher infection rate of Helicobacter pylori (HP) infection than non-smokers and, as since the HP-infected subjects show enhanced plasma levels of gastrin, we decided 1) to compare the seroprevalence of HP and the expression of its cytotoxin, CagA, in lung cancer patients with those in the age- and gender-matched controls without cancer; 2) to determine the gene expression for gastrin and its receptors (CCKB-R) in lung cancer, 3) to assess the gastrin levels in plasma bronchial lavage and in tumor tissue and 4) to examine the expression of cyclooxygenase (COX)-1 and COX-2 in cancer tissue resection margin and intact bronchial mucosa.Material/Methods: The trial material included 50 patients with lung carcinoma and 100 age- and gender-matched controls. Anti-HP and anti-CagA IgG seroprevalence was estimated by specific antisera using ELISA tests. Gene expression of gastrin, CCKB-R, COX-1 and COX-2 was examined using RT-PCR, while gastrin was measured by specific RIA.Results: The seroprevalence of HP, especially that expressing CagA, is significantly higher in lung cancers than in healthy controls. Both gastrin and CCKB-R mRNA were detected in the cancer tissue and at the resection margin and similarly COX-2 mRNA was expressed in most cancers and resection margin but not in bronchial mucosa where only COX-1 was found. The lung cancer tissue and resection margin contained many folds larger amounts of immunoreactive gastrin than intact bronchial mucosa.
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