Publication:
When dormancy fuels tumour relapse.

dc.contributor.authorSantos-de-Frutos, Karla
dc.contributor.authorDjouder, Nabil
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.contributor.funderAsociación Española Contra el Cáncer
dc.date.accessioned2024-02-08T20:51:58Z
dc.date.available2024-02-08T20:51:58Z
dc.date.issued2021-06-16
dc.description.abstractTumour recurrence is a serious impediment to cancer treatment, but the mechanisms involved are poorly understood. The most frequently used anti-tumour therapies-chemotherapy and radiotherapy-target highly proliferative cancer cells. However non- or slow-proliferative dormant cancer cells can persist after treatment, eventually causing tumour relapse. Whereas the reversible growth arrest mechanism allows quiescent cells to re-enter the cell cycle, senescent cells are largely thought to be irreversibly arrested, and may instead contribute to tumour growth and relapse through paracrine signalling mechanisms. Thus, due to the differences in their growth arrest mechanism, metabolic features, plasticity and adaptation to their respective tumour microenvironment, dormant-senescent and -quiescent cancer cells could have different but complementary roles in fuelling tumour growth. In this review article, we discuss the implication of dormant cancer cells in tumour relapse and the need to understand how quiescent and senescent cells, respectively, may play a part in this process.es_ES
dc.description.peerreviewedes_ES
dc.description.sponsorshipThis work was funded by the State Research Agency (AEI, 10.13039/501100011033) from the Spanish Ministry of Science and Innovation (projects granted to N.D. SAF201676598-R, SAF2017-92733-EXP, RTI2018-094834-B-I00 and RED2018-102723-T), cofounded by European Regional Development Fund (ERDF). K.S.D.F. is recipient of a fellowship from the AECC Scientific Foundation (Madrid). This work was developed at the CNIO funded by the Health Institute Carlos III (ISCIII) and the Spanish Ministry of Science and Innovation.es_ES
dc.format.number1es_ES
dc.format.page747es_ES
dc.format.volume4es_ES
dc.identifier.citationCommun Biol . 2021 ;4(1):747.es_ES
dc.identifier.doi10.1038/s42003-021-02257-0es_ES
dc.identifier.e-issn2399-3642es_ES
dc.identifier.journalCommunications biologyes_ES
dc.identifier.pubmedID34135460es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/17668
dc.language.isoenges_ES
dc.publisherNature Publishing Group
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/SAF201676598-Res_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/SAF2017-92733-EXPes_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/RTI2018-094834-B-I00es_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/RED2018-102723-Tes_ES
dc.relation.publisherversionhttps://doi.org/10.1038/s42003-021-02257-0.es_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Grupo de Factores de Crecimiento, Nutrientes y Cánceres_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.meshCell Cyclees_ES
dc.subject.meshCell Plasticityes_ES
dc.subject.meshCell Proliferationes_ES
dc.subject.meshCellular Senescencees_ES
dc.subject.meshHumanses_ES
dc.subject.meshNeoplasm Recurrence, Locales_ES
dc.subject.meshNeoplasmses_ES
dc.subject.meshSignal Transductiones_ES
dc.subject.meshTumor Microenvironmentes_ES
dc.titleWhen dormancy fuels tumour relapse.es_ES
dc.typejournal articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
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