p53 at the crossroads between stress response signaling and tumorigenesis: From molecular mechanisms to therapeutic opportunities

The p53 tumor suppressor is a transcription factor that integrates signals from numerous stress-activated signaling pathways and regulates the expression of specific target genes. p53 activation triggers a variety of cellular responses that ensure tumor suppression, including cell cycle arrest, apop...

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Autores principales: Giono, L.E., Ladelfa, M.F., Monte, M.
Formato: CHAP
Materias:
p53
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_97894017_v_n_p51_Giono
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spelling todo:paper_97894017_v_n_p51_Giono2023-10-03T16:45:23Z p53 at the crossroads between stress response signaling and tumorigenesis: From molecular mechanisms to therapeutic opportunities Giono, L.E. Ladelfa, M.F. Monte, M. Apoptosis Cancer Cell cycle Cell signaling DNA damage Metabolism Mutation Oncogene p53 Senescence Therapy Tumor suppressor The p53 tumor suppressor is a transcription factor that integrates signals from numerous stress-activated signaling pathways and regulates the expression of specific target genes. p53 activation triggers a variety of cellular responses that ensure tumor suppression, including cell cycle arrest, apoptosis and senescence. In addition, p53 tumor suppressive activity also involves the maintenance of cellular homeostasis through the regulation of metabolic pathways and the protection of stemness. Mutation of p53 protein or inactivation of the p53 pathway is the most frequent alteration found in human cancer. Loss of p53 function leads to tumorigenesis and is associated with poor prognosis and therapy resistance in cancer patients. Moreover, mutant p53 often exhibits gain of function activities that contribute to the tumoral phenotype. Over 30 years of basic research on p53 structure and function have placed p53 at the center of cancer investigation. Numerous cellular and mouse models have demonstrated that restoration of p53 function may stop tumor progression or even promote tumor regression. Now, these observations lead to the development of multiple anti-cancer therapeutic strategies that rely on activation of wild-type p53 or reactivation of mutant p53, as well as other p53-based approaches. Rational drug design and functional screenings have allowed for the identification of small molecule compounds, some of which are currently being tested in clinical trials. © Springer Science+Business Media Dordrecht 2015. Fil:Giono, L.E. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Ladelfa, M.F. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. CHAP info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_97894017_v_n_p51_Giono
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Apoptosis
Cancer
Cell cycle
Cell signaling
DNA damage
Metabolism
Mutation
Oncogene
p53
Senescence
Therapy
Tumor suppressor
spellingShingle Apoptosis
Cancer
Cell cycle
Cell signaling
DNA damage
Metabolism
Mutation
Oncogene
p53
Senescence
Therapy
Tumor suppressor
Giono, L.E.
Ladelfa, M.F.
Monte, M.
p53 at the crossroads between stress response signaling and tumorigenesis: From molecular mechanisms to therapeutic opportunities
topic_facet Apoptosis
Cancer
Cell cycle
Cell signaling
DNA damage
Metabolism
Mutation
Oncogene
p53
Senescence
Therapy
Tumor suppressor
description The p53 tumor suppressor is a transcription factor that integrates signals from numerous stress-activated signaling pathways and regulates the expression of specific target genes. p53 activation triggers a variety of cellular responses that ensure tumor suppression, including cell cycle arrest, apoptosis and senescence. In addition, p53 tumor suppressive activity also involves the maintenance of cellular homeostasis through the regulation of metabolic pathways and the protection of stemness. Mutation of p53 protein or inactivation of the p53 pathway is the most frequent alteration found in human cancer. Loss of p53 function leads to tumorigenesis and is associated with poor prognosis and therapy resistance in cancer patients. Moreover, mutant p53 often exhibits gain of function activities that contribute to the tumoral phenotype. Over 30 years of basic research on p53 structure and function have placed p53 at the center of cancer investigation. Numerous cellular and mouse models have demonstrated that restoration of p53 function may stop tumor progression or even promote tumor regression. Now, these observations lead to the development of multiple anti-cancer therapeutic strategies that rely on activation of wild-type p53 or reactivation of mutant p53, as well as other p53-based approaches. Rational drug design and functional screenings have allowed for the identification of small molecule compounds, some of which are currently being tested in clinical trials. © Springer Science+Business Media Dordrecht 2015.
format CHAP
author Giono, L.E.
Ladelfa, M.F.
Monte, M.
author_facet Giono, L.E.
Ladelfa, M.F.
Monte, M.
author_sort Giono, L.E.
title p53 at the crossroads between stress response signaling and tumorigenesis: From molecular mechanisms to therapeutic opportunities
title_short p53 at the crossroads between stress response signaling and tumorigenesis: From molecular mechanisms to therapeutic opportunities
title_full p53 at the crossroads between stress response signaling and tumorigenesis: From molecular mechanisms to therapeutic opportunities
title_fullStr p53 at the crossroads between stress response signaling and tumorigenesis: From molecular mechanisms to therapeutic opportunities
title_full_unstemmed p53 at the crossroads between stress response signaling and tumorigenesis: From molecular mechanisms to therapeutic opportunities
title_sort p53 at the crossroads between stress response signaling and tumorigenesis: from molecular mechanisms to therapeutic opportunities
url http://hdl.handle.net/20.500.12110/paper_97894017_v_n_p51_Giono
work_keys_str_mv AT gionole p53atthecrossroadsbetweenstressresponsesignalingandtumorigenesisfrommolecularmechanismstotherapeuticopportunities
AT ladelfamf p53atthecrossroadsbetweenstressresponsesignalingandtumorigenesisfrommolecularmechanismstotherapeuticopportunities
AT montem p53atthecrossroadsbetweenstressresponsesignalingandtumorigenesisfrommolecularmechanismstotherapeuticopportunities
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