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[Cancer Research 60, 2786-2789, June 1, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

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 Carcinoma1

Konstadinos Salassidis, Jochen Bruch, Horst Zitzelsberger, Edmund Lengfelder, Albrecht M. Kellerer and Manfred Bauchinger2

Institute of Radiation Biology, Ludwig Maximilians University, D-80336 München [K. S., H. Z., E. L., A. M. K.], and Institute of Radiobiology, GSF-National Research Center for Environment and Health, D-85764 Neuherberg [K. S., J. B., H. Z., M. B.], Germany

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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