Loss of Fhit is frequent in stage I non-small cell lung cancer and in the lungs of chronic smokers.

摘要: Abnormalities of FHIT , a candidate tumor suppressor gene at 3p14.2, have been found frequently in multiple types including non-small cell lung cancer (NSCLC). To investigate whether inactivation plays role early tumorigenesis, Fhit levels were determined by immunohistochemistry tumors from 87 patients with stage I NSCLC and 372 bronchial biopsy specimens 86 chronic smokers without evidence malignancy. We that 49% demonstrated significantly decreased staining or lack for Fhit. However, expression status was not associated disease-free survival overall survival. Analysis subset 76 on which microsatellite analysis the locus performed did show strong association between loss heterozygosity expression, suggesting presence complex mechanisms inactivation. Of biopsies smokers, (23%) exhibited expression. In 37 (43%) subjects, observed least one site. Loss higher metaplastic lesions (23 49 lesions, 47%) than histologically normal epithelium (63 323 specimens, 20%; P 15% had frequency those metaplasia index ≤15% ( = 0.015). Interestingly, current rate former 0.02). Our data indicate is reduced substantial number early-stage preneoplastic smokers. The cigarette smoking suggests initiation smoking-related tumorigenesis.