PATHOLOGY & ONCOLOGY RESEARCHVol. 12 No. 2, 2006

 Review

Leptin - From Regulation of fat Metabolism to Stimulation of Breast Cancer Growth

Mariola SULKOWSKA, Jolanta GOLASZEWSKA, Andrzej WINCEWICZ, Mariusz KODA, Marek BALTAZIAK, Stanislaw SULKOWSKI

Department of Pathology, Collegium Pathologicum, Medical University of Bialystok, Bialystok, Poland

 

Leptin restricts intake of calories as a satiety hormone. It probably stimulates neoplastic proliferation in breast cancer, too. Growth of malignant cells could be regulated by various leptin-induced second messengers like STAT3 (signal transducers and activators of transcription 3), AP-1 (transcription activator protein 1), MAPK (mitogen-activated protein kinase) and ERKs (extracellular signal-regulated kinases). They seem to be involved in aromatase expression, generation of estrogens and activation of estrogen receptor ? (ER?) in malignant breast epithelium. Leptin may maintain resistance to antiestrogen therapy. Namely, it increased activation of estrogen receptors, therefore, it was suspected to reduce or even overcome the inhibitory effect of tamoxifen on breast cell proliferation. Although several valuable reviews have been focused on the role of leptin in breast cancer, the status of knowledge in this field changes quickly and our insight should be continuously revised. In this summary, we provide refreshed interpretation of intensively reported scientific queries of the topic. Pathology & Oncology Research, Vol 12, Nr 2, 69-72, 2006

Key words: leptin; leptin receptor; signal transducer and activator of transcription 3; estrogen receptor alpha; antiestrogen resistance


Received: Oct 18, 2005; accepted: Mar 5, 2006
Correspondence: Stanislaw SULKOWSKI, Department of Pathology, Collegium Pathologicum, Medical University of Bialystok, Waszyngtona St 13 Bialystok 15-269, Poland; Tel: +48-85-748 59 45, Fax: +48-85-748 59 44; E-mail: sulek@zeus.amb.edu.pl

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