ArticleThe American journal of pathology2006
Prolactin potentiates transforming growth factor alpha induction of mammary neoplasia in transgenic mice.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- ERBB Receptors and Their Ligands in the Developing Mammary Glands of Different Species: Fifteen Characters in Search of an Author.Journal of mammary gland biology and neoplasia · 2023Review
- Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022Review
- Article
- Cyclophilin A Function in Mammary Epithelium Impacts Jak2/Stat5 Signaling, Morphogenesis, Differentiation, and Tumorigenesis in the Mammary Gland.Cancer research · 2018Article
- Epiregulin contributes to breast tumorigenesis through regulating matrix metalloproteinase 1 and promoting cell survival.Molecular cancer · 2015Article
- Modeling prolactin actions in breast cancer in vivo: insights from the NRL-PRL mouse.Advances in experimental medicine and biology · 2015Article
- Prolactin activates ERα in the absence of ligand in female mammary development and carcinogenesis in vivo.Endocrinology · 2013Article
- Stiff collagen matrices increase tumorigenic prolactin signaling in breast cancer cells.The Journal of biological chemistry · 2013Article
- Autocrine prolactin: an emerging market for homegrown (prolactin) despite the imports.Genes & development · 2012Article
- Prolactin promotes mammary pathogenesis independently from cyclin D1.The American journal of pathology · 2012Article
- Prolactin-induced mouse mammary carcinomas model estrogen resistant luminal breast cancer.Breast cancer research : BCR · 2011Article
- Mouse models of estrogen receptor-positive breast cancer.Journal of carcinogenesis · 2011Article
- Janus kinase 2 is required for the initiation but not maintenance of prolactin-induced mammary cancer.Oncogene · 2010Article
- Prolactin enhances insulin-like growth factor I receptor phosphorylation by decreasing its association with the tyrosine phosphatase SHP-2 in MCF-7 breast cancer cells.The Journal of biological chemistry · 2010Article
- Ovarian hormones are not required for PRL-induced mammary tumorigenesis, but estrogen enhances neoplastic processes.The Journal of endocrinology · 2009Article
- Complex prolactin crosstalk in breast cancer: new therapeutic implications.Molecular and cellular endocrinology · 2009Article
- Prolactin-growth factor crosstalk reduces mammary estrogen responsiveness despite elevated ERalpha expression.The American journal of pathology · 2009Article
- SRC family kinases accelerate prolactin receptor internalization, modulating trafficking and signaling in breast cancer cells.Molecular endocrinology (Baltimore, Md.) · 2009Article
- From bench to bedside: future potential for the translation of prolactin inhibitors as breast cancer therapeutics.Journal of mammary gland biology and neoplasia · 2008Review
- Transgenic models to study actions of prolactin in mammary neoplasia.Journal of mammary gland biology and neoplasia · 2008Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 3 countries.
Funding
Abstract
Prolactin influences mammary development and carcinogenesis through endocrine and autocrine/paracrine mechanisms. In virgin female mice, pro-lactin overexpression under control of a mammary selective nonhormonally responsive promoter, neu-related lipocalin, results in estrogen receptor alpha (ERalpha)-positive and ERalpha-negative adenocarcinomas. However, disease in vivo occurs in the context of dysregulation of multiple pathways. In this study, we investigated the ability of prolactin to modulate carcinogenesis when co-expressed with the potent oncogene transforming growth factor alpha (TGFalpha) in bitransgenic mice. Prolactin and TGFalpha cooperated to reduce dramatically the latency of mammary macrocyst development, the principal lesion type induced by TGFalpha. In combination, prolactin and TGFalpha also increased the incidence and reduced the latency of other preneoplastic lesions and increased cellular turnover in structurally normal alveoli and ducts compared with single transgenic females. Bitransgenic glands contained higher levels of phosphorylated ERK1/2 compared with single TGFalpha transgenic glands, suggesting that this kinase may be a point of signaling crosstalk. Furthermore, transgenic prolactin also reversed the decrease in ERalpha induced by neu-related lipocalin-TGFalpha. Our findings demonstrate that locally produced prolactin can strikingly potentiate the carcinogenic actions of another oncogene and modify ovarian hormone responsiveness, suggesting that prolactin signaling may be a potential therapeutic target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.