Treatment of secondary cultures of hamster embryonic cells with an excess of thymidine (5mM) caused an inhibition of DNA synthesis which was reversible. This treatment permitted a study of the effects of polycyclic hydrocarbons on cells inhibited at the G1-S boundary and on cells entering the S phase of the cell cycle. Cytotoxic damage caused by 7,12dimethylbenz(a)anthracene (DMBA) treatment of...

We demonstrate that although IGF-II gene expression is approximately 3-fold higher in 9,10-dimethyl-1,2-benzanthracine (DMBA)-induced rat mammary tumors (MTs) than in nonneoplastic breast tissue, IGF-II mRNA abundance in DMBA-induced MTs is approximately 130-fold higher in pregnant as compared to nonpregnant hosts. This correlated with accelerated tumor growth in pregnant hosts. Immunohistochem...

Dimethylbenz(a)anthracene (DMBA) is a potent inducer of mammary tumors in intact female Sprague-Dawley rats, but not in males or ovariectomized females (OVX). Qualitative and quantitative aspects of hepatic metabolism of DMBA were examined in these three groups of rats, using the nonrecirculating perfused liver, to determine whether the production of proximate carcinogenic metabolites of DMBA b...

Chemical induction of mammary tumors in mice requires usually a long latency period and is often complicated by high non-mammary tumor related mortality. Classically hormone stimulation has been used as the means to increase tumor incidence. The synthetic progestin medroxyprogesterone acetate (MPA) was postulated by some authors to increase mammary tumor incidence in various rodent models. Howe...

Mammary carcinomas induced by the administration of 7,12-dimethylbenz(a)anthracene (DMBA) to young virgin rats arise from undifferentiated terminal ductal structures called terminal end buds (TEBs). TEBs that normally differentiate into alveolar buds (ABs) and lobules under the influence of DMBA develop intraductal proliferations which progress to carcinoma. The high susceptibility of the young...

BACKGROUND The present study has evaluated the Emodin efficacy on the Akt, MAPK, ERK and DNMT expression pattern during 7,12-dimethylbenz[a]anthracene (DMBA)-induced oral carcinoma in golden Syrian hamsters, in order to explore its antitumor potential. MATERIALS AND METHODS Oral tumors were developed in the buccal pouches of golden Syrian hamsters using the carcinogen, DMBA. RESULTS While t...

Apoptosis (programmed cell death) is regulated by a number of inhibitory or stimulatory factors. One such family of antiapoptotic proteins is the inhibitors of apoptosis proteins (IAPs), of which survivin and X chromosome-linked IAP (XIAP) are members. The expression of survivin and XIAP, as well as their association with p53, in chemically-induced experimental oral carcinogenesis is not comple...

BACKGROUND There has been no dearth of scientific literature that genotoxic agents have a causative effect in the pathogenesis of carcinomas. 7,12 dimethylbenz(a)anthracene (DMBA), which is a potent organ specific carcinogen, has been found to produce mutagenic effects on cells. Annona squamosa has a long history in traditional Indian medicine for being used to treat several diseases including ...

Experiments were conducted to determine whether two-stage carcinogenesis could be observed in rat tracheal epithelium using 7,12-dimethylbenz(a)anthracene (DMBA) as initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as promoter. Heterotopic tracheal transplants in Fischer 344 rats were first exposed to 188 microgram of DMBA delivered over a four-week period and subsequently to 100 microgr...