Journal article

Publication year: 2009

Pages: 571-576

Journal: Epigenetics

Volume number: 4

Issue number: 8

ISSN: 1559-2294

eISSN: 1559-2308

Open access status: Bronze

DOI Link: https://doi.org/10.4161/epi.4.8.10056

Publisher: Taylor and Francis Group

Abstract: 

The Ras association domain family (RASS F) encodes for distinct tumor suppressors and several members are frequently silenced in human cancer. In our study, we analyzed the role of a novel RASS F member termed RASS F10 in thyroid carcinogenesis. The RASSF10 CpG island promoter was intensively methylated in nine thyroid cancer cell lines and in 66% of primary thyroid carcinomas. RASSF10 methylation was significantly increased in primary thyroid carcinoma compared to normal thyroid and follicular adenoma (0 and 10%, respectively; p < 0.004). Patients with cancerous lymph nodes were significantly hypermethylated for RASSF10 in primary thyroid tumors compared to those with non-affected lymph nodes (79 vs. 36%; p = 0.047). RASSF10 promoter hypermethylation correlated with a reduced expression and treatment with a DNA methylation inhibitor reactivated RASSF10 transcription. In summary, our data show frequent epigenetic inactivation of RASSF10 in thyroid cancer. These results suggest that RASSF10 may encode a novel epigenetically inactivated candidate tumor suppressor gene in thyroid carcinogenesis.

Harvard Citation style: Schagdarsurengin, U., Richter, A., Wöhler, C. and Dammann, R. (2009) Frequent epigenetic inactivation of RASSF10 in thyroid cancer, Epigenetics, 4(8), pp. 571-576. https://doi.org/10.4161/epi.4.8.10056

APA Citation style: Schagdarsurengin, U., Richter, A., Wöhler, C., & Dammann, R. (2009). Frequent epigenetic inactivation of RASSF10 in thyroid cancer. Epigenetics. 4(8), 571-576. https://doi.org/10.4161/epi.4.8.10056