Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/23858
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dc.contributor.authorDall, Genevieve V-
dc.contributor.authorVieusseux, Jessica-
dc.contributor.authorSeyed-Razavi, Yashar-
dc.contributor.authorGodde, Nathan-
dc.contributor.authorLudford-Menting, Mandy-
dc.contributor.authorRussell, Sarah M-
dc.contributor.authorAshworth, Alan-
dc.contributor.authorAnderson, Robin L-
dc.contributor.authorRisbridger, Gail P-
dc.contributor.authorShackleton, Mark-
dc.contributor.authorBritt, Kara L-
dc.date2020-07-21-
dc.date.accessioned2020-07-27T05:09:33Z-
dc.date.available2020-07-27T05:09:33Z-
dc.date.issued2020-10-
dc.identifier.citationBreast cancer research and treatment 2020; 183(3): 565-575-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/23858-
dc.description.abstractBreast 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 (CD24midCD49fhi)-enriched populations. We also developed a novel serial transplant method to enable us to assess self-renewal of MaSC following pregnancy. Lastly, as each pregnancy confers additional BCa protection, we subjected mice to multiple rounds of pregnancy to assess whether additional pregnancies impact MaSC activity. 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+CD49fhi) numbers or function. Self-renewal was unaffected by parity and additional rounds of pregnancy also did not lead to a decrease in MaSC activity. Our data show instead that parity impacts on the stem-like activity of cells outside the MaSC population.-
dc.language.isoeng-
dc.subjectBreast cancer-
dc.subjectMammary fat pad transplants-
dc.subjectParity-
dc.subjectStem cells-
dc.titleParity reduces mammary repopulating activity but does not affect mammary stem cells defined as CD24 + CD29/CD49fhi in mice.-
dc.typeJournal Article-
dc.identifier.journaltitleBreast cancer research and treatment-
dc.identifier.affiliationHelen Diller Comprehensive Cancer Center, University of California, San Francisco, CA, USAen
dc.identifier.affiliationImmune Signaling Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC, Australiaen
dc.identifier.affiliationThe Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC, Australiaen
dc.identifier.affiliationPathology and Pathogenesis Group, CSIRO Australian Animal Health Laboratory, Geelong, VIC, Australiaen
dc.identifier.affiliationBreast Cancer Risk and Prevention Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC, Australiaen
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Bundoora, VIC, Australiaen
dc.identifier.affiliationDepartment of Anatomy and Developmental Biology, Monash University, Melbourne, VIC, Australiaen
dc.identifier.affiliationCancer Development and Treatment, Alfred Hospital, Monash University, Melbourne, VIC, Australiaen
dc.identifier.affiliationMetastasis Research Laboratory, Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationCentre for Micro-Photonics, Swinburne University, Hawthorn, VIC, Australiaen
dc.identifier.doi10.1007/s10549-020-05804-1-
dc.identifier.orcid0000-0001-6069-7856-
dc.identifier.orcid0000-0002-6841-7422-
dc.identifier.pubmedid32696317-
dc.type.austinJournal Article-
local.name.researcherAnderson, Robin L
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairetypeJournal Article-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
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