Activation of c‐Ki‐ras coexists with c‐myc amplification in cells from a nude mouse tumor induced by the human breast carcinoma cell line SW 613‐S

Abstract

In vitro transfection experiments have shown that cooperation between two different oncogenes can confer a fully malignant phenotype to primary rodent cells. We have previously reported that SW 613-Tul cells, derived from a tumor induced in a nude mouse by the human breast carcinoma cell line SW 613-S showed a 30-fold amplification of the c-m_rc gene. In the present work, we show that these cells also harbor an activated c-Ki-ras gene capable of inducing the formation of foci upon transfection of NIH 3T3 cells with SW 613-Tul genomic DNA. Our results suggest that both the c-myc and c-Ki-ras oncogenes, activated by two different mechanisms, may cooperate in the full expression of the tumorigenic phenotype of SW 613-Tul cells.

Oncogenic activation of glypican-3 by c-Myc in human hepatocellular carcinoma

“…To further investigate the effects of c‐Myc on GPC3 levels, we assessed the mRNA and protein levels of c‐Myc and GPC3 in HCC samples. In human malignancies, the overexpression of proto‐oncogenes has been found to result from chromosomal translocation, gene amplification, and/or specific point mutations 21. Because increased c‐Myc protein levels have been associated with gene amplification, we evaluated the amplification of the c‐Myc gene in HCC samples and their respective tissues.…”