NDLI: Leptin — From regulation of fat metabolism to stimulation of breast cancer growth

Content Provider	Springer Nature Link
Author	Sulkowska, Mariola Golaszewska, Jolanta Wincewicz, Andrzej Koda, Mariusz Baltaziak, Marek Sulkowski, Stanislaw
Copyright Year	2006
Abstract	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 leptininduced second messengers like STAT3 (signal transducers and activators of transcription 3), AP-1 (transcription activator protein 1), MAPK (mitogenactivated protein kinase) and ERKs (extracellular signalregulated kinases). They seem to be involved in aromatase expression, generation of estrogens and activation of estrogen receptor α (ERα) 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, No 2, 69–72)
Starting Page	69
Ending Page	72
Page Count	4
File Format	PDF
ISSN	12194956
Journal	Pathology & Oncology Research
Volume Number	12
Issue Number	2
e-ISSN	15322807
Language	English
Publisher	Springer Netherlands
Publisher Date	2006-01-01
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	leptin leptin receptor signal transducer and activator of transcription 3 estrogen receptor α antiestrogen resistance Cancer Research Oncology Pathology Immunology Biomedicine general
Content Type	Text
Resource Type	Article
Subject	Cancer Research Pathology and Forensic Medicine Oncology

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