Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Pregnancy and stem cell behavior.

Kay-Uwe Wagner1, Gilbert H Smith

  • 1Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Nebraska Medical Center, Omaha, Nebraska 68198, USA. kuwagner@unmc.edu

Journal of Mammary Gland Biology and Neoplasia
|May 12, 2005
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Intestinal epithelial cell-specific deletion of Jak2 disrupts gut homeostasis.

Scientific reports·2026
Same author

STAT-independent functions of Janus kinases 1 and 2 are obligatory for the postnatal development of mammary epithelial ducts.

Cell reports·2025
Same author

Platelet Jak2 deficiency accelerates atherosclerosis with increased inflammatory response.

The Journal of biological chemistry·2025
Same author

Cardiomyocyte Janus kinase 1 (JAK1) signaling is required for cardiac homeostasis and cytokine-dependent activation of STAT3.

Journal of molecular and cellular cardiology·2025
Same author

Overexpression of TSG101 causes the development of adenosquamous mammary carcinoma.

Breast cancer research : BCR·2025
Same author

Neuronal Deletion of <i>Tumor Susceptibility Gene 101</i> (<i>Tsg101</i>) Causes Rapid Apoptotic Loss of Hippocampal CA3 Neurons.

Biomolecules·2025

Pregnancy induces specific mammary epithelial cells (PI-MECs) that persist lifelong and possess stem cell-like properties. These cells are implicated as targets in pregnancy-enhanced breast tumorigenesis.

Area of Science:

  • Mammary gland biology
  • Cancer stem cell research
  • Reproductive endocrinology

Background:

  • Reproductive history significantly influences breast tumorigenesis.
  • Pregnancy and lactation may permanently alter mammary progenitor cell susceptibility.
  • Understanding these effects is crucial for breast cancer prevention and treatment.

Purpose of the Study:

  • To identify and characterize mammary epithelial subtypes affected by pregnancy.
  • To investigate the long-term fate and stem cell-like properties of these pregnancy-induced cells.
  • To determine the role of these cells in pregnancy-associated mammary tumorigenesis.

Main Methods:

  • Utilized Cre-lox technology for genetic labeling of pregnancy-hormone-responsive cells.
  • Analyzed mammary epithelial cell populations in parous vs. nulliparous female animal models.

Related Experiment Videos

  • Assessed stem cell-like features (self-renewal, differentiation potential) and apoptosis during postlactational remodeling.
  • Investigated PI-MECs as cellular targets in pregnancy-enhanced mammary tumorigenesis models.
  • Main Results:

    • Identified a novel mammary epithelial subtype, pregnancy-induced mammary epithelial cells (PI-MECs), abundant in parous females.
    • PI-MECs originate from differentiating cells during the first pregnancy/lactation cycle and persist throughout life.
    • These cells exhibit stem cell-like characteristics, including self-renewal and multipotency.
    • Demonstrated that PI-MECs are cellular targets for pregnancy-enhanced mammary tumorigenesis.

    Conclusions:

    • Pregnancy establishes a long-lived mammary epithelial cell population (PI-MECs) with stem cell properties.
    • PI-MECs are critical players in the increased susceptibility to mammary tumors observed after pregnancy.
    • These findings offer new insights into breast cancer development influenced by reproductive factors.