Open AccessEXPRESSION OF Ha‐ ras ONCOGENE PRODUCT IN RAT GASTROINTESTINAL CARCINOMAS INDUCED BY CHEMICAL CARCINOGENS
Author(s) -
Yasui Wataru,
Sumiyoshi Hiromichi,
Yamamoto Tetsuro,
Oda Noriko,
Kameda Takashi,
Tanaka* Takeo,
Tahara Eiichi
Publication year - 1987
Publication title -
acta patholigica japonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
ISSN - 0001-6632
DOI - 10.1111/j.1440-1827.1987.tb02867.x
Subject(s) - carcinogen , oncogene , pathology , cancer research , immunohistochemistry , biology , medicine , cancer , biochemistry , cell cycle
The expression of Ha ras oncogene product in rat gastrointestinal carcinomas induced by N‐methyl‐N‐nitro‐N‐nitrosoguanidine (MNNG) or 1, 2‐dimethylhydrazine (DMH) was studied by Western blotting and immunohistochemistry using anti‐Ha ras p 21 oncoprotein antibody. In Western blotting, high levels of c‐Ha ras p 21 were found in serially transplantable rat duodenal carcinomas induced by MNNG and rat colon carcinomas induced by DMH. mmunohistochemically, c‐Ha ras p21 immunoreactivity was detected in 3 (16.7%) of 17 MNNG‐induced stomach carcinomas and in 21 (63.6%) of 33 DMH‐induced colon carcinomas, respectively. In the colon carcinomas, c‐Ha‐ ras p 21 immunoreactivity in deeply invasive tumors was stronger than that in superficially invasive tumors and was expressed in all subserosal tumors. Moreover, all of the metastatic colon carcinomas had c‐Ha‐ ras p 21 immuno‐reactive tumor cells. These findings suggest that c‐Ha‐ ras p21 expression plays an important role in tumor proliferation, invasion and metastasis of DMH‐induced colon carcinoma. ACTA PATHOL. JPN. 37: 1731–1741, 1987.