AustralieFrV1, PubMed, Corpus, bibRecord, 002065

Do cell-autonomous and non-cell-autonomous effects drive the structure of tumor ecosystems?

Identifieur interne : 002065 ( PubMed/Corpus ); précédent : 002064; suivant : 002066

Do cell-autonomous and non-cell-autonomous effects drive the structure of tumor ecosystems?

Auteurs : Tazzio Tissot ; Beata Ujvari ; Eric Solary ; Patrice Lassus ; Benjamin Roche ; Frédéric Thomas

Source :

Biochimica et biophysica acta [ 0006-3002 ] ; 2016.

RBID : pubmed:26845682

English descriptors

KwdEn :
- Disease Progression, Ecosystem, Humans, Mutation, Neoplasms (pathology), Tumor Microenvironment.
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

Links to Exploration step

pubmed:26845682

Le document en format XML

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<author><name sortKey="Ujvari, Beata" sort="Ujvari, Beata" uniqKey="Ujvari B" first="Beata" last="Ujvari">Beata Ujvari</name>
<affiliation><nlm:affiliation>Centre for Integrative Ecology, School of Life and Environmental Sciences, Deakin University, Waurn Ponds, Australia.</nlm:affiliation>
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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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Do cell-autonomous and non-cell-autonomous effects drive the structure of tumor ecosystems?

Do cell-autonomous and non-cell-autonomous effects drive the structure of tumor ecosystems?

Source :

English descriptors

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki