Cdkn2a inactivation promotes malignant transformation of mouse immature thymocytes before the β-selection checkpoint

Detalhes bibliográficos
Autor(a) principal: Catarino, Telmo A.
Data de Publicação: 2022
Outros Autores: Pacheco-Leyva, Ivette, Kindi, Faiza Al, Ghezzo, Marinella N., Fernandes, Mónica T., Costa, Telma, Rodrigues Dos Santos, Nuno
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/10400.1/20189
Resumo: CDKN2A deletion is the most frequent genetic alteration in T-cell acute lymphoblastic leukemia (T-ALL), occurring across all molecular and immunophenotypic subtypes. CDKN2A encodes two functionally unrelated tumor suppressor proteins, ARF and INK4a, which are critical regulators of cell cycle and proliferation. Arf has been reported to suppress T-ALL development in post−b-selection thymocytes, but whether CDKN2A acts as a tumor suppressor gene in immature, pre−b-selection thymocytes remains to be elucidated. Resorting to a Rag2-deficient model of T-ALL, driven by the ETV6:: JAK2 fusion, we report that Cdkn2a haploinsufficiency at early stages of T-cell development facilitates leukemia development
id RCAP_aed70c7c85c830af34bdfabaedeb6247
oai_identifier_str oai:sapientia.ualg.pt:10400.1/20189
network_acronym_str RCAP
network_name_str Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
repository_id_str 7160
spelling Cdkn2a inactivation promotes malignant transformation of mouse immature thymocytes before the β-selection checkpointPt-alphaNotch1 mutationsTumor-suppressorExpressionTcrLocusCDKN2A deletion is the most frequent genetic alteration in T-cell acute lymphoblastic leukemia (T-ALL), occurring across all molecular and immunophenotypic subtypes. CDKN2A encodes two functionally unrelated tumor suppressor proteins, ARF and INK4a, which are critical regulators of cell cycle and proliferation. Arf has been reported to suppress T-ALL development in post−b-selection thymocytes, but whether CDKN2A acts as a tumor suppressor gene in immature, pre−b-selection thymocytes remains to be elucidated. Resorting to a Rag2-deficient model of T-ALL, driven by the ETV6:: JAK2 fusion, we report that Cdkn2a haploinsufficiency at early stages of T-cell development facilitates leukemia developmentPPBI-POCI-01-0145-FEDER-022122; POCI-01-0145-FEDER-007274; NORTE01-0145-FEDER-000029SapientiaCatarino, Telmo A.Pacheco-Leyva, IvetteKindi, Faiza AlGhezzo, Marinella N.Fernandes, Mónica T.Costa, TelmaRodrigues Dos Santos, Nuno2023-12-07T11:16:25Z20222022-01-01T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10400.1/20189eng0301-472X10.1016/j.exphem.2022.10.001info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-12-13T02:00:44Zoai:sapientia.ualg.pt:10400.1/20189Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-20T00:42:22.142553Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse
dc.title.none.fl_str_mv Cdkn2a inactivation promotes malignant transformation of mouse immature thymocytes before the β-selection checkpoint
title Cdkn2a inactivation promotes malignant transformation of mouse immature thymocytes before the β-selection checkpoint
spellingShingle Cdkn2a inactivation promotes malignant transformation of mouse immature thymocytes before the β-selection checkpoint
Catarino, Telmo A.
Pt-alpha
Notch1 mutations
Tumor-suppressor
Expression
Tcr
Locus
title_short Cdkn2a inactivation promotes malignant transformation of mouse immature thymocytes before the β-selection checkpoint
title_full Cdkn2a inactivation promotes malignant transformation of mouse immature thymocytes before the β-selection checkpoint
title_fullStr Cdkn2a inactivation promotes malignant transformation of mouse immature thymocytes before the β-selection checkpoint
title_full_unstemmed Cdkn2a inactivation promotes malignant transformation of mouse immature thymocytes before the β-selection checkpoint
title_sort Cdkn2a inactivation promotes malignant transformation of mouse immature thymocytes before the β-selection checkpoint
author Catarino, Telmo A.
author_facet Catarino, Telmo A.
Pacheco-Leyva, Ivette
Kindi, Faiza Al
Ghezzo, Marinella N.
Fernandes, Mónica T.
Costa, Telma
Rodrigues Dos Santos, Nuno
author_role author
author2 Pacheco-Leyva, Ivette
Kindi, Faiza Al
Ghezzo, Marinella N.
Fernandes, Mónica T.
Costa, Telma
Rodrigues Dos Santos, Nuno
author2_role author
author
author
author
author
author
dc.contributor.none.fl_str_mv Sapientia
dc.contributor.author.fl_str_mv Catarino, Telmo A.
Pacheco-Leyva, Ivette
Kindi, Faiza Al
Ghezzo, Marinella N.
Fernandes, Mónica T.
Costa, Telma
Rodrigues Dos Santos, Nuno
dc.subject.por.fl_str_mv Pt-alpha
Notch1 mutations
Tumor-suppressor
Expression
Tcr
Locus
topic Pt-alpha
Notch1 mutations
Tumor-suppressor
Expression
Tcr
Locus
description CDKN2A deletion is the most frequent genetic alteration in T-cell acute lymphoblastic leukemia (T-ALL), occurring across all molecular and immunophenotypic subtypes. CDKN2A encodes two functionally unrelated tumor suppressor proteins, ARF and INK4a, which are critical regulators of cell cycle and proliferation. Arf has been reported to suppress T-ALL development in post−b-selection thymocytes, but whether CDKN2A acts as a tumor suppressor gene in immature, pre−b-selection thymocytes remains to be elucidated. Resorting to a Rag2-deficient model of T-ALL, driven by the ETV6:: JAK2 fusion, we report that Cdkn2a haploinsufficiency at early stages of T-cell development facilitates leukemia development
publishDate 2022
dc.date.none.fl_str_mv 2022
2022-01-01T00:00:00Z
2023-12-07T11:16:25Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://hdl.handle.net/10400.1/20189
url http://hdl.handle.net/10400.1/20189
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 0301-472X
10.1016/j.exphem.2022.10.001
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação
instacron:RCAAP
instname_str Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação
instacron_str RCAAP
institution RCAAP
reponame_str Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
collection Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
repository.name.fl_str_mv Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação
repository.mail.fl_str_mv
_version_ 1799136324958027776

Registros relacionados