[Methylation status of c-fms oncogene in hepatocellular carcinoma and its relation with clinical pathology].
OBJECTIVE
To study the methylation status change of c-fms oncogene in hepatocellular carcinogenesis, and to clarify the abnormal highly expressing mechanism of c-fms/CSF-1R in hepatocellular carcinoma (HCC).


METHODS
Genome DNA of 30 cases of HCC tissue and matching surrounding-cancer tissue were digested with restrictive endonucleases Hpa II/Msp I. Methylation status of c-fms oncogene was tested with Southern blot. Methylation status of c-fms oncogene in the HCC tissue and the matching surrounding-cancer tissue was compared. The relation between methylation status of c-fms oncogene and clinical pathology of HCC was determined.


RESULTS
Methylation status of c-fms oncogene decreased in 36.7% (11/30) HCC tissue and 13.3% (4/30) matching surrounding-cancer tissue. The hypomethylation rate of c-fms oncogene in the HCC tissue was higher than that in the matching surrounding-cancer tissue. There was significant correlation between Edmondson scale of HCC and hypomethylation of c-fms oncogene. The hypomethylation rate of HCC in Edmondson III-IV was higher than that in Edmondson I-II.


CONCLUSIONS
Hypomethylation of c-fms oncogene may be an important molecular mechanism leading to abnormally high expressing of CSF-1R, which contributes to occurrence and deterioration of HCC.
Cui
J
J
Department of Gastroenterology, Zhujiang Hospital, First Military Medical University, Guangzhou 510282, China.
Yang
D
D
D000328:Adult; D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000473:pathology; D019175:DNA Methylation; D005260:Female; D016236:Genes, fms; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics* / Q000473:pathology; D008297:Male; D008875:Middle Aged