Inactivation of phosphatidylethanolamine N-methyltransferase-2 in aflatoxin-induced liver cancer and partial reversion of the neoplastic phenotype by PEMT transfection of hepatoma cells.

Phosphatidylethanolamine N-methyltransferase(PEMT) is an enzyme in liver that catalyzes the stepwise methylation of phosphatidylethanolamine to phosphatidylcholine, in addition to the main pathway that synthesizes phosphatidylcholine directly from choline. We have reported that PEMT is permanently inactivated in liver cancer induced by the Solt and Farber model. Here we studied, (i) whether similar changes also occur in the progression of hepatocarcinoma triggered by aflatoxin B(1) (AFB(1)) in rats; (ii) whether the hepatoma phenotype could be reversed by over-expression of PEMT2.

Expression of phosphatidylethanolamine N-methyltransferase in Yoshida ascites hepatoma cells and the livers of host rats.

Previous studies have implicated phosphatidylethanolamine N-methyltransferase-2 (PEMT2) in the regulation of non-neoplastic liver growth [Tessitore,L., Cui,Z. and Vance,E.

Fasting/re-feeding before initiation enhances the growth of aberrant crypt foci induced by azoxymethane in rat colon and rectum.

In contrast to the protective effect of chronic caloric restriction on tumor development, we have shown that fasting sustained tumor initiation in rat liver by a noninitiating dose of diethylnitrosamine. Here we investigated whether fasting had a similar favorable effect on initiation in the colorectal mucosa in 80 male F344 rats. Animals fasted for 4 days were given a single s.

Fasting-refeeding stimulates the development of mammary tumors induced by 7,12-dimethylbenz[a]anthracene.

The effect of fasting-refeeding during the promotion phase of dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis has been investigated. Female Sprague-Dawley rats were given 130 mg/kg of DMBA and divided into four groups: Group 1 was fed ad libitum; Group 2 was fed ad libitum and, in addition, received daily subcutaneous injections of beta-estradiol and haloperidol for eight days, beginning two weeks after DMBA administration; Group 3 was exposed to three days of fasting one week after carcinogen injection, then fed ad libitum until the end of the experiment; Group 4 was treated as Group 2, except the animals were fasted for three days beginning one week after DMBA administration. Treatment with beta-estradiol and haloperidol enhanced the development of DMBA-induced mammary tumors.

Fasting during promotion, but not during initiation, enhances the growth of methylnitrosourea-induced mammary tumours.

The purpose of this work was to investigate the effect of fasting on the induction and growth of chemically-induced mammary carcinogenesis. Female Sprague-Dawley rats were given methylnitrosourea (MNU) i.p.