Increased high molecular weight FGF2 in endocrine-resistant breast cancer

Autores
Sahores, Ana; Figueroa, Virginia; May, Maria; Liguori, Marcos; Rubstein, Adrián; Fuentes, Cynthia Analia; Jacobsen, Britta M.; Elia, Andres Maximiliano; Rojas, Paola Andrea; Sequeira, Gonzalo Ricardo; Álvarez, Michelle M.; González, Pedro; Gass, Hugo; Hewitt, Stephen; Molinolo, Alfredo; Lanari, Claudia Lee Malvina; Lamb, Caroline Ana
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Endocrine resistance may develop as a consequence of enhanced growth factor signaling. Fibroblast growth factor 2 (FGF2) consists of a low and several high molecular weight forms (HMW-FGF2). We previously demonstrated that antiprogestin-resistant mammary carcinomas display lower levels of progesterone receptor A isoforms (PRA) than B isoforms (PRB). Our aim was to evaluate the role of FGF2 isoforms in breast cancer progression. We evaluated FGF2 expression, cell proliferation, and pathway activation in models with different PRA/PRB ratios. We performed lentiviral infections of different FGF2 isoforms using the human hormone-responsive T47D-YA cells, engineered to only express PRA, and evaluated tumor growth, metastatic dissemination, and endocrine responsiveness. We assessed FGF2 expression and localization in 81 human breast cancer samples. Antiprogestin-resistant experimental mammary carcinomas with low PRA/PRB ratios and T47D-YB cells, which only express PRB, displayed higher levels of HMW-FGF2 than responsive variants. HMW-FGF2 overexpression in T47D-YA cells induced increased tumor growth, lung metastasis, and antiprogestin resistance compared to control tumors. In human breast carcinomas categorized by their PRA/PRB ratio, we found nuclear FGF2 expression in 55.6% of tumor cells. No differences were found between nuclear FGF2 expression and Ki67 proliferation index, tumor stage, or tumor grade. In low-grade tumor samples, moderate to high nuclear FGF2 levels were associated to carcinomas with low PRA/PRB ratio. In conclusion, we show that HMW-FGF2 isoforms are PRB targets which confer endocrine resistance and are localized in the nuclei of breast cancer samples. Hence, targeting intracellular FGF2 may contribute to overcome tumor progression.
Fil: Sahores, Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentina
Fil: Figueroa, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: May, Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Liguori, Marcos. Hospital de Agudos Magdalena V. de Martínez; Argentina
Fil: Rubstein, Adrián. Merck Argentina; Argentina
Fil: Fuentes, Cynthia Analia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Jacobsen, Britta M.. University Of Colorado Anschutz Medical Campus.; Estados Unidos
Fil: Elia, Andres Maximiliano. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Rojas, Paola Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Sequeira, Gonzalo Ricardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Álvarez, Michelle M.. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: González, Pedro. Hospital de Agudos Magdalena V de Martínez; Argentina
Fil: Gass, Hugo. Hospital de Agudos Magdalena V de Martínez; Argentina
Fil: Hewitt, Stephen. National Institute Of Dental And Craniofacial Research; Estados Unidos
Fil: Molinolo, Alfredo. University of California at San Diego; Estados Unidos
Fil: Lanari, Claudia Lee Malvina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Lamb, Caroline Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Materia
ANTIPROGESTIN
BREAST CANCER
ENDOCRINE RESISTANCE
FGF2
HMW-FGF2
PROGESTERONE RECEPTOR
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:11336/85381
Acceder
id CONICETDig_b82fbd4d6056cbffdedafa82100e90e4
oai_identifier_str oai:ri.conicet.gov.ar:11336/85381
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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Increased high molecular weight FGF2 in endocrine-resistant breast cancerSahores, AnaFigueroa, VirginiaMay, MariaLiguori, MarcosRubstein, AdriánFuentes, Cynthia AnaliaJacobsen, Britta M.Elia, Andres MaximilianoRojas, Paola AndreaSequeira, Gonzalo RicardoÁlvarez, Michelle M.González, PedroGass, HugoHewitt, StephenMolinolo, AlfredoLanari, Claudia Lee MalvinaLamb, Caroline AnaANTIPROGESTINBREAST CANCERENDOCRINE RESISTANCEFGF2HMW-FGF2PROGESTERONE RECEPTORTUMOR PROGRESSIONhttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Endocrine resistance may develop as a consequence of enhanced growth factor signaling. Fibroblast growth factor 2 (FGF2) consists of a low and several high