Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes

Autores
Mavingire, Nicole; Campbell, Petreena; Wooten, Jonathan; Aja, Joyce; Davis, Melissa B; Loaiza Perez, Andrea Irene; Brantley, Eileen
Año de publicación
2021
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Breast cancer stem cells (BCSCs) promote endocrine therapy (ET) resistance, also known as endocrine resistance in hormone receptor (HR) positive breast cancer. Endocrine resistance occurs via mechanisms that are not yet fully understood. In vitro, in vivo and clinical data suggest that signaling cascades such as Notch, hypoxia inducible factor (HIF), and integrin/Akt promote BCSC-mediated endocrine resistance. Once HR positive breast cancer patients relapse on ET, targeted therapy agents such as cyclin dependent kinase inhibitors are frequently implemented, though secondary resistance remains a threat. Here, we discuss Notch, HIF, and integrin/Akt pathway regulation of BCSC activity and potential strategies to target these pathways to counteract endocrine resistance. We also discuss a plausible link between elevated BCSC-regulatory gene levels and reduced survival observed among African American women with basal-like breast cancer which lacks HR expression. Should future studies reveal a similar link for patients with luminal breast cancer, then the use of agents that impede BCSC activity could prove highly effective in improving clinical outcomes among African American breast cancer patients.
Fil: Mavingire, Nicole. Loma Linda University Health School of Medicine; Estados Unidos
Fil: Campbell, Petreena. Loma Linda University Health School of Medicine; Estados Unidos
Fil: Wooten, Jonathan. Loma Linda University Health School of Medicine; Estados Unidos
Fil: Aja, Joyce. University of the Philippines Diliman; Filipinas
Fil: Davis, Melissa B. New York Presbyterian Hospital; Estados Unidos
Fil: Loaiza Perez, Andrea Irene. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina
Fil: Brantley, Eileen. Loma Linda University Health School of Medicine; Estados Unidos
Materia
BREAST CANCER
DISPARITIES
ENDOCRINE RESISTANCE
ENDOCRINE THERAPY
STEM CELLS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/150047
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomesMavingire, NicoleCampbell, PetreenaWooten, JonathanAja, JoyceDavis, Melissa BLoaiza Perez, Andrea IreneBrantley, EileenBREAST CANCERDISPARITIESENDOCRINE RESISTANCEENDOCRINE THERAPYSTEM CELLShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Breast cancer stem cells (BCSCs) promote endocrine therapy (ET) resistance, also known as endocrine resistance in hormone receptor (HR) positive breast cancer. Endocrine resistance occurs via mechanisms that are not yet fully understood. In vitro, in vivo and clinical data suggest that signaling cascades such as Notch, hypoxia inducible factor (HIF), and integrin/Akt promote BCSC-mediated endocrine resistance. Once HR positive breast cancer patients relapse on ET, targeted therapy agents such as cyclin dependent kinase inhibitors are frequently implemented, though secondary resistance remains a threat. Here, we discuss Notch, HIF, and integrin/Akt pathway regulation of BCSC activity and potential strategies to target these pathways to counteract endocrine resistance. We also discuss a plausible link between elevated BCSC-regulatory gene levels and reduced survival observed among African American women with basal-like breast cancer which lacks HR expression. Should future studies reveal a similar link for patients with luminal breast cancer, then the use of agents that impede BCSC activity could prove highly effective in improving clinical outcomes among African American breast cancer patients.Fil: Mavingire, Nicole. Loma Linda University Health School of Medicine; Estados UnidosFil: Campbell, Petreena. Loma Linda University Health School of Medicine; Estados UnidosFil: Wooten, Jonathan. Loma Linda University Health School of Medicine; Estados UnidosFil: Aja, Joyce. University of the Philippines Diliman; FilipinasFil: Davis, Melissa B. New York Presbyterian Hospital; Estados UnidosFil: Loaiza Perez, Andrea Irene. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; ArgentinaFil: Brantley, Eileen. Loma Linda University Health School of Medicine; Estados UnidosElsevier Ireland2021-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/150047Mavingire, Nicole; Campbell, Petreena; Wooten, Jonathan; Aja, Joyce; Davis, Melissa B; et al.; Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes; Elsevier Ireland; Cancer Letters; 500; 3-2021; 64-740304-3835CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.canlet.2020.12.014info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0304383520306649info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:03:12Zoai:ri.conicet.gov.ar:11336/150047instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:03:13.221CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes
title Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes
spellingShingle Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes
Mavingire, Nicole
BREAST CANCER
DISPARITIES
ENDOCRINE RESISTANCE
