Background: To investigate the relationship between loss of heterozygosity (LOH) of the allele genes on 3p and the pathogenesis of NSCLC.
Methods: Using polymerase chain reaction-based assays for dinucleotide repeat polymorphisms to analyze allele loss of 3p in 162 NSCLC samples.
Results: Of the 162 cases with NSCLC , 108 (66. 67 %) had LOH on 3p. Among them , 65 cases (40. 12 %) had LOH at 3p14 , 84 cases (51. 85 %) had LOH at 3p25 , and 41 cases (25. 31 %) occured co-deletion of 3p14 and 3p25. No 3p LOH were observed in 85 paracancerous lung tissues and 5 tissues of the pulmonary benign diseases. The total frequency of LOH at 3p did not relate to TNM staging and pathological classification in NSCLC ( P > 0. 05) . However , the co2deletion rate of 3p14 and 3p25 was significantly higher in adenocarcinoma (38 % , 19/ 50) than that in squamous cell carcinoma (19. 51 % ,16/82) ( P < 0. 05) . And 3p LOH rate in stage II(51. 28 % ,20/ 39) and stage III(44. 93 % ,31/ 69) were both remarkably higher than that of stage I(25. 93 % ,14/ 54) ( P < 0. 05) .
Conclusions: 3p LOH occur commonly in human NSCLC. It suggests that each region harbor one or more tumor suppressor genes , the inactivation of which might be critical for the oncogenesis and development of lung cancer.