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English Abstract
Journal Article
Research Support, Non-U.S. Gov't
[Hypermethylation of promoter region of RASSF1A gene in ovarian malignant epithelial tumors].
Zhonghua Zhong Liu za Zhi [Chinese Journal of Oncology] 2005 November
OBJECTIVE: To investigate hypermethylation of promoter region of RASSF1A and its relationship with ovarian malignant epithelial tumors.
METHODS: Methylation-specific PCR (MSP) was used to determine the hypermethylation of promoter region of ras association domain family 1 (RASSF1A) gene in 80 cases of ovarian malignant epithelial tumors.
RESULTS: No methylation of promoter region of RASSF1A gene was found in all 80 normal control tissues (0). Of 80 ovarian malignant epithelial tumors 42 were hypermethylated in promoter region of RASSF1A gene (52.5%). There was no statistically significant difference in the frequency of hypermethylation of RASSF1A gene among serious adenocarcinomas, mucinous adenocarcinomas and endometrioid adenocarcinomas (54.2%, 52.4% and 45.5%, respectively; P > 0.05). Hypermethylation of RASSF1A gene happened more often in tumors in stage III and IV (66.7% and 77.8%) than that in stage I and II (21.4% and 16.7%; P < 0.05). It was less frequently observed in well and moderately differentiated tumors (34.5% and 35.0%) than in poorly differentiated tumors (80.6%; P < 0.05).
CONCLUSION: High frequency of methylation of RASSF1A promoter exists in ovarian malignant epithelial tumors as a tumor suppressor gene, its suppressor activity may be abrogated by an epigenetic mechanism. Hypermethylation of RASSF1A promoter in patients with epithelial malignant ovarian tumors is related to clinical stage and histopathological grade. It indicates poor prognosis.
METHODS: Methylation-specific PCR (MSP) was used to determine the hypermethylation of promoter region of ras association domain family 1 (RASSF1A) gene in 80 cases of ovarian malignant epithelial tumors.
RESULTS: No methylation of promoter region of RASSF1A gene was found in all 80 normal control tissues (0). Of 80 ovarian malignant epithelial tumors 42 were hypermethylated in promoter region of RASSF1A gene (52.5%). There was no statistically significant difference in the frequency of hypermethylation of RASSF1A gene among serious adenocarcinomas, mucinous adenocarcinomas and endometrioid adenocarcinomas (54.2%, 52.4% and 45.5%, respectively; P > 0.05). Hypermethylation of RASSF1A gene happened more often in tumors in stage III and IV (66.7% and 77.8%) than that in stage I and II (21.4% and 16.7%; P < 0.05). It was less frequently observed in well and moderately differentiated tumors (34.5% and 35.0%) than in poorly differentiated tumors (80.6%; P < 0.05).
CONCLUSION: High frequency of methylation of RASSF1A promoter exists in ovarian malignant epithelial tumors as a tumor suppressor gene, its suppressor activity may be abrogated by an epigenetic mechanism. Hypermethylation of RASSF1A promoter in patients with epithelial malignant ovarian tumors is related to clinical stage and histopathological grade. It indicates poor prognosis.
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