Targeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance

Jennifer S Carew1, Steffan T Nawrocki1, Francis J Giles1, John L Cleveland21The CTRC Institute for Drug Development, University of Texas Health Science Center San Antonio, San Antonio, TX, USA; 2The Department of Cancer Biology, The Scripps Research Institute, Jupiter, FL, USAAbstract: Autophagy is...

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Autores principales:	Jennifer S Carew, Steffan T Nawrocki, Francis J Giles, John L Cleveland
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2008
Materias:	Medicine (General) R5-920
Acceso en línea:	https://doaj.org/article/c53d4c8306034bdb8fb9674d50370ccc
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spelling	oai:doaj.org-article:c53d4c8306034bdb8fb9674d50370ccc2021-12-02T02:16:25ZTargeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance1177-54751177-5491https://doaj.org/article/c53d4c8306034bdb8fb9674d50370ccc2008-06-01T00:00:00Zhttp://www.dovepress.com/targeting-autophagy-a-novel-anticancer-strategy-with-therapeutic-impli-a1726https://doaj.org/toc/1177-5475https://doaj.org/toc/1177-5491Jennifer S Carew1, Steffan T Nawrocki1, Francis J Giles1, John L Cleveland21The CTRC Institute for Drug Development, University of Texas Health Science Center San Antonio, San Antonio, TX, USA; 2The Department of Cancer Biology, The Scripps Research Institute, Jupiter, FL, USAAbstract: Autophagy is an ancient, intracellular degradative system which plays important roles in regulating protein homeostasis and which is essential for survival when cells are faced with metabolic stress. Increasing evidence suggests that autophagy also functions as a tumor suppressor mechanism that harnesses the growth and/or survival of cells as they transition towards a rapidly dividing malignant state. However, the impact of autophagy on cancer progression and on the efficacy of cancer therapeutics is controversial. In particular, although the induction of autophagy has been reported after treatment with a number of therapeutic agents, including imatinib, this response has variously been suggested to either impair or contribute to the effects of anticancer agents. More recent studies support the notion that autophagy compromises the efficacy of anticancer agents, where agents such as chloroquine (CQ) that impair autophagy augment the anticancer activity of histone deacetylase (HDAC) inhibitors and alkylating agents. Inhibition of autophagy is a particularly attractive strategy for the treatment of imatinib-refractory chronic myelogenous leukemia (CML) since a combination of CQ with the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) compromises the survival of even BCR-ABL-T315I+ imatinib-resistant CML. Additional studies are clearly needed to establish the clinical utility of autophagy inhibitors and to identify patients most likely to benefit from this novel therapeutic approach.Keywords: autophagy, imatinib, resistance, chronic myelogenous leukemia Jennifer S CarewSteffan T NawrockiFrancis J GilesJohn L ClevelandDove Medical PressarticleMedicine (General)R5-920ENBiologics: Targets & Therapy, Vol 2008, Iss Issue 2, Pp 201-204 (2008)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine (General) R5-920
spellingShingle	Medicine (General) R5-920 Jennifer S Carew Steffan T Nawrocki Francis J Giles John L Cleveland Targeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance
description	Jennifer S Carew1, Steffan T Nawrocki1, Francis J Giles1, John L Cleveland21The CTRC Institute for Drug Development, University of Texas Health Science Center San Antonio, San Antonio, TX, USA; 2The Department of Cancer Biology, The Scripps Research Institute, Jupiter, FL, USAAbstract: Autophagy is an ancient, intracellular degradative system which plays important roles in regulating protein homeostasis and which is essential for survival when cells are faced with metabolic stress. Increasing evidence suggests that autophagy also functions as a tumor suppressor mechanism that harnesses the growth and/or survival of cells as they transition towards a rapidly dividing malignant state. However, the impact of autophagy on cancer progression and on the efficacy of cancer therapeutics is controversial. In particular, although the induction of autophagy has been reported after treatment with a number of therapeutic agents, including imatinib, this response has variously been suggested to either impair or contribute to the effects of anticancer agents. More recent studies support the notion that autophagy compromises the efficacy of anticancer agents, where agents such as chloroquine (CQ) that impair autophagy augment the anticancer activity of histone deacetylase (HDAC) inhibitors and alkylating agents. Inhibition of autophagy is a particularly attractive strategy for the treatment of imatinib-refractory chronic myelogenous leukemia (CML) since a combination of CQ with the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) compromises the survival of even BCR-ABL-T315I+ imatinib-resistant CML. Additional studies are clearly needed to establish the clinical utility of autophagy inhibitors and to identify patients most likely to benefit from this novel therapeutic approach.Keywords: autophagy, imatinib, resistance, chronic myelogenous leukemia
format	article
author	Jennifer S Carew Steffan T Nawrocki Francis J Giles John L Cleveland
author_facet	Jennifer S Carew Steffan T Nawrocki Francis J Giles John L Cleveland
author_sort	Jennifer S Carew
title	Targeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance
title_short	Targeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance
title_full	Targeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance
title_fullStr	Targeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance
title_full_unstemmed	Targeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance
title_sort	targeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance
publisher	Dove Medical Press
publishDate	2008
url	https://doaj.org/article/c53d4c8306034bdb8fb9674d50370ccc
work_keys_str_mv	AT jenniferscarew targetingautophagyanovelanticancerstrategywiththerapeuticimplicationsforimatinibresistance AT steffantnawrocki targetingautophagyanovelanticancerstrategywiththerapeuticimplicationsforimatinibresistance AT francisjgiles targetingautophagyanovelanticancerstrategywiththerapeuticimplicationsforimatinibresistance AT johnlcleveland targetingautophagyanovelanticancerstrategywiththerapeuticimplicationsforimatinibresistance
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Targeting autophagy: a novel anticancer strategy with therapeutic implications for imatinib resistance

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