Biochemistry of essential

508 hal; 22 c

Intisari biokimia./ Schumm

477 hal. : ill. ; 23 cm

Intisari biokimia./ Schumm

477 hal. : ill. ; 23 cm

Nucleocytoplasmic Release of Repetitive DNA Transcripts in Carcinogenesis Correlates With a 60 Kilodalton Cytoplasmic Protein

Treatment of rats with the hepatocarcinogen 3′-methyl-4-dimethylaminoazobenzene (3′-MeDAB) causes the appearance in the liver cytosol of a 60 kilodalton oncofetal protein. The appearance of this factor occurs within 40 h of treatment and coincides with the increase in the amount of rapidly labeled RNA released from nuclei in a reconstituted cell-free system. Cross-over experiments show that this increase is due to an enhanced transport capacity of the cytosol. The 60 kilodalton RNA transport factor is also present in the cytosol of tumor cells. Addition of the 60 kilodalton factor to normal liver cytosol causes the transport of repetitive RNA sequences similar to those transported from liver nuclei to tumor cell cytosol and those transported to the tumor cell cytoplasm in vivo. This factor modifies nuclear RNA restriction, at least in part, by eliciting the transport of repetitive RNA normally retained within the nucleus of the normal cell

A carcinogenesis- and tumorigenesis-associated rat fetal protein: An immuno-histochemical and immuno-biochemical study utilizing a new monoclonal antibody, MOFP

An oncofetal protein (OFP), which is a potential marker for carcinogenesis and tumorigenesis, was evaluated with monoclonal antibodies shown to be specific for the antigen. Treatment of partially hepatectomized rats with a single non-necrogenic dose of diethylnitrosamine induced OFP in the liver. Its concentration, as measured by a dual immunol/bioassay, increased steadily over a 5-week period of observation before reaching a constant level. Immunohistochemical localization of OFP in liver sections from rats treated with N-nitroso-N-diethyl-nitrosamine showed that the factor was primarily localized to the cell cytoplasm in cells of most of the altered hepatic foci although some of this shedding antigen was also extracellular. Monoclonal antibody 17-1A specific for 17-1A antigen, an established surface marker for adenocarcinomas of the gastrointestinal tract, showed a similar distribution in liver from the carcinogentreated rats, but localized to the cell membrane and cytoplasm. Scattered cells surrounding the altered hepatic foci were also positive for both monoclonal antibodies. Immunolocalization studies showed fetal rat liver and hepatoma were positive for OFP but adult normal or regenerating liver was negative. It was not detected in cells which morphologically could be classified as oval cells. As assessed by immuno/bioassay, the OFP released to the peripheral blood (plasma) of hepato-carcinogen-treated rats increased for 3 weeks, before undergoing a transitory decrease. Circulating antibodies specific for the factor were detected in the blood around 3-5 weeks post-treatment. Development of Western blots of the OFP with antiphosphotyrosine IgG indicates that the marker protein contains phosphotyrosine. © 1989 Oxford University Press