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Murine study supports hypothesis that leptin may play role in tumorigenesis.

Women's Health Weekly

| September 02, 2004 | COPYRIGHT 2004 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2004 SEP 2 - (NewsRx.com & NewsRx.net) -- Leptin receptor-deficient female mice do not develop mammary tumors despite having increased circulating leptin levels, researchers report.

The finding adds to the body of evidence supporting a role for leptin in the development of cancerous mammary tumors.

"Being overweight is a risk factor for postmenopausal breast cancer and is associated with an increased incidence and shortened latency of spontaneous and chemically-induced mammary tumors in rodents. However, leptin-deficient obese Lep(ob)Lep(ob) female mice have reduced incidences of spontaneous and oncogene-induced mammary tumors," according to M.P. Cleary and colleagues, University of Minnesota.

These researchers further explored the observation that "leptin enhances the proliferation of human breast cancer cell lines in which leptin receptors are expressed, which suggests that leptin signaling plays a role in tumor development."

"We evaluated oncogene-induced mammary tumor development in obese MMTV-TGF-alpha/Lepr(db)Lepr(db) mice that exhibit a defect in OB-Rb, which is considered to be the major signaling isoform of the leptin receptor. Lepr and MMTV-TGF-alpha mice were crossed, and the offspring were genotyped for oncogene expression and the determination of Lepr status.

"Lean MMTV-TGF-alpha/Lepr()Lepr() (homozygous) and MMTV-TGF-alpha/Lepr()Lepr(db) (heterozygous) mice and obese MMTV-TGF-alpha/Lepr(db) were monitored until age 104 weeks," Cleary and coworkers wrote.

The MMTV-TGF-alpha/Lepr(db)Lepr(db) mice had significantly heavier body weights than lean mice.

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