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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/85381
Ver los metadatos del registro completo
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oai:ri.conicet.gov.ar:11336/85381 |
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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 Técnicas2025-09-29T10:07:25Zoai: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:34982025-09-29 10:07:25.744CONICET 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) 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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13.070432 |