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
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/126192
Ver los metadatos del registro completo
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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 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://sedici.unlp.edu.ar/handle/10915/126192 |
url |
http://sedici.unlp.edu.ar/handle/10915/126192 |
dc.language.none.fl_str_mv |
eng |
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eng |
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