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

Exp Clin Endocrinol Diabetes. 2000;108(1):49-53. doi: 10.1055/s-0032-1329215.

Abstract

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.

MeSH terms

  • Base Sequence
  • Carcinoma, Medullary / genetics*
  • Codon
  • Genes, ras / genetics*
  • Humans
  • Mutation*
  • Polymerase Chain Reaction
  • Proto-Oncogene Proteins p21(ras) / genetics
  • Thyroid Neoplasms / genetics*

Substances

  • Codon
  • HRAS protein, human
  • Proto-Oncogene Proteins p21(ras)