Santoro M, Melillo R M, Grieco M, Berlingieri M T, Vecchio G, Fusco A
Dipartimento di Biologia e Patologia Cellulare e Molecolare L. Califano, II Facoltà di Medicina e Chirurgia, Università degli Studi di Napoli, Italy.
Cell Growth Differ. 1993 Feb;4(2):77-84.
We have recently reported that about 50% of papillary thyroid carcinomas harbor an activated TRK or RET oncogene. Two retroviral vectors containing the activated TRK or RET/PTC oncogene have been used to infect a differentiated rat thyroid epithelial cell line, namely the PC Clone 3 cell line. Upon infection with the TRK virus, the PC Clone 3 cells lost only the ability to trap iodide and to express the thyroperoxidase gene. Conversely, when infected with the PTC virus, the PC Clone 3 cells completely lost all of their differentiated functions. However, both the PC-TRK and PC-PTC cell lines were unable to grow in soft agar, and they were not tumorigenic when injected into nude mice. A completely undifferentiated and malignant phenotype was obtained by the cooperation between the TRK or RET and the viral Ha-ras or Ki-ras oncogenes.
