2026-04-29T19:07:21Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/176682024-11-29T18:14:22Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud
author
Santos-de-Frutos, Karla
author
Djouder, Nabil
funder
Ministerio de Ciencia e Innovación (España)
funder
Asociación Española Contra el Cáncer
2024-02-08T20:51:58Z
2024-02-08T20:51:58Z
2021-06-16
Commun Biol . 2021 ;4(1):747.
10.1038/s42003-021-02257-0
2399-3642
Communications biology
34135460
http://hdl.handle.net/20.500.12105/17668
Tumour 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.
eng
When dormancy fuels tumour relapse.
journal article
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URL
https://repisalud.isciii.es/bitstreams/451518c7-9400-48d0-bdf8-7caac6de9f70/download
File
MD5
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application/pdf
whendornacy_2021.pdf
URL
https://repisalud.isciii.es/bitstreams/cf978766-1e8b-43ad-95a7-e514b3965275/download
File
MD5
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text/plain
whendornacy_2021.pdf.txt