Prolactin in Human Breast Cancer Development

Vonderhaar, Barbara K.

doi:10.1007/978-1-59259-223-4_7

Cited by 8 publications

(5 citation statements)

References 119 publications

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“…A number of epidemiological studies have demonstrated a consistent correlation between prolactin levels and well-confirmed breast cancer risk factors such as parity and age at menarche [177]. Most breast cancer cell lines express the prolactin receptor, and exogenously added prolactin has modest trophic effects on human tumor tissues and cells in vitro [179]. Prolactin has been demonstrated to stimulate proliferation in prostate and endometrial cancer cells as well [178].…”

Section: Other Stress Mediatorsmentioning

confidence: 99%

Impact of Stress on Cancer Metastasis

2010

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The influence of psychosocial factors on the development and progression of cancer has been a longstanding hypothesis since ancient times. In fact, epidemiological and clinical studies over the past 30 years have provided strong evidence for links between chronic stress, depression and social isolation and cancer progression. By contrast, there is only limited evidence for the role of these behavioral factors in cancer initiation. Recent cellular and molecular studies have identified specific signaling pathways that impact cancer growth and metastasis. This article provides an overview of the relationship between psychosocial factors, specifically chronic stress, and cancer progression. Keywordscancer; catecholamine; metastasis; signaling pathway; stress The major cause of death from cancer is metastasis that is resistant to conventional therapy [1]. Primary neoplasms are biologically heterogeneous and the process of metastasis consists of a series of sequential and selective steps that few cells can successfully complete. The outcome of cancer metastasis depends on multiple interactions between metastatic cells and homeostatic mechanisms that are unique to a given organ micro environment [2]. Therefore, the treatment of metastasis should be targeted not only against cancer cells, but also against the host factors that contribute to and support the progressive growth and survival of metastatic cancer cells. Clinical and epidemiological studies over the last 30 years have identified psychosocial factors including stress, chronic depression and lack of social support as risk factors for cancer progression [3][4][5][6]. Whereas evidence for the role of psychosocial factors in cancer initiation is limited and some-what contradictory [7][8][9][10], support is stronger for links between psychological factors such as stress, depression and social isolation and disease progression [11,12]. Chronicity of negative affect, as manifested by depressed mood or hopelessness, appears to have stronger relationships with outcomes NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript than do stressful events, suggesting that sustained activation of negative affective pathways may provide the strongest links to cancer progression [13][14][15][16]. Moderators of stress, such as social support, have been frequently studied with respect to cancer outcomes. Social support refers to an individual's perceived satisfaction with social relationships and is thought to play a major role in buffering psychological and biological stress responses [17]. Several studies have linked high levels of social support to improved clinical outcomes in cancer patients. For example, in breast cancer patients, social support has been related to longer survival in several large-scale studies [18][19][20], although negative findings were noted in some studies [21][22][23]. Collectively, emerging evidence has shown stress and specific psychosocial factors to be associated with key elements of the metastatic cascade in both animal ...

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Section: Other Stress Mediatorsmentioning

confidence: 99%

Impact of Stress on Cancer Metastasis

2010

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“…Considering the breadth of genotypes in the mammary tumor cell lines that have been examined, the evidence for a mitogenic action of PRL is remarkably consistent. Exogenously added PRL has modest trophic effects on human tumor tissue and cells in vitro (144). However, it is now clear that this relatively low activity is in part due to PRL synthesized by the mammary cells themselves.…”

Section: B Proliferationmentioning

confidence: 99%

The Role of Prolactin in Mammary Carcinoma

et al. 2003

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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 networks 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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“…PRL is critical for both mammogenesis and lactation, and accumulating evidence indicates that it may play a role in mammary carcinogenesis as well (for review see Refs. [3][4][5]. In rodent models, systemic PRL treatment or pituitary transplants increased development of spontaneous, chemically induced, and oncogene-initiated mammary tumors (6 -8), and mammary transgenic PRL induced tumors in virgin females (9,10).…”

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confidence: 99%

Inhibition of Prolactin (PRL)-Induced Proliferative Signals in Breast Cancer Cells by a Molecular Mimic of Phosphorylated PRL, S179D-PRL

et al. 2003

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Posttranslational modifications of prolactin (PRL), including phosphorylation, vary with physiologic state and alter biologic activity. In light of the growing evidence for a role for PRL in proliferation in mammary cancer, we examined the ability of a mimic of phosphorylated human PRL, S179D-PRL, to initiate signals to several pathways in mammary tumor cells alone and in combination with unmodified PRL. Unmodified PRL employed multiple pathways to increase cellular proliferation and cyclin D1 levels in PRL-deficient MCF-7 cells. S179D-PRL was a weak agonist compared with unmodified PRL with regard to cellular proliferation, cyclin D1 levels, and phosphorylation of signal transducer and activator of transcription 5 and ERKs. However, S179D-PRL was a potent antagonist of unmodified PRL to these endpoints. In contrast to the reduced levels of the long isoform of the PRL receptor observed in response to a 3-d incubation with unmodified PRL, S179D-PRL up-regulated expression of this isoform, 4-fold. These studies support the utility of this mutant as a PRL antagonist to proliferative signals in mammary epithelial cells, including a potential role in breast cancer therapeutics.

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Prolactin in Human Breast Cancer Development

Cited by 8 publications

References 119 publications

Impact of Stress on Cancer Metastasis

Impact of Stress on Cancer Metastasis

The Role of Prolactin in Mammary Carcinoma

Inhibition of Prolactin (PRL)-Induced Proliferative Signals in Breast Cancer Cells by a Molecular Mimic of Phosphorylated PRL, S179D-PRL

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