期刊
ENDOCRINE REVIEWS
卷 24, 期 1, 页码 1-27出版社
ENDOCRINE SOC
DOI: 10.1210/er.2001-0036
关键词
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资金
- NCI NIH HHS [R01 CA069294, CA-49449, P01 CA087969, R01 CA067262, CA-8312, U01 CA067262, CA-87969, CA-67262, R01 CA049449, R01 CA078312, U01 CA049449, R01 CA-69294] Funding Source: Medline
- NICHD NIH HHS [T32 HD007259, T32 HD-07259] Funding Source: Medline
- NIDDK NIH HHS [DK-92265] Funding Source: Medline
The contribution of prolactin (PRL) to the pathogenesis and progression of human breast cancer at the cellular, transgenic, and epidemiological levels is increasingly appreciated. Acting at the endocrine and autocrine/paracrine levels, PRL functions to stimulate the growth and motility of human breast cancer cells. The actions of this ligand are mediated by at least six recognized PRL receptor isoforms found on, or secreted by, human breast epithelium. The PRL/PRL receptor complex associates with and activates several signaling net-works that are shared with other members of the cytokine receptor superfamily. Coupled with the recently identified intranuclear function of PRL, these networks are integrated into the in vitro and in vivo actions induced by ligand. These findings indicate that antagonists of PRL/PRL receptor interaction or PRL receptor-associated signal transduction may be of considerable utility in the treatment of human breast cancer.
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