Chromosome I rearrangements involving the genes TPR and NTRKI produce structurally different thyroid-specific TRK oncogenes

Angela Greco, Claudia Miranda, Sonia Pagliardini, Lisa Fusetti, Italia Bongarzone, Marco A. Pierotti

Research output: Contribution to journalArticlepeer-review

Abstract

The NTRKI gene in the q arm of chromosome I encodes one of the receptors for the nerve growth factor and is frequently activated as an oncogene in papillary thyroid carcinomas. The activation is due to chromosomal rearrangements juxtaposing the NTRKI tyrosine kinase domain to 5'-end sequences from different genes. The thyroid TRK oncogenes are activated by recombination with at least three different genes: the gene coding for tropomyosin and TPR, both on chromosome I, and TFG on chromosome 3. In a previous study, we showed that two tumors carrying the TPRINTRKI rearrangement contained structurally different oncogenes named TRK-TI and TRK-T2. In this paper, we report (1) the cDNA structure of TRK-T2, (2) evidence that TRK-T2 is generated by different rearrangements in two thyroid tumors, and (3) a detailed analysis of the three different TPR/NTRKI rearrangements. With molecular studies based on Southern blot hybridization, cloning, and sequencing, we show that all the rearrangements are nearly balanced, involving deletion, insertion, or duplication of only few nucleotides. In one case, an additional rearrangement involving sequences derived from chromosome 17 was detected.

Original languageEnglish
Pages (from-to)112-123
Number of pages12
JournalGenes Chromosomes and Cancer
Volume19
Issue number2
DOIs
Publication statusPublished - 1997

ASJC Scopus subject areas

  • Cancer Research
  • Genetics

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