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Related Experiment Video

Updated: Jun 13, 2026

X-Ray Visualization of Intraductal Ethanol-Based Ablative Treatment for Prevention of Breast Cancer in Rat Models
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Published on: December 9, 2022

Prolactin and human tumourogenesis.

I Fernandez1, P Touraine, V Goffin

  • 1Inserm, Unit 845, Research Center Growth and Signalling, University Paris Descartes, Faculty of Medicine, Necker site, Paris, France.

Journal of Neuroendocrinology
|May 12, 2010
PubMed
Summary

Prolactin

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • The role of prolactin in human tumourogenesis remains debated.
  • Previous studies in the 1980s yielded inconclusive results in human species.
  • Rodent models provided early evidence for prolactin's role in breast cancer.

Purpose of the Study:

  • To discuss recent advancements in understanding prolactin's nonclassical mechanisms in tumor growth.
  • To explore the potential of targeting prolactin signaling in future cancer therapies.
  • To review novel actions of prolactin in breast cancer cells.

Main Methods:

  • Review of recent scientific literature on prolactin and tumourogenesis.
  • Analysis of data from genetically-modified mouse models.

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Last Updated: Jun 13, 2026

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  • Examination of genetic variants of the prolactin receptor.
  • Main Results:

    • Two novel mechanisms of prolactin action in tumor growth have emerged: autocrine/paracrine prolactin production and constitutively active prolactin receptor variants.
    • Genetically-modified models show prolactin's tumorigenic potential in prostate and mammary glands.
    • A prolactin receptor variant with constitutive activity identified in breast tumor patients suggests sustained signaling in tumourogenesis.

    Conclusions:

    • Local prolactin production and prolactin receptor variants represent key nonclassical mechanisms in tumourogenesis.
    • These findings open new avenues for inhibiting prolactin signaling in cancer therapy.
    • Further research is needed to develop targeted therapies against prolactin receptor signaling.