Abstract |
With a rapid-emergence, chemically induced animal model for breast cancer, an experiment designed to test the hypothesis that energy restriction (ER) induces the loss of carcinogen-initiated cells from the mammary gland, thereby conferring a permanent protective effect against the development of cancer, failed to support this hypothesis. Nonetheless, this experiment served to define an experimental approach and a time frame on which to focus mechanistic inquiry. With an ER and energy repletion (ER-REP) protocol as a tool for identifying potential mediators of the cancer-inhibitory activity of ER, concomitant changes in plasma corticosterone and insulin-like growth factor 1 during energy restriction and repletion were observed. The relationship of the timing of these hormonal changes to the time frame of change in the carcinogenic response during ER-REP was consistent with the role of both hormones in mediating the protective effects of ER. However, a similar pattern of change in the energy-regulated hormone leptin indicated that its role in cancer inhibition also merits consideration.
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Authors | Zongjian Zhu, Weiqin Jiang, Henry J Thompson |
Journal | Molecular carcinogenesis
(Mol Carcinog)
Vol. 35
Issue 2
Pg. 51-6
(Oct 2002)
ISSN: 0899-1987 [Print] United States |
PMID | 12325034
(Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Copyright | Copyright 2002 Wiley-Liss, Inc. |
Chemical References |
- Leptin
- Receptors, Estrogen
- Insulin-Like Growth Factor I
- Methylnitrosourea
- Corticosterone
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Topics |
- Adenocarcinoma
(chemically induced, metabolism, prevention & control)
- Animals
- Caloric Restriction
- Corticosterone
(blood)
- Diet
- Energy Metabolism
- Female
- Insulin-Like Growth Factor I
(metabolism)
- Leptin
(blood)
- Mammary Glands, Animal
(pathology)
- Mammary Neoplasms, Experimental
(chemically induced, metabolism, prevention & control)
- Methylnitrosourea
- Rats
- Rats, Sprague-Dawley
- Receptors, Estrogen
(metabolism)
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