Notch partners in the long journey of T-ALL pathogenesis

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological disease that arises from the oncogenic transformation of developing T cells during T-lymphopoiesis. Although T-ALL prognosis has improved markedly in recent years, relapsing and refractory patients with dismal outcomes still...

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Detalles Bibliográficos
Autores: Toribio, María Luisa, González García, Sara
Tipo de recurso: artículo
Fecha de publicación:2023
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/94978
Acceso en línea:https://hdl.handle.net/20.500.14352/94978
Access Level:acceso abierto
Palabra clave:577.2
NOTCH
T-cell acute lymphoblastic leukemia (T-ALL)
T-cell development
Gamma secretase inhibitors (GSI)
Targeted therapies
Thymus
Biología
2412 Inmunología
2415 Biología Molecular
2407 Biología Celular
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oai_identifier_str oai:docta.ucm.es:20.500.14352/94978
network_acronym_str ES
network_name_str España
repository_id_str
spelling Notch partners in the long journey of T-ALL pathogenesisToribio, María LuisaGonzález García, Sara577.2NOTCHT-cell acute lymphoblastic leukemia (T-ALL)T-cell developmentGamma secretase inhibitors (GSI)Targeted therapiesThymusBiología2412 Inmunología2415 Biología Molecular2407 Biología CelularT-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological disease that arises from the oncogenic transformation of developing T cells during T-lymphopoiesis. Although T-ALL prognosis has improved markedly in recent years, relapsing and refractory patients with dismal outcomes still represent a major clinical issue. Consequently, understanding the pathological mechanisms that lead to the appearance of this malignancy and developing novel and more effective targeted therapies is an urgent need. Since the discovery in 2004 that a major proportion of T-ALL patients carry activating mutations that turn NOTCH1 into an oncogene, great efforts have been made to decipher the mechanisms underlying constitutive NOTCH1 activation, with the aim of understanding how NOTCH1 dysregulation converts the physiological NOTCH1-dependent T-cell developmental program into a pathological T-cell transformation process. Several molecular players have so far been shown to cooperate with NOTCH1 in this oncogenic process, and different therapeutic strategies have been developed to specifically target NOTCH1-dependent T-ALLs. Here, we comprehensively analyze the molecular bases of the cross-talk between NOTCH1 and cooperating partners critically involved in the generation and/or maintenance and progression of T-ALL and discuss novel opportunities and therapeutic approaches that current knowledge may open for future treatment of T-ALL patients.MDPIUniversidad Complutense de Madrid20232023-01-1020232023-01-10journal articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/20.500.14352/94978reponame:Docta Complutenseinstname:Universidad Complutense de Madrid (UCM)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Attribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:docta.ucm.es:20.500.14352/949782026-06-02T12:44:21Z
dc.title.none.fl_str_mv Notch partners in the long journey of T-ALL pathogenesis
title Notch partners in the long journey of T-ALL pathogenesis
spellingShingle Notch partners in the long journey of T-ALL pathogenesis
Toribio, María Luisa
577.2
NOTCH
T-cell acute lymphoblastic leukemia (T-ALL)
T-cell development
Gamma secretase inhibitors (GSI)
Targeted therapies
Thymus
Biología
2412 Inmunología
2415 Biología Molecular
2407 Biología Celular
title_short Notch partners in the long journey of T-ALL pathogenesis
title_full Notch partners in the long journey of T-ALL pathogenesis
title_fullStr Notch partners in the long journey of T-ALL pathogenesis
title_full_unstemmed Notch partners in the long journey of T-ALL pathogenesis
title_sort Notch partners in the long journey of T-ALL pathogenesis
dc.creator.none.fl_str_mv Toribio, María Luisa
González García, Sara
author Toribio, María Luisa
author_facet Toribio, María Luisa
González García, Sara
author_role author
author2 González García, Sara
author2_role author
dc.contributor.none.fl_str_mv Universidad Complutense de Madrid
dc.subject.none.fl_str_mv 577.2
NOTCH
T-cell acute lymphoblastic leukemia (T-ALL)
T-cell development
Gamma secretase inhibitors (GSI)
Targeted therapies
Thymus
Biología
2412 Inmunología
2415 Biología Molecular
2407 Biología Celular
topic 577.2
NOTCH
T-cell acute lymphoblastic leukemia (T-ALL)
T-cell development
Gamma secretase inhibitors (GSI)
Targeted therapies
Thymus
Biología
2412 Inmunología
2415 Biología Molecular
2407 Biología Celular
description T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological disease that arises from the oncogenic transformation of developing T cells during T-lymphopoiesis. Although T-ALL prognosis has improved markedly in recent years, relapsing and refractory patients with dismal outcomes still represent a major clinical issue. Consequently, understanding the pathological mechanisms that lead to the appearance of this malignancy and developing novel and more effective targeted therapies is an urgent need. Since the discovery in 2004 that a major proportion of T-ALL patients carry activating mutations that turn NOTCH1 into an oncogene, great efforts have been made to decipher the mechanisms underlying constitutive NOTCH1 activation, with the aim of understanding how NOTCH1 dysregulation converts the physiological NOTCH1-dependent T-cell developmental program into a pathological T-cell transformation process. Several molecular players have so far been shown to cooperate with NOTCH1 in this oncogenic process, and different therapeutic strategies have been developed to specifically target NOTCH1-dependent T-ALLs. Here, we comprehensively analyze the molecular bases of the cross-talk between NOTCH1 and cooperating partners critically involved in the generation and/or maintenance and progression of T-ALL and discuss novel opportunities and therapeutic approaches that current knowledge may open for future treatment of T-ALL patients.
publishDate 2023
dc.date.none.fl_str_mv 2023
2023-01-10
2023
2023-01-10
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/20.500.14352/94978
url https://hdl.handle.net/20.500.14352/94978
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution 4.0 International
http://creativecommons.org/licenses/by/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution 4.0 International
http://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv reponame:Docta Complutense
instname:Universidad Complutense de Madrid (UCM)
instname_str Universidad Complutense de Madrid (UCM)
reponame_str Docta Complutense
collection Docta Complutense
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,300719

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