Journalartikel

Jahr der Veröffentlichung: 2005

Seiten: 1-7

Zeitschrift: Experimental and Clinical Endocrinology & Diabetes

Bandnummer: 113

Heftnummer: 1

ISSN: 0947-7349

eISSN: 1439-3646

DOI Link: https://doi.org/10.1055/s-2004-830522

Verlag: Thieme Publishing

Abstract: 
Hypermethylation of CpG island promoters is associated with transcriptional inactivation of tumor suppressor genes in neoplasia. Inactivation of p16 and Pten was related to the development of pheochromocytomas. In this report, we investigated the methylation status of the p16(INK4a) cell cycle inhibitor gene and other prominent tumor-related genes (PTEN, RASSF1 A, CDH1, MSH2, MLH1, VHL, and TIMP3) in sporadic and multiple endocrine neoplasia type 2 (MEN2) pheochromocytomas by methylation-specific PCR. Hypermethylation was detected in 48% of pheochromocytomas for RASSF1 A, 24% for p16, 36% for MSH2, 16% for CDH1, and 8% for PTEN. No VHL, MLH1, and TIMP3 methylation was observed. Interestingly, the frequency of p16 inactivation in familial tumors was higher (5 out of 12, 42%) than in sporadic tumors (1 out of 13, 8%; p = 0.047) and RASSF1 A inactivation was more common in the hereditary tumors (58%) compared to the sporadic tumors (38%). Combined methylation of RASSF1 A and p 16 was found only in MEN2-related pheochromocytomas. Thus, a subset of hereditary pheochromocytomas displays preferential methylation of p 16 and RASSF1 A.

Harvard-Zitierstil: Dammann, R., Schagdarsurengin, U., Seidel, C., Trümpler, C., Hoang-Vu, C., Gimm, O., et al. (2005) Frequent promoter methylation of tumor-related genes in sporadic and Men2-associated pheochromocytomas, Experimental and Clinical Endocrinology & Diabetes, 113(1), pp. 1-7. https://doi.org/10.1055/s-2004-830522

APA-Zitierstil: Dammann, R., Schagdarsurengin, U., Seidel, C., Trümpler, C., Hoang-Vu, C., Gimm, O., Dralle, H., Pfeifer, G., & Brauckhoff, M. (2005). Frequent promoter methylation of tumor-related genes in sporadic and Men2-associated pheochromocytomas. Experimental and Clinical Endocrinology & Diabetes. 113(1), 1-7. https://doi.org/10.1055/s-2004-830522