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in lasiocarpine model are resistant to megalocytic effect of
Senecio alkaloid. These selective resistances to cytotoxicity
[8]
models appear to be precursor lesions for hepatocellular
carcinoma development.

REFERENCES

1. Roomi MW, Gaal K, Yuan QX, French BA, Fu P, Bardag-Gorce F,
French SW. Preneoplastic liver cell foci expansion induced by
thioacetamide toxicity in drug-primed mice. Exp Mol Pathol
2006;81:8-14.
2. Tazawa J, Irie T, French SW. Mallory body formation runs parallel to
gamma-glutamyl transferase induction in hepatocytes of griseofulvin-fed
mice. Hepatology 1983;3:989-1001.
3. Oliva J, Bardag-Gorce F, French BA, Li J, McPhaul L, Amidi F, Dedes J,
Figure 2: Liver from a mouse fed diethyl 1, 4-dihydro, 1, 4, 6-trimethyl 3, 5-pyridine Habibi A, Nguyen S, French SW. Fat10 is an epigenetic marker for liver
decarboxylate (DDC) for 5 months, then withdrawn from DDC for 1 month, then preneoplasia in a drug-primed mouse model of tumorigenesis. Exp Mol
refed DDC for 3 days (×567). Note that the hyperplastic nodule stained red for Pathol 2008;84:102-12.
gamma-glutamyl transferase is devoid of protoporphyrin pigment whereas the 4. Nagao Y, Wan YJ, Yuan QX, Kachi K, Marceau N, French SW. Mouse
normal liver parenchyma has numerous protoporphyrin deposits as shown model of hepatocellular hyperplastic nodule formation characterization
of mRNA expression. Hepatol Res 1999;15:110-23.
manipulations. HN is a population of cells from which 5. Solt DB, Medline A, Farber E. Rapid emergence of carcinogen-induced
hepatocelluar carcinoma can develop. The HN studied hyperplastic lesions in a new model for the sequential analysis of liver
carcinogenesis. Am J Pathol 1977;88:595-618.
here resembles resistant phenotypes which grow in an 6. Shinozuka H, Sells MA, Katyal SL, Sell S, Lombardi B. Effects of a
otherwise toxic environment of potent porphyrinogenic choline-devoid diet on the emergence of gamma-glutamyltranspeptidase-
drugs DDC and GF. The HN is resistant to protoporphyrin positive foci in the liver of carcinogen-treated rats. Cancer Res
accumulation whereas the surrounding normal liver is filled 7. 1979;39:2515-21.
Rao PM, Nagamine Y, Roomi MW, Rajalakshmi S, Sarma DS.
with protoporphyrin. This observation is further supported Orotic acid, a new promoter for experimental liver carcinogenesis.
by the fact that HNs generated by diethylnitrosamine Toxicol Pathol 1984;12:173-8.
initiation and various promoting regimens are resistant 8. Hayes MA, Roberts E, Farber E. Initiation and selection of resistant
to their own promoting agents. For example, the nodules hepatocyte nodules in rats given the pyrrolizidine alkaloids lasiocarpine
and senecionine. Cancer Res 1985;45:3726-34.
produced by resistance to a cytotoxicity model using 2-acetyl
[5]
aminofluorene (2-AAF) are resistant to 2-AAF metabolism. How to cite this article: French SW, Roomi MW. Preneoplastic foci in
The nodules produced by choline methionine deficient diet mice fed diethyl 1, 4-dihydro, 1, 4, 6-trimethyl 3, 5-pyridine decarboxylate
[6]
are resistant to fat accumulation. The HN nodules generated are resistant to protoporphyrin accumulation. Hepatoma Res 2015;1:50-1.
in orotic acid models are resistant to imbalances of
nucleotide pools created by orotic acid; nodules generated Source of Support: Nil. Confl ict of Interest: None declared.
[7]

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