The RET/PTC oncogene is frequently activated in oncocytic thyroid tumors (Hurthle cell adenomas and carcinomas), but not in oncocytic hyperplastic lesions

J Clin Endocrinol Metab. 2002 Jan;87(1):364-9. doi: 10.1210/jcem.87.1.8180.


Hurthle cell adenomas and carcinomas, characterized by the presence of oncocytic cells, are unusual thyroid neoplasms, the treatment of which is still controversial. We analyzed specimens from 49 patients with oncocytic cell nodular lesions including 20 adenomas, 19 carcinomas, and 10 hyperplasias for RET/PTC (papillary thyroid carcinoma) activation, which is the most frequent genetic alteration in PTCs. RET/PTC activation was detected in a significant number of cases of Hurthle cell adenomas and carcinomas, but in 0 of 10 patients with hyperplastic nodules. In particular, the RET/PTC1 isoform was found in 7 of 12 adenomas and 4 of 7 carcinomas. These results would indicate that RET/PTC is a genetic event common to papillary carcinomas and to Hurthle cell neoplasias.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoma, Oxyphilic / metabolism*
  • Adenoma, Oxyphilic / pathology
  • Carcinoma / metabolism*
  • Carcinoma / pathology
  • Humans
  • Hyperplasia / metabolism
  • Immunohistochemistry
  • Oncogene Proteins, Fusion / metabolism*
  • Protein-Tyrosine Kinases
  • Reverse Transcriptase Polymerase Chain Reaction
  • Thyroid Gland / metabolism
  • Thyroid Neoplasms / metabolism*
  • Thyroid Neoplasms / pathology


  • Oncogene Proteins, Fusion
  • Protein-Tyrosine Kinases
  • ret-PTC fusion oncoproteins, human