Parity reduces mammary repopulating activity but does not affect mammary stem cells defined as CD24 + CD29/CD49fhi in mice.


Journal

Breast cancer research and treatment
ISSN: 1573-7217
Titre abrégé: Breast Cancer Res Treat
Pays: Netherlands
ID NLM: 8111104

Informations de publication

Date de publication:
Oct 2020
Historique:
received: 23 05 2020
accepted: 11 07 2020
pubmed: 23 7 2020
medline: 24 6 2021
entrez: 23 7 2020
Statut: ppublish

Résumé

Breast cancer (BCa) mortality is decreasing with early detection and improvement in therapies. The incidence of BCa, however, continues to increase, particularly estrogen-receptor-positive (ER +) subtypes. One of the greatest modifiers of ER + BCa risk is childbearing (parity), with BCa risk halved in young multiparous mothers. Despite convincing epidemiological data, the biology that underpins this protection remains unclear. Parity-induced protection has been postulated to be due to a decrease in mammary stem cells (MaSCs); however, reports to date have provided conflicting data. We have completed rigorous functional testing of repopulating activity in parous mice using unfractionated and MaSC (CD24 Here, we report that while repopulating activity in the mammary gland is reduced by parity in the unfractionated gland, it is not due to a loss in the classically defined MaSC (CD24 Our data show instead that parity impacts on the stem-like activity of cells outside the MaSC population.

Sections du résumé

BACKGROUND BACKGROUND
Breast cancer (BCa) mortality is decreasing with early detection and improvement in therapies. The incidence of BCa, however, continues to increase, particularly estrogen-receptor-positive (ER +) subtypes. One of the greatest modifiers of ER + BCa risk is childbearing (parity), with BCa risk halved in young multiparous mothers. Despite convincing epidemiological data, the biology that underpins this protection remains unclear. Parity-induced protection has been postulated to be due to a decrease in mammary stem cells (MaSCs); however, reports to date have provided conflicting data.
METHODS METHODS
We have completed rigorous functional testing of repopulating activity in parous mice using unfractionated and MaSC (CD24
RESULTS RESULTS
Here, we report that while repopulating activity in the mammary gland is reduced by parity in the unfractionated gland, it is not due to a loss in the classically defined MaSC (CD24
CONCLUSIONS CONCLUSIONS
Our data show instead that parity impacts on the stem-like activity of cells outside the MaSC population.

Identifiants

pubmed: 32696317
doi: 10.1007/s10549-020-05804-1
pii: 10.1007/s10549-020-05804-1
doi:

Substances chimiques

Integrin beta1 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

565-575

Auteurs

Genevieve V Dall (GV)

Department of Anatomy and Developmental Biology, Monash University, Melbourne, VIC, Australia.
Breast Cancer Risk and Prevention Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC, Australia.

Jessica Vieusseux (J)

Breast Cancer Risk and Prevention Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC, Australia.

Yashar Seyed-Razavi (Y)

Department of Anatomy and Developmental Biology, Monash University, Melbourne, VIC, Australia.

Nathan Godde (N)

Pathology and Pathogenesis Group, CSIRO Australian Animal Health Laboratory, Geelong, VIC, Australia.
The Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC, Australia.

Mandy Ludford-Menting (M)

Immune Signaling Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC, Australia.
Centre for Micro-Photonics, Swinburne University, Hawthorn, VIC, Australia.

Sarah M Russell (SM)

Immune Signaling Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC, Australia.
Centre for Micro-Photonics, Swinburne University, Hawthorn, VIC, Australia.
The Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC, Australia.

Alan Ashworth (A)

Helen Diller Comprehensive Cancer Center, University of California, San Francisco, CA, USA.

Robin L Anderson (RL)

The Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC, Australia.
Metastasis Research Laboratory, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC, 3084, Australia.
School of Cancer Medicine, La Trobe University, Bundoora, VIC, Australia.

Gail P Risbridger (GP)

Department of Anatomy and Developmental Biology, Monash University, Melbourne, VIC, Australia.
The Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC, Australia.

Mark Shackleton (M)

The Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC, Australia.
Cancer Development and Treatment, Alfred Hospital, Monash University, Melbourne, VIC, Australia.

Kara L Britt (KL)

Breast Cancer Risk and Prevention Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC, Australia. kara.britt@petermac.org.
The Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC, Australia. kara.britt@petermac.org.

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Classifications MeSH