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Translocation t(10;14)(q11.2:q22.1) fusing the kinectin to the RET gene creates a novel rearranged form (PTC8) of the RET proto-oncogene in radiation-induced childhood papillary thyroid carcinoma.
Cancer Res. 60, 2786-2679 (2000)
Publ. Version/Full Text Volltext
PMC
Evaluation of 20 cases of radiation-induced childhood papillary thyroid carcinoma using fluorescence in situ hybridization demonstrated the presence of clonal translocations affecting the RET locus. Semiquantitative reverse transcription-PCR indicated overexpression of the RET tyrosine kinase (TK) domain in four cases. In two cases, the RET rearrangements PTC6 and PTC7 were identified and assigned to balanced translocations t(7;10)(q32;q11.2) and t(1;10)(p13;q11.2), respectively. In one case with a balanced translocation t(10;14)(q11.2;q22.1), 5' rapid amplification of cDNA ends revealed a novel type of RET oncogenic activation (PTC8), arising from a fusion of the 5' part of the kinectin (KTN1) gene to the TK domain of the RET gene. The presence of coiled-coil domains in the resulting ktn1/ret fusion protein suggests ligand-independent dimerization and thus constitutive activation of the ret TK domain.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
KINESIN-BINDING PROTEIN; CHERNOBYL; CHILDREN; ACCIDENT; BYELARUS; CLONING; CANCER; TUMORS
ISSN (print) / ISBN
0008-5472
e-ISSN
1538-7445
Journal
Cancer Research
Quellenangaben
Volume: 60,
Issue: 11,
Pages: 2786-2679
Publisher
American Association for Cancer Research (AACR)
Publishing Place
Philadelphia, Pa.
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Molecular Radiation Biology (IMS)