[Alterations of FHIT gene and p16 gene in lung cancer and metastatic hilar lymph nodes].
OBJECTIVE
To investigate alterations of fragile histidine triad (FHIT) gene and p16 gene in lung cancer.


METHODS
Forty-nine lung cancer specimens and 16 matched metastatic hilar lymph nodes of lung cancer patients were examined for abnormalities of p16 and FHIT genes by using RT-PCR and RT-PCR-SSCP.


RESULTS
Thirty-two of 47(68.1%) samples of primary lung cancer and 15 of 16 (93.8%) samples of metastatic hilar lymph nodes exhibited loss of FHIT gene transcripts. In 14 of the 47 samples of primary lung cancer(29.8%), and 9 of 16 samples of metastatic hilar lymph nodes(56.3%), FHIT gene transcripts were deleted in exones 1-4. The deletion rate of p16 gene transcripts in exons 2-3 was 36.7% (18/49) in primary and 56.3% (9/16) in metastatic lymph nodes, respectively. The loss of p16 or FHIT expression did not correlate with sex, smoking, TNM stage, but was more frequently observed in poorly differentiated cancer. No mutation of FHIT and p16 cDNA was found by SSCP.


CONCLUSIONS
Loss of FHIT and p16 gene transcript is frequent in lung cancer and may be an early event in lung carcinogenesis. Mutations may not be the major mechanisms of p16 and FHIT gene inactivation. Lung cancer with FHIT and p16 gene alterations have more malignant phenotype and behavior.
Wang
X
X
Department of Medical Oncology, National Laboratory of Molecular Oncology, Cancer Institute (Hospital), Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100021.
Sun
Y
Y
Li
W
W
D017766:Acid Anhydride Hydrolases; D017353:Gene Deletion; D019942:Genes, p16; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics* / Q000473:pathology; D008207:Lymphatic Metastasis; D009154:Mutation; D009363:Neoplasm Proteins / Q000235:genetics*; D000099170:Bis(5'-adenosyl)triphosphatase
D017766:Acid Anhydride Hydrolases; D009363:Neoplasm Proteins; D000099170:Bis(5'-adenosyl)triphosphatase