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Targeting Metabolism and Autophagy in the Context of Haematologic Malignancies

Autophagy is a cellular process that maintains the homeostasis of the normal cell. It not only allows for cell survival in times of metabolic stress with nutrient recycling but also is able to lead to cell death when required. During malignant transformation the cell is able to proliferate and survi...

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Detalles Bibliográficos
Autores principales: Banerji, Versha, Gibson, Spencer B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399452/
https://www.ncbi.nlm.nih.gov/pubmed/22829831
http://dx.doi.org/10.1155/2012/595976
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author Banerji, Versha
Gibson, Spencer B.
author_facet Banerji, Versha
Gibson, Spencer B.
author_sort Banerji, Versha
collection PubMed
description Autophagy is a cellular process that maintains the homeostasis of the normal cell. It not only allows for cell survival in times of metabolic stress with nutrient recycling but also is able to lead to cell death when required. During malignant transformation the cell is able to proliferate and survive. This is due to altered cell metabolism and the presence of altered genetic changes that maintain the cell survival. Metabolism was considered an innocent bystander that was a consequence of the increased nutrient requirement for the survival and proliferation of haematological malignancies. The interdependency of metabolism and cellular mechanisms such as autophagy are becoming more evident and important. This interdependence contributes to increased cancer progression and drug resistance. In this paper we aim to discuss autophagy, how it pertains to metabolism in the context of hematologic malignancies, and the implications for therapy.
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spelling pubmed-33994522012-07-24 Targeting Metabolism and Autophagy in the Context of Haematologic Malignancies Banerji, Versha Gibson, Spencer B. Int J Cell Biol Review Article Autophagy is a cellular process that maintains the homeostasis of the normal cell. It not only allows for cell survival in times of metabolic stress with nutrient recycling but also is able to lead to cell death when required. During malignant transformation the cell is able to proliferate and survive. This is due to altered cell metabolism and the presence of altered genetic changes that maintain the cell survival. Metabolism was considered an innocent bystander that was a consequence of the increased nutrient requirement for the survival and proliferation of haematological malignancies. The interdependency of metabolism and cellular mechanisms such as autophagy are becoming more evident and important. This interdependence contributes to increased cancer progression and drug resistance. In this paper we aim to discuss autophagy, how it pertains to metabolism in the context of hematologic malignancies, and the implications for therapy. Hindawi Publishing Corporation 2012 2012-07-08 /pmc/articles/PMC3399452/ /pubmed/22829831 http://dx.doi.org/10.1155/2012/595976 Text en Copyright © 2012 V. Banerji and S. B. Gibson. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Banerji, Versha
Gibson, Spencer B.
Targeting Metabolism and Autophagy in the Context of Haematologic Malignancies
title Targeting Metabolism and Autophagy in the Context of Haematologic Malignancies
title_full Targeting Metabolism and Autophagy in the Context of Haematologic Malignancies
title_fullStr Targeting Metabolism and Autophagy in the Context of Haematologic Malignancies
title_full_unstemmed Targeting Metabolism and Autophagy in the Context of Haematologic Malignancies
title_short Targeting Metabolism and Autophagy in the Context of Haematologic Malignancies
title_sort targeting metabolism and autophagy in the context of haematologic malignancies
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399452/
https://www.ncbi.nlm.nih.gov/pubmed/22829831
http://dx.doi.org/10.1155/2012/595976
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