Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients

Autores
Sales, Maria Elena
Año de publicación
2012
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
In developed countries, cancer has replaced infectious diseases as a major cause of death. Currently, efforts in the immunoprevention of cancer are beginning to resemble those presented by the prevention of infectious diseases by immunization a century ago. Breast cancer is the most frequent type of tumor in women and is the second leading cause of death by this illness, among them. Moreover, cancer incidence will grow during next years. Some findings in autoimmunity related to breast cancer in animal models have been important to clarify mechanisms that potentiate tumor growth. Clinical and experimental data now clearly indicate that chronic inflammation significantly contributes to cancer development. Emerging out of these studies is an appreciation that persistent humoral immune responses exacerbate recruitment and activation of innate immune cells in the neoplastic microenvironment where they regulate tissue remodeling, pro-angiogenic and pro-survival pathways that together potentiate cancer development. Generally, antigens involved in autoimmune response in breast cancer are modified self-proteins or over-expressed normal proteins that induce autoantibodies (autoAbs) formation, which exhibit tumor promoting actions. Very frequently muscarinic acetylcholine receptors (mAChR) are up-regulated in different types of tumors appearing in different animal species. mAChR have the ability to act as autoantigens for tumor bearers. This article will review recent results concerning to the ability of mAChR expressed in transformed breast cells to trigger autoAbs formation either in experimental models or in breast cancer patients. We will also discuss the action of these antibodies as agonists of mAChR.
Fil: Sales, Maria Elena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Materia
Autoantibodies
Muscarinic Receptors
Breast Cancer
Tumor Growth
Mcf-7 T1n0mx Breast Tumors
Autoantigens
Cells Proliferation
Inositol Monophosphate
Nitric Oxide Synthase
Phospholipase Cβ2
Protein Kinase C
Tumor Progression
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:11336/17236

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network_name_str CONICET Digital (CONICET)
spelling Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patientsSales, Maria ElenaAutoantibodiesMuscarinic ReceptorsBreast CancerTumor GrowthMcf-7 T1n0mx Breast TumorsAutoantigensCells ProliferationInositol MonophosphateNitric Oxide SynthasePhospholipase Cβ2Protein Kinase CTumor Progressionhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3In developed countries, cancer has replaced infectious diseases as a major cause of death. Currently, efforts in the immunoprevention of cancer are beginning to resemble those presented by the prevention of infectious diseases by immunization a century ago. Breast cancer is the most frequent type of tumor in women and is the second leading cause of death by this illness, among them. Moreover, cancer incidence will grow during next years. Some findings in autoimmunity related to breast cancer in animal models have been important to clarify mechanisms that potentiate tumor growth. Clinical and experimental data now clearly indicate that chronic inflammation significantly contributes to cancer development. Emerging out of these studies is an appreciation that persistent humoral immune responses exacerbate recruitment and activation of innate immune cells in the neoplastic microenvironment where they regulate tissue remodeling, pro-angiogenic and pro-survival pathways that together potentiate cancer development. Generally, antigens involved in autoimmune response in breast cancer are modified self-proteins or over-expressed normal proteins that induce autoantibodies (autoAbs) formation, which exhibit tumor promoting actions. Very frequently muscarinic acetylcholine receptors (mAChR) are up-regulated in different types of tumors appearing in different animal species. mAChR have the ability to act as autoantigens for tumor bearers. This article will review recent results concerning to the ability of mAChR expressed in transformed breast cells to trigger autoAbs formation either in experimental models or in breast cancer patients. We will also discuss the action of these antibodies as agonists of mAChR.Fil: Sales, Maria Elena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaBentham Science Publishers2012-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/mswordapplication/pdfhttp://hdl.handle.net/11336/17236Sales, Maria Elena; Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients; Bentham Science Publishers; Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry; 12; 3; 4-2012; 208-2151871-5222enginfo:eu-repo/semantics/altIdentifier/url/http://www.ingentaconnect.com/content/ben/iemamc/2012/00000012/00000003/art00004?crawler=trueinfo:eu-repo/semantics/altIdentifier/doi/10.2174/187152212802001839info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:56:48Zoai:ri.conicet.gov.ar:11336/17236instacron: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 09:56:49.189CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients
title Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients
spellingShingle Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients
Sales, Maria Elena
Autoantibodies
Muscarinic Receptors
Breast Cancer
Tumor Growth
Mcf-7 T1n0mx Breast Tumors
Autoantigens
Cells Proliferation
Inositol Monophosphate
Nitric Oxide Synthase
Phospholipase Cβ2
Protein Kinase C
Tumor Progression
title_short Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients
title_full Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients
title_fullStr Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients
title_full_unstemmed Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients
title_sort Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients
dc.creator.none.fl_str_mv Sales, Maria Elena
author Sales, Maria Elena
author_facet Sales, Maria Elena
author_role author
dc.subject.none.fl_str_mv Autoantibodies
Muscarinic Receptors
Breast Cancer
Tumor Growth
Mcf-7 T1n0mx Breast Tumors
Autoantigens
Cells Proliferation
Inositol Monophosphate
Nitric Oxide Synthase
Phospholipase Cβ2
Protein Kinase C
Tumor Progression
topic Autoantibodies
Muscarinic Receptors
Breast Cancer
Tumor Growth
Mcf-7 T1n0mx Breast Tumors
Autoantigens
Cells Proliferation
Inositol Monophosphate
Nitric Oxide Synthase
Phospholipase Cβ2
Protein Kinase C
Tumor Progression
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv In developed countries, cancer has replaced infectious diseases as a major cause of death. Currently, efforts in the immunoprevention of cancer are beginning to resemble those presented by the prevention of infectious diseases by immunization a century ago. Breast cancer is the most frequent type of tumor in women and is the second leading cause of death by this illness, among them. Moreover, cancer incidence will grow during next years. Some findings in autoimmunity related to breast cancer in animal models have been important to clarify mechanisms that potentiate tumor growth. Clinical and experimental data now clearly indicate that chronic inflammation significantly contributes to cancer development. Emerging out of these studies is an appreciation that persistent humoral immune responses exacerbate recruitment and activation of innate immune cells in the neoplastic microenvironment where they regulate tissue remodeling, pro-angiogenic and pro-survival pathways that together potentiate cancer development. Generally, antigens involved in autoimmune response in breast cancer are modified self-proteins or over-expressed normal proteins that induce autoantibodies (autoAbs) formation, which exhibit tumor promoting actions. Very frequently muscarinic acetylcholine receptors (mAChR) are up-regulated in different types of tumors appearing in different animal species. mAChR have the ability to act as autoantigens for tumor bearers. This article will review recent results concerning to the ability of mAChR expressed in transformed breast cells to trigger autoAbs formation either in experimental models or in breast cancer patients. We will also discuss the action of these antibodies as agonists of mAChR.
Fil: Sales, Maria Elena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
description In developed countries, cancer has replaced infectious diseases as a major cause of death. Currently, efforts in the immunoprevention of cancer are beginning to resemble those presented by the prevention of infectious diseases by immunization a century ago. Breast cancer is the most frequent type of tumor in women and is the second leading cause of death by this illness, among them. Moreover, cancer incidence will grow during next years. Some findings in autoimmunity related to breast cancer in animal models have been important to clarify mechanisms that potentiate tumor growth. Clinical and experimental data now clearly indicate that chronic inflammation significantly contributes to cancer development. Emerging out of these studies is an appreciation that persistent humoral immune responses exacerbate recruitment and activation of innate immune cells in the neoplastic microenvironment where they regulate tissue remodeling, pro-angiogenic and pro-survival pathways that together potentiate cancer development. Generally, antigens involved in autoimmune response in breast cancer are modified self-proteins or over-expressed normal proteins that induce autoantibodies (autoAbs) formation, which exhibit tumor promoting actions. Very frequently muscarinic acetylcholine receptors (mAChR) are up-regulated in different types of tumors appearing in different animal species. mAChR have the ability to act as autoantigens for tumor bearers. This article will review recent results concerning to the ability of mAChR expressed in transformed breast cells to trigger autoAbs formation either in experimental models or in breast cancer patients. We will also discuss the action of these antibodies as agonists of mAChR.
publishDate 2012
dc.date.none.fl_str_mv 2012-04
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/11336/17236
Sales, Maria Elena; Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients; Bentham Science Publishers; Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry; 12; 3; 4-2012; 208-215
1871-5222
url http://hdl.handle.net/11336/17236
identifier_str_mv Sales, Maria Elena; Tumor growth is stimulated by muscarinic receptors agonism: role of autoantibodies in breast cancer patients; Bentham Science Publishers; Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry; 12; 3; 4-2012; 208-215
1871-5222
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.ingentaconnect.com/content/ben/iemamc/2012/00000012/00000003/art00004?crawler=true
info:eu-repo/semantics/altIdentifier/doi/10.2174/187152212802001839
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/msword
application/pdf
dc.publisher.none.fl_str_mv Bentham Science Publishers
publisher.none.fl_str_mv Bentham Science Publishers
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
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