A t(10;17) translocation creates the RET/PTC2 chimeric transforming sequence in papillary thyroid carcinoma

G. Sozzi, I. Bongarzone, M. Miozzo, M. G. Borrello, M. G. Butti, S. Pilotti, G. Della Porta, M. A. Pierotti

Research output: Contribution to journalArticlepeer-review

Abstract

Activation of the RET protooncogene tyrosine kinase (tk) by fusion with other genes is a frequent finding in papillary thyroid carcinoma. The tk domain of proto-RET can be fused either with the D10S170 gene generating the RET/PTC1 transforming sequence or with sequences belonging to the gene encoding the regulatory subunit RIA of c-AMP-dependent protein kinase A, thus forming the RET/PTC2 oncogene. We have previously shown that an inversion of chromosome 10, inv(10)(q11.2q21), is responsible for the generation of the RET/PTC1. Here we report that a chromosomal translocation, t(10;17)(q11.2;q23), juxtaposes the tk domain of the RET protooncogene, which resides on chromosome 10, to a 5' portion of the RIA gene on chromosome 17, leading to the formation of the chimeric transforming gene RET/PTC2. The finding of the transforming protein in primary tumor cell extracts supports the conclusion that RET/PTC2 activation plays a role in papillary thyroid tumorigenesis.

Original languageEnglish
Pages (from-to)244-250
Number of pages7
JournalGenes Chromosomes and Cancer
Volume9
Issue number4
Publication statusPublished - 1994

ASJC Scopus subject areas

  • Cancer Research
  • Genetics

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