ENDOCRINE THERAPY
STEM CELLS
title_short Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes
title_full Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes
title_fullStr Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes
title_full_unstemmed Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes
title_sort Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes
dc.creator.none.fl_str_mv Mavingire, Nicole
Campbell, Petreena
Wooten, Jonathan
Aja, Joyce
Davis, Melissa B
Loaiza Perez, Andrea Irene
Brantley, Eileen
author Mavingire, Nicole
author_facet Mavingire, Nicole
Campbell, Petreena
Wooten, Jonathan
Aja, Joyce
Davis, Melissa B
Loaiza Perez, Andrea Irene
Brantley, Eileen
author_role author
author2 Campbell, Petreena
Wooten, Jonathan
Aja, Joyce
Davis, Melissa B
Loaiza Perez, Andrea Irene
Brantley, Eileen
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv BREAST CANCER
DISPARITIES
ENDOCRINE RESISTANCE
ENDOCRINE THERAPY
STEM CELLS
topic BREAST CANCER
DISPARITIES
ENDOCRINE RESISTANCE
ENDOCRINE THERAPY
STEM CELLS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Breast cancer stem cells (BCSCs) promote endocrine therapy (ET) resistance, also known as endocrine resistance in hormone receptor (HR) positive breast cancer. Endocrine resistance occurs via mechanisms that are not yet fully understood. In vitro, in vivo and clinical data suggest that signaling cascades such as Notch, hypoxia inducible factor (HIF), and integrin/Akt promote BCSC-mediated endocrine resistance. Once HR positive breast cancer patients relapse on ET, targeted therapy agents such as cyclin dependent kinase inhibitors are frequently implemented, though secondary resistance remains a threat. Here, we discuss Notch, HIF, and integrin/Akt pathway regulation of BCSC activity and potential strategies to target these pathways to counteract endocrine resistance. We also discuss a plausible link between elevated BCSC-regulatory gene levels and reduced survival observed among African American women with basal-like breast cancer which lacks HR expression. Should future studies reveal a similar link for patients with luminal breast cancer, then the use of agents that impede BCSC activity could prove highly effective in improving clinical outcomes among African American breast cancer patients.
Fil: Mavingire, Nicole. Loma Linda University Health School of Medicine; Estados Unidos
Fil: Campbell, Petreena. Loma Linda University Health School of Medicine; Estados Unidos
Fil: Wooten, Jonathan. Loma Linda University Health School of Medicine; Estados Unidos
Fil: Aja, Joyce. University of the Philippines Diliman; Filipinas
Fil: Davis, Melissa B. New York Presbyterian Hospital; Estados Unidos
Fil: Loaiza Perez, Andrea Irene. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina
Fil: Brantley, Eileen. Loma Linda University Health School of Medicine; Estados Unidos
description Breast cancer stem cells (BCSCs) promote endocrine therapy (ET) resistance, also known as endocrine resistance in hormone receptor (HR) positive breast cancer. Endocrine resistance occurs via mechanisms that are not yet fully understood. In vitro, in vivo and clinical data suggest that signaling cascades such as Notch, hypoxia inducible factor (HIF), and integrin/Akt promote BCSC-mediated endocrine resistance. Once HR positive breast cancer patients relapse on ET, targeted therapy agents such as cyclin dependent kinase inhibitors are frequently implemented, though secondary resistance remains a threat. Here, we discuss Notch, HIF, and integrin/Akt pathway regulation of BCSC activity and potential strategies to target these pathways to counteract endocrine resistance. We also discuss a plausible link between elevated BCSC-regulatory gene levels and reduced survival observed among African American women with basal-like breast cancer which lacks HR expression. Should future studies reveal a similar link for patients with luminal breast cancer, then the use of agents that impede BCSC activity could prove highly effective in improving clinical outcomes among African American breast cancer patients.
publishDate 2021
dc.date.none.fl_str_mv 2021-03
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/150047
Mavingire, Nicole; Campbell, Petreena; Wooten, Jonathan; Aja, Joyce; Davis, Melissa B; et al.; Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes; Elsevier Ireland; Cancer Letters; 500; 3-2021; 64-74
0304-3835
CONICET Digital
CONICET
url http://hdl.handle.net/11336/150047
identifier_str_mv Mavingire, Nicole; Campbell, Petreena; Wooten, Jonathan; Aja, Joyce; Davis, Melissa B; et al.; Cancer stem cells: Culprits in endocrine resistance and racial disparities in breast cancer outcomes; Elsevier Ireland; Cancer Letters; 500; 3-2021; 64-74
0304-3835
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.canlet.2020.12.014
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0304383520306649
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Ireland
publisher.none.fl_str_mv Elsevier Ireland
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1842269788969107456
score 13.13397

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