molecular weight forms (HMW-FGF2). We previously demonstrated that antiprogestin-resistant mammary carcinomas display lower levels of progesterone receptor A isoforms (PRA) than B isoforms (PRB). Our aim was to evaluate the role of FGF2 isoforms in breast cancer progression. We evaluated FGF2 expression, cell proliferation, and pathway activation in models with different PRA/PRB ratios. We performed lentiviral infections of different FGF2 isoforms using the human hormone-responsive T47D-YA cells, engineered to only express PRA, and evaluated tumor growth, metastatic dissemination, and endocrine responsiveness. We assessed FGF2 expression and localization in 81 human breast cancer samples. Antiprogestin-resistant experimental mammary carcinomas with low PRA/PRB ratios and T47D-YB cells, which only express PRB, displayed higher levels of HMW-FGF2 than responsive variants. HMW-FGF2 overexpression in T47D-YA cells induced increased tumor growth, lung metastasis, and antiprogestin resistance compared to control tumors. In human breast carcinomas categorized by their PRA/PRB ratio, we found nuclear FGF2 expression in 55.6% of tumor cells. No differences were found between nuclear FGF2 expression and Ki67 proliferation index, tumor stage, or tumor grade. In low-grade tumor samples, moderate to high nuclear FGF2 levels were associated to carcinomas with low PRA/PRB ratio. In conclusion, we show that HMW-FGF2 isoforms are PRB targets which confer endocrine resistance and are localized in the nuclei of breast cancer samples. Hence, targeting intracellular FGF2 may contribute to overcome tumor progression.Fil: Sahores, Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Figueroa, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: May, Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Liguori, Marcos. Hospital de Agudos Magdalena V. de Martínez; ArgentinaFil: Rubstein, Adrián. Merck Argentina; ArgentinaFil: Fuentes, Cynthia Analia. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Jacobsen, Britta M.. University Of Colorado Anschutz Medical Campus.; Estados UnidosFil: Elia, Andres Maximiliano. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Rojas, Paola Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Sequeira, Gonzalo Ricardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Álvarez, Michelle M.. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: González, Pedro. Hospital de Agudos Magdalena V de Martínez; ArgentinaFil: Gass, Hugo. Hospital de Agudos Magdalena V de Martínez; ArgentinaFil: Hewitt, Stephen. National Institute Of Dental And Craniofacial Research; Estados UnidosFil: Molinolo, Alfredo. University of California at San Diego; Estados UnidosFil: Lanari, Claudia Lee Malvina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Lamb, Caroline Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaSpringer US2018-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/85381Sahores, Ana; Figueroa, Virginia; May, Maria; Liguori, Marcos; Rubstein, Adrián; et al.; Increased high molecular weight FGF2 in endocrine-resistant breast cancer; Springer US; Hormones and Cancer; 9; 5; 10-2018; 338-3481868-8500CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1007/s12672-018-0339-4info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8054767/info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007/s12672-018-0339-4info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:04:26Zoai:ri.conicet.gov.ar:11336/85381instacron: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:34982025-10-15 15:04:26.414CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Increased high molecular weight FGF2 in endocrine-resistant breast cancer
title Increased high molecular weight FGF2 in endocrine-resistant breast cancer
spellingShingle Increased high molecular weight FGF2 in endocrine-resistant breast cancer
Sahores, Ana
ANTIPROGESTIN
BREAST CANCER
ENDOCRINE RESISTANCE
FGF2
HMW-FGF2
PROGESTERONE RECEPTOR
TUMOR PROGRESSION
title_short Increased high molecular weight FGF2 in endocrine-resistant breast cancer
title_full Increased high molecular weight FGF2 in endocrine-resistant breast cancer
title_fullStr Increased high molecular weight FGF2 in endocrine-resistant breast cancer
title_full_unstemmed Increased high molecular weight FGF2 in endocrine-resistant breast cancer
title_sort Increased high molecular weight FGF2 in endocrine-resistant breast cancer
dc.creator.none.fl_str_mv Sahores, Ana
Figueroa, Virginia
May, Maria
Liguori, Marcos
Rubstein, Adrián
Fuentes, Cynthia Analia
Jacobsen, Britta M.
Elia, Andres Maximiliano
Rojas, Paola Andrea
Sequeira, Gonzalo Ricardo
Álvarez, Michelle M.
González, Pedro
Gass, Hugo
Hewitt, Stephen
Molinolo, Alfredo
Lanari, Claudia Lee Malvina
Lamb, Caroline Ana
author Sahores, Ana
author_facet Sahores, Ana
Figueroa, Virginia
May, Maria
Liguori, Marcos
Rubstein, Adrián
Fuentes, Cynthia Analia
Jacobsen, Britta M.
Elia, Andres Maximiliano
Rojas, Paola Andrea
Sequeira, Gonzalo Ricardo
Álvarez, Michelle M.
González, Pedro
Gass, Hugo
Hewitt, Stephen
Molinolo, Alfredo
Lanari, Claudia Lee Malvina
Lamb, Caroline Ana
author_role author
author2 Figueroa, Virginia
May, Maria
Liguori, Marcos
Rubstein, Adrián
Fuentes, Cynthia Analia
Jacobsen, Britta M.
Elia, Andres Maximiliano
Rojas, Paola Andrea
Sequeira, Gonzalo Ricardo
Álvarez, Michelle M.
González, Pedro
Gass, Hugo
Hewitt, Stephen
Molinolo, Alfredo
Lanari, Claudia Lee Malvina
Lamb, Caroline Ana
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv ANTIPROGESTIN
BREAST CANCER
ENDOCRINE RESISTANCE
FGF2
HMW-FGF2
PROGESTERONE RECEPTOR
TUMOR PROGRESSION
topic ANTIPROGESTIN
BREAST CANCER
ENDOCRINE RESISTANCE
FGF2
HMW-FGF2
PROGESTERONE RECEPTOR
TUMOR PROGRESSION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Endocrine resistance may develop as a consequence of enhanced growth factor signaling. Fibroblast growth factor 2 (FGF2) consists of a low and several high molecular weight forms (HMW-FGF2). We previously demonstrated that antiprogestin-resistant mammary carcinomas display lower levels of progesterone receptor A isoforms (PRA) than B isoforms (PRB). Our aim was to evaluate the role of FGF2 isoforms in breast cancer progression. We evaluated FGF2 expression, cell proliferation, and pathway activation in models with different PRA/PRB ratios. We performed lentiviral infections of different FGF2 isoforms using the human hormone-responsive T47D-YA cells, engineered to only express PRA, and evaluated tumor growth, metastatic dissemination, and endocrine responsiveness. We assessed FGF2 expression and localization in 81 human breast cancer samples. Antiprogestin-resistant experimental mammary carcinomas with low PRA/PRB ratios and T47D-YB cells, which only express PRB, displayed higher levels of HMW-FGF2 than responsive variants. HMW-FGF2 overexpression in T47D-YA cells induced increased tumor growth, lung metastasis, and antiprogestin resistance compared to control tumors. In human breast carcinomas categorized by their PRA/PRB ratio, we found nuclear FGF2 expression in 55.6% of tumor cells. No differences were found between nuclear FGF2 expression and Ki67 proliferation index, tumor stage, or tumor grade. In low-grade tumor samples, moderate to high nuclear FGF2 levels were associated to carcinomas with low PRA/PRB ratio. In conclusion, we show that HMW-FGF2 isoforms are PRB targets which confer endocrine resistance and are localized in the nuclei of breast cancer samples. Hence, targeting intracellular FGF2 may contribute to overcome tumor progression.
Fil: Sahores, Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentina
Fil: Figueroa, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: May, Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Liguori, Marcos. Hospital de Agudos Magdalena V. de Martínez; Argentina
Fil: Rubstein, Adrián. Merck Argentina; Argentina
Fil: Fuentes, Cynthia Analia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Jacobsen, Britta M.. University Of Colorado Anschutz Medical Campus.; Estados Unidos
Fil: Elia, Andres Maximiliano. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Rojas, Paola Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Sequeira, Gonzalo Ricardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Álvarez, Michelle M.. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: González, Pedro. Hospital de Agudos Magdalena V de Martínez; Argentina
Fil: Gass, Hugo. Hospital de Agudos Magdalena V de Martínez; Argentina
Fil: Hewitt, Stephen. National Institute Of Dental And Craniofacial Research; Estados Unidos
Fil: Molinolo, Alfredo. University of California at San Diego; Estados Unidos
Fil: Lanari, Claudia Lee Malvina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Lamb, Caroline Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
description Endocrine resistance may develop as a consequence of enhanced growth factor signaling. Fibroblast growth factor 2 (FGF2) consists of a low and several high molecular weight forms (HMW-FGF2). We previously demonstrated that antiprogestin-resistant mammary carcinomas display lower levels of progesterone receptor A isoforms (PRA) than B isoforms (PRB). Our aim was to evaluate the role of FGF2 isoforms in breast cancer progression. We evaluated FGF2 expression, cell proliferation, and pathway activation in models with different PRA/PRB ratios. We performed lentiviral infections of different FGF2 isoforms using the human hormone-responsive T47D-YA cells, engineered to only express PRA, and evaluated tumor growth, metastatic dissemination, and endocrine responsiveness. We assessed FGF2 expression and localization in 81 human breast cancer samples. Antiprogestin-resistant experimental mammary carcinomas with low PRA/PRB ratios and T47D-YB cells, which only express PRB, displayed higher levels of HMW-FGF2 than responsive variants. HMW-FGF2 overexpression in T47D-YA cells induced increased tumor growth, lung metastasis, and antiprogestin resistance compared to control tumors. In human breast carcinomas categorized by their PRA/PRB ratio, we found nuclear FGF2 expression in 55.6% of tumor cells. No differences were found between nuclear FGF2 expression and Ki67 proliferation index, tumor stage, or tumor grade. In low-grade tumor samples, moderate to high nuclear FGF2 levels were associated to carcinomas with low PRA/PRB ratio. In conclusion, we show that HMW-FGF2 isoforms are PRB targets which confer endocrine resistance and are localized in the nuclei of breast cancer samples. Hence, targeting intracellular FGF2 may contribute to overcome tumor progression.
publishDate 2018
dc.date.none.fl_str_mv 2018-10
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/11336/85381
Sahores, Ana; Figueroa, Virginia; May, Maria; Liguori, Marcos; Rubstein, Adrián; et al.; Increased high molecular weight FGF2 in endocrine-resistant breast cancer; Springer US; Hormones and Cancer; 9; 5; 10-2018; 338-348
1868-8500
CONICET Digital
CONICET
url http://hdl.handle.net/11336/85381
identifier_str_mv Sahores, Ana; Figueroa, Virginia; May, Maria; Liguori, Marcos; Rubstein, Adrián; et al.; Increased high molecular weight FGF2 in endocrine-resistant breast cancer; Springer US; Hormones and Cancer; 9; 5; 10-2018; 338-348
1868-8500
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1007/s12672-018-0339-4
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8054767/
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007/s12672-018-0339-4
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
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Springer US
publisher.none.fl_str_mv Springer US
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
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reponame_str CONICET Digital (CONICET)
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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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