Do cell-autonomous and non-cell-autonomous effects drive the structure of tumor ecosystems?
Identifieur interne : 002075 ( Main/Exploration ); précédent : 002074; suivant : 002076Do cell-autonomous and non-cell-autonomous effects drive the structure of tumor ecosystems?
Auteurs : Tazzio Tissot [France] ; Beata Ujvari [Australie] ; Eric Solary [France] ; Patrice Lassus [France] ; Benjamin Roche [France] ; Frédéric Thomas [France]Source :
- Biochimica et biophysica acta [ 0006-3002 ] ; 2016.
Descripteurs français
- KwdFr :
- MESH :
- anatomopathologie : Tumeurs.
- Humains, Microenvironnement tumoral, Mutation, Écosystème, Évolution de la maladie.
English descriptors
- KwdEn :
- MESH :
- pathology : Neoplasms.
- Disease Progression, Ecosystem, Humans, Mutation, Tumor Microenvironment.
Abstract
By definition, a driver mutation confers a growth advantage to the cancer cell in which it occurs, while a passenger mutation does not: the former is usually considered as the engine of cancer progression, while the latter is not. Actually, the effects of a given mutation depend on the genetic background of the cell in which it appears, thus can differ in the subclones that form a tumor. In addition to cell-autonomous effects generated by the mutations, non-cell-autonomous effects shape the phenotype of a cancer cell. Here, we review the evidence that a network of biological interactions between subclones drives cancer cell adaptation and amplifies intra-tumor heterogeneity. Integrating the role of mutations in tumor ecosystems generates innovative strategies targeting the tumor ecosystem's weaknesses to improve cancer treatment.
DOI: 10.1016/j.bbcan.2016.01.005
PubMed: 26845682
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">By definition, a driver mutation confers a growth advantage to the cancer cell in which it occurs, while a passenger mutation does not: the former is usually considered as the engine of cancer progression, while the latter is not. Actually, the effects of a given mutation depend on the genetic background of the cell in which it appears, thus can differ in the subclones that form a tumor. In addition to cell-autonomous effects generated by the mutations, non-cell-autonomous effects shape the phenotype of a cancer cell. Here, we review the evidence that a network of biological interactions between subclones drives cancer cell adaptation and amplifies intra-tumor heterogeneity. Integrating the role of mutations in tumor ecosystems generates innovative strategies targeting the tumor ecosystem's weaknesses to improve cancer treatment.</div>
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