Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism

Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2•−and H2O2. It has also been proposed that cancer cells increase glucose and hydrope...
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Autor*in:	Bryan G. Allen [verfasserIn] Sudershan K. Bhatia [verfasserIn] Carryn M. Anderson [verfasserIn] Julie M. Eichenberger-Gilmore [verfasserIn] Zita A. Sibenaller [verfasserIn] Kranti A. Mapuskar [verfasserIn] Joshua D. Schoenfeld [verfasserIn] John M. Buatti [verfasserIn] Douglas R. Spitz [verfasserIn] Melissa A. Fath [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Ketogenic diet Oxidative stress Cancer therapy

Übergeordnetes Werk:	In: Redox Biology - Elsevier, 2013, 2(2014), C, Seite 963-970
Übergeordnetes Werk:	volume:2 ; year:2014 ; number:C ; pages:963-970

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.redox.2014.08.002

Katalog-ID:	DOAJ035338946

Internformat


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520			\|a Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2•−and H2O2. It has also been proposed that cancer cells increase glucose and hydroperoxide metabolism to compensate for increased levels of ROS. Given this theoretical construct, it is reasonable to propose that forcing cancer cells to use mitochondrial oxidative metabolism by feeding ketogenic diets that are high in fats and low in glucose and other carbohydrates, would selectively cause metabolic oxidative stress in cancer versus normal cells. Increased metabolic oxidative stress in cancer cells would in turn be predicted to selectively sensitize cancer cells to conventional radiation and chemotherapies. This review summarizes the evidence supporting the hypothesis that ketogenic diets may be safely used as an adjuvant therapy to conventional radiation and chemotherapies and discusses the proposed mechanisms by which ketogenic diets may enhance cancer cell therapeutic responses.
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allfields	10.1016/j.redox.2014.08.002 doi (DE-627)DOAJ035338946 (DE-599)DOAJb33c13805b3e4342821a2e82435b3589 DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Bryan G. Allen verfasserin aut Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2•−and H2O2. It has also been proposed that cancer cells increase glucose and hydroperoxide metabolism to compensate for increased levels of ROS. Given this theoretical construct, it is reasonable to propose that forcing cancer cