Cellules souches cancéreuses

Résumé

Les cellules souches cancéreuses (CSCs) sont des cellules cancéreuses (présentes dans les tumeurs dites « solides » ou les cancers hématologiques) qui possèdent des caractéristiques associées aux cellules souches normales, notamment la capacité de donner naissance aux différentes populations de cellules présentes dans une tumeur particulière. Les CSCs sont donc tumorigènes (formant des tumeurs), peut-être à la différence d'autres cellules cancéreuses non tumorigènes. Les CSCs peuvent générer des tumeurs grâce aux processus d'auto-renouvellement et de différenciation des cellules souches vers l’ensemble des composants cellulaires formant la tumeur. On suppose que ces cellules persistent dans les tumeurs comme une population distincte et provoquent des rechutes et des métastases en donnant naissance à de nouvelles tumeurs. Par conséquent, le développement de thérapies spécifiques ciblées sur les CSCs permet d'espérer une amélioration de la survie et de la qualité de vi

Source officielle

https://fr.wikipedia.org/wiki/Cellules_souches_canc%C3%A9reuses

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Metastasis is an inefficient process and most cancer cells fail to colonize secondary sites. There are several possible reasons for this. First, the nature of the infiltrating cells is important as a small population of cancer stem cells has been shown to have exclusive metastasis-initiating potential. Secondly, supportive niches are required to promote the outgrowth of disseminated tumour cells. S uch niches are either produced prior to the arrival of cancer cells in the target organ or are induced ad hoc upon cell infiltration. Components of the extracellular matrix (ECM) have been found to play a role in establishing these niches. This has highlighted the importance of the ECM for metastatic progression, and suggests that such components may provide alternative targets for treatment of metastastic disease. © 2012 The Association for the Publication of the Journal of Internal Medicine.

Wiley-Blackwell2013

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Hierarchical organization of tissues relies on stem cells, which either self-renew or produce committed progenitors predestined for lineage differentiation. Here we identify HOXA5 as an important repressor of intestinal stem cell fate in vivo and identify a reciprocal feedback between HOXA5 and Wnt signaling. HOXA5 is suppressed by the Wnt pathway to maintain stemness and becomes active only outside the intestinal crypt where it inhibits Wnt signaling to enforce differentiation. In colon cancer, HOXA5 is downregulated, and its re-expression induces loss of the cancer stem cell phenotype, preventing tumor progression and metastasis. Tumor regression by HOXA5 induction can be triggered by retinoids, which represent tangible means to treat colon cancer by eliminating cancer stem cells.

Elsevier2015

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Cutaneous cancer stem cell maintenance is dependent on beta-catenin signalling

Deepika Kassen, Ilaria Malanchi

Continuous turnover of epithelia is ensured by the extensive self-renewal capacity of tissue-specific stem cells. Similarly, epithelial tumour maintenance relies on cancer stem cells (CSCs), which co-opt stem cell properties. For most tumours, the cellular origin of these CSCs and regulatory pathways essential for sustaining stemness have not been identified. In murine skin, follicular morphogenesis is driven by bulge stem cells that specifically express CD34. Here we identify a population of cells in early epidermal tumours characterized by phenotypic and functional similarities to normal bulge skin stem cells. This population contains CSCs, which are the only cells with tumour initiation properties. Transplants derived from these CSCs preserve the hierarchical organization of the primary tumour. We describe beta-catenin signalling as being essential in sustaining the CSC phenotype. Ablation of the beta-catenin gene results in the loss of CSCs and complete tumour regression. In addition, we provide evidence for the involvement of increased beta-catenin signalling in malignant human squamous cell carcinomas. Because Wnt/beta-catenin signalling is not essential for normal epidermal homeostasis, such a mechanistic difference may thus be targeted to eliminate CSCs and consequently eradicate squamous cell carcinomas.

2008

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