New forms of induction of apoptosis in aggressive lymphoma using peptides that interrupt the RAS / RAF interaction

Autores
Bergna, Cecilia; Marín, Gustavo Horacio; Maiz, Mercedes Guadalupe; Bruzzoni Giovanelli, H.; Ponzinibbio, Carlos; Schinella, Guillermo Raúl; Errecalde, Jorge Oscar; Rebollo, Angelita
Año de publicación
2019
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
RAS-RAF-MEK-ERK is a key pathway for apoptosis regulation in cancer cells. B-Raf-inhibitors such as PLX4032 peptide was developed by Institute Curie-Université Pierre et Marie Curie in order to induce apoptosis in cancer cells. Objective: To demonstrate pro-apoptotic properties and survival outcome of EP2014/064243 peptide in murine aggressive lymphoma. Material and methods: BALBc mice with T-lymphoma were randomized assigned either in Group A (peptide+cyclophosphamide-CFM); Group B (peptides), Group C (CFM-control) or Control D (Cl-Na 0.9%-SF control group). Survival probability was calculated by Kaplan-Meier analysis. Apoptosis was detected using TUNEL technique. The protocol was approved by the Institutional Committee for Animal Care (CICUAL: T04-01-2015). Results: The median survival was 24 days (21.6-26.4) for placebo, 33 days (28.0-35.4) for the CFM monotherapy group, 33 (27.1-35.8) for the peptide group and 34 days (24,4-40) for CFM-peptide combined treatment (p < 0.05). In lymph node tissue the mean TUNEL positive cells per field for each treatment group was 2, 12 and 13 and 35 for SF, CFM, peptide and combined therapy (p < 0.05). Conclusion: These findings suggest that in murine aggressive lymphoma treated by an experimental peptide in addition with CFM, had an exponentially pro-apoptotic effect than CFM alone, suggesting that the peptide potentiated the anti-tumoural effect of CFM.
Facultad de Ciencias Médicas
Materia
Medicina
T-LYMPHOMA
NHL-T
Peptides
Apoptosis
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/126192

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oai_identifier_str oai:sedici.unlp.edu.ar:10915/126192
network_acronym_str SEDICI
repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling New forms of induction of apoptosis in aggressive lymphoma using peptides that interrupt the RAS / RAF interactionBergna, CeciliaMarín, Gustavo HoracioMaiz, Mercedes GuadalupeBruzzoni Giovanelli, H.Ponzinibbio, CarlosSchinella, Guillermo RaúlErrecalde, Jorge OscarRebollo, AngelitaMedicinaT-LYMPHOMANHL-TPeptidesApoptosisRAS-RAF-MEK-ERK is a key pathway for apoptosis regulation in cancer cells. B-Raf-inhibitors such as PLX4032 peptide was developed by Institute Curie-Université Pierre et Marie Curie in order to induce apoptosis in cancer cells. Objective: To demonstrate pro-apoptotic properties and survival outcome of EP2014/064243 peptide in murine aggressive lymphoma. Material and methods: BALBc mice with T-lymphoma were randomized assigned either in Group A (peptide+cyclophosphamide-CFM); Group B (peptides), Group C (CFM-control) or Control D (Cl-Na 0.9%-SF control group). Survival probability was calculated by Kaplan-Meier analysis. Apoptosis was detected using TUNEL technique. The protocol was approved by the Institutional Committee for Animal Care (CICUAL: T04-01-2015). Results: The median survival was 24 days (21.6-26.4) for placebo, 33 days (28.0-35.4) for the CFM monotherapy group, 33 (27.1-35.8) for the peptide group and 34 days (24,4-40) for CFM-peptide combined treatment (p < 0.05). In lymph node tissue the mean TUNEL positive cells per field for each treatment group was 2, 12 and 13 and 35 for SF, CFM, peptide and combined therapy (p < 0.05). Conclusion: These findings suggest that in murine aggressive lymphoma treated by an experimental peptide in addition with CFM, had an exponentially pro-apoptotic effect than CFM alone, suggesting that the peptide potentiated the anti-tumoural effect of CFM.Facultad de Ciencias Médicas2019info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf46-51http://sedici.unlp.edu.ar/handle/10915/126192enginfo:eu-repo/semantics/altIdentifier/issn/0009-0875info:eu-repo/semantics/altIdentifier/issn/2386-1274info:eu-repo/semantics/altIdentifier/pmid/31455066info:eu-repo/semantics/altIdentifier/doi/10.4038/cmj.v64i2.8890info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:30:22Zoai:sedici.unlp.edu.ar:10915/126192Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:30:23.202SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv New forms of induction of apoptosis in aggressive lymphoma using peptides that interrupt the RAS / RAF interaction
title New forms of induction of apoptosis in aggressive lymphoma using peptides that interrupt the RAS / RAF interaction
spellingShingle New forms of induction of apoptosis in aggressive lymphoma using peptides that interrupt the RAS / RAF interaction
Bergna, Cecilia
Medicina
T-LYMPHOMA
NHL-T
Peptides
Apoptosis
title_short New forms of induction of apoptosis in aggressive lymphoma using peptides that interrupt the RAS / RAF interaction
title_full New forms of induction of apoptosis in aggressive lymphoma using peptides that interrupt the RAS / RAF interaction
title_fullStr New forms of induction of apoptosis in aggressive lymphoma using peptides that interrupt the RAS / RAF interaction
title_full_unstemmed New forms of induction of apoptosis in aggressive lymphoma using peptides that interrupt the RAS / RAF interaction
title_sort New forms of induction of apoptosis in aggressive lymphoma using peptides that interrupt the RAS / RAF interaction
dc.creator.none.fl_str_mv Bergna, Cecilia
Marín, Gustavo Horacio
Maiz, Mercedes Guadalupe
Bruzzoni Giovanelli, H.
Ponzinibbio, Carlos
Schinella, Guillermo Raúl
Errecalde, Jorge Oscar
Rebollo, Angelita
author Bergna, Cecilia
author_facet Bergna, Cecilia
Marín, Gustavo Horacio
Maiz, Mercedes Guadalupe
Bruzzoni Giovanelli, H.
Ponzinibbio, Carlos
Schinella, Guillermo Raúl
Errecalde, Jorge Oscar
Rebollo, Angelita
author_role author
author2 Marín, Gustavo Horacio
Maiz, Mercedes Guadalupe
Bruzzoni Giovanelli, H.
Ponzinibbio, Carlos
Schinella, Guillermo Raúl
Errecalde, Jorge Oscar
Rebollo, Angelita
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Medicina
T-LYMPHOMA
NHL-T
Peptides
Apoptosis
topic Medicina
T-LYMPHOMA
NHL-T
Peptides
Apoptosis
dc.description.none.fl_txt_mv RAS-RAF-MEK-ERK is a key pathway for apoptosis regulation in cancer cells. B-Raf-inhibitors such as PLX4032 peptide was developed by Institute Curie-Université Pierre et Marie Curie in order to induce apoptosis in cancer cells. Objective: To demonstrate pro-apoptotic properties and survival outcome of EP2014/064243 peptide in murine aggressive lymphoma. Material and methods: BALBc mice with T-lymphoma were randomized assigned either in Group A (peptide+cyclophosphamide-CFM); Group B (peptides), Group C (CFM-control) or Control D (Cl-Na 0.9%-SF control group). Survival probability was calculated by Kaplan-Meier analysis. Apoptosis was detected using TUNEL technique. The protocol was approved by the Institutional Committee for Animal Care (CICUAL: T04-01-2015). Results: The median survival was 24 days (21.6-26.4) for placebo, 33 days (28.0-35.4) for the CFM monotherapy group, 33 (27.1-35.8) for the peptide group and 34 days (24,4-40) for CFM-peptide combined treatment (p < 0.05). In lymph node tissue the mean TUNEL positive cells per field for each treatment group was 2, 12 and 13 and 35 for SF, CFM, peptide and combined therapy (p < 0.05). Conclusion: These findings suggest that in murine aggressive lymphoma treated by an experimental peptide in addition with CFM, had an exponentially pro-apoptotic effect than CFM alone, suggesting that the peptide potentiated the anti-tumoural effect of CFM.
Facultad de Ciencias Médicas
description RAS-RAF-MEK-ERK is a key pathway for apoptosis regulation in cancer cells. B-Raf-inhibitors such as PLX4032 peptide was developed by Institute Curie-Université Pierre et Marie Curie in order to induce apoptosis in cancer cells. Objective: To demonstrate pro-apoptotic properties and survival outcome of EP2014/064243 peptide in murine aggressive lymphoma. Material and methods: BALBc mice with T-lymphoma were randomized assigned either in Group A (peptide+cyclophosphamide-CFM); Group B (peptides), Group C (CFM-control) or Control D (Cl-Na 0.9%-SF control group). Survival probability was calculated by Kaplan-Meier analysis. Apoptosis was detected using TUNEL technique. The protocol was approved by the Institutional Committee for Animal Care (CICUAL: T04-01-2015). Results: The median survival was 24 days (21.6-26.4) for placebo, 33 days (28.0-35.4) for the CFM monotherapy group, 33 (27.1-35.8) for the peptide group and 34 days (24,4-40) for CFM-peptide combined treatment (p < 0.05). In lymph node tissue the mean TUNEL positive cells per field for each treatment group was 2, 12 and 13 and 35 for SF, CFM, peptide and combined therapy (p < 0.05). Conclusion: These findings suggest that in murine aggressive lymphoma treated by an experimental peptide in addition with CFM, had an exponentially pro-apoptotic effect than CFM alone, suggesting that the peptide potentiated the anti-tumoural effect of CFM.
publishDate 2019
dc.date.none.fl_str_mv 2019
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
Articulo
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info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/126192
url http://sedici.unlp.edu.ar/handle/10915/126192
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/0009-0875
info:eu-repo/semantics/altIdentifier/issn/2386-1274
info:eu-repo/semantics/altIdentifier/pmid/31455066
info:eu-repo/semantics/altIdentifier/doi/10.4038/cmj.v64i2.8890
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
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instname:Universidad Nacional de La Plata
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instname_str Universidad Nacional de La Plata
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repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
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