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| The relationship between point mutation and abnormal expression of c-fms oncogene in hepatocellular carcinoma |
| Dong-Hua Yang, Wei Huang, Jun Cui, Jian-Chang Shu, Shao-Hui Tang, Wen-Jie Zhang and Jie-Hua Liang |
Guangzhou, China
Author Affiliations: Department of Gastroenterology, First Affiliated Hospital of Jinan University, Guangzhou 510630, China (Yang DH, Huang W, Cui J, Shu JC, Tang SH, Zhang WJ and Liang JH)
Corresponding Author: Dong-Hua Yang, MD, Department of Gastroenterology, First Affiliated Hospital, Jinan University, Guangzhou 510630, China (Tel: 86-20-38688633; Fax: 86-20-38688000; Email: thdyang@jnu.edu.cn) |
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Abstract BACKGROUND: Recent research found abnormal expression of the c-fms oncogene, which encodes the macrophage colony-stimulating factor receptor (CSF-1R), in several human carcinomas including hepatocellular carcinoma (HCC). But the relationship between the point mutation and abnormal expressing of c-fms oncogene in HCC was not clear. This study is to investigate the relationship between point mutation and abnormal expression of c-fms oncogene in hepatocellular carcinoma (HCC) and to clarify the mechanism of HCC.
METHODS: The expression of c-fms oncogene at different levels of cell, protein and transcription was observed using immune histological ABC, Western blot and Northern blot. PCR-single strand conformation polymorphism and gene sequencing were used to detect the mutation of c-fms in HCC tissues and their surrounding tissues of 30 patients.
RESULTS: The expression of c-fms was significantly higher in HCC tissues than in their surrounding tissues (P<0.01). Point mutation of Leu (TTG)→Ser (TCG) at codon 301 of c-fms amino acids was observed in 21.4% (3/14) HCC tissues. No mutation of c-fms oncogene was detected in the surrounding cancerous tissues.
CONCLUSION: Point mutation at codon 301 of c-fms oncogene is one of the mechanisms of abnormal over-expression in HCC.
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2004, Vol. 3 
