Overexpression of human H-ras transgene is responsible for tumors induced by chemical carcinogens in mice

Level of human prototype H-ras transgene expression in tumors induced by ch emical carcinogens (N-ethyl-N-nitrosourea and N-methyl-N-nitrosourea) was a nalyzed in human H-rns transgenic mice (CB6F1-TgrasH2 Jic mice). All forest omach tumors examined revealed about 2-fold overexpression of the human H-r as transgene with or without point mutation at codon 12 or codon 61. Howeve r, endogenous mouse H- and K-ras genes exhibited neither point mutation nor overexpression. These results suggested that increased levels of ras gene products in the cell played an important role in facilitating chemical carc inogenesis in transgenic mice.