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Recent high-profile reports have reignited an interest in acetate metabolism in cancer. Acetyl-CoA synthetases that catalyse the conversion of acetate to acetyl-CoA have now been implicated in the growth of hepatocellular carcinoma, glioblastoma, breast cancer and prostate cancer. In this Review, we discuss how acetate functions as a nutritional source for tumours and as a regulator of cancer cell stress, and how preventing its (re)capture by cancer cells may provide an opportunity for therapeutic intervention.

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Schug, Zachary T. -  Vande Voorde, Johan -  Gottlieb, Eyal - 

Id.: 69789651

Versión: 1.0

Estado: Final

Tipo de recurso: Articles  -  PeerReviewed  - 

Tipo de Interactividad: Expositivo

Nivel de Interactividad: muy bajo

Audiencia: Estudiante  -  Profesor  -  Autor  - 

Estructura: Atomic

Coste: no

Copyright: sí

Requerimientos técnicos:  Browser: Any - 

Relación: [References] http://eprints.gla.ac.uk/139817/
[References] 10.1038/nrc.2016.87

Fecha de contribución: 08-nov-2017


* Schug, Z. T., Vande Voorde, J. and Gottlieb, E. (2016) The metabolic fate of acetate in cancer. Nature Reviews Cancer , 16(11), pp. 708-717. (doi:10.1038/nrc.2016.87 ) (PMID:27562461)

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