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Exp Clin Endocrinol Diabetes 2000; 108(1): 49-53
DOI: 10.1055/s-0032-1329215
Original Article
© Georg Thieme Verlag Stuttgart - New York

Absence of H- and K-ras oncogene mutations in sporadic medullary thyroid carcinoma

M. Bockhorn
1   Department of General and Transplantation Surgery, University Clinic Essen, Germany
,
A. Frilling
1   Department of General and Transplantation Surgery, University Clinic Essen, Germany
,
V. Kalinin
2   Department of General Surgery, University Clinic Eppendorf, Hamburg, Germany
,
S. Schröder
3   Institute of Immunology, Pathology and Molecular Biology, Hamburg, Germany
,
C. E. Broelsch
1   Department of General and Transplantation Surgery, University Clinic Essen, Germany
› Institutsangaben
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Publikationsdatum:
24. September 2012 (online)

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Summary:

Medullary thyroid carcinoma (MTC) occurs sporadically (sMTC) or as part of the inherited cancer syndrome, multiple endocrine neoplasia type 2 (MEN 2). While the occurence of the MEN 2 syndrome is associated with mutations in the RET protooncogene, the reason for carcinogenesis in sMTC still remains unclear.

Ras is a frequently mutated oncogene in a broad spectrum of human tumors and has been found in about 50% of follicular, papillary or anaplastic thyroid carcinomas. The purpose of this study was to determine, whether mutations in the ras oncogene could play a possible role in the carcinogenesis of sMTC.

In this study we analyzed 15 sMTC for mutations in the hotspots codon 12, 13 and 61 of the H- and K-ras oncogene. We used the direct sequencing technique. In none of the examined tumors we were able to detect a mutation in the codon 12, 13 and 61 of the H-ras and K-ras oncogene.

Based upon these results, we conclude that H- and K-ras do not play an important role in the carcinogenesis of sMTC.

Key words:

ras oncogene - sporadic medullary thyroid carcinoma - multiple endocrine neoplasia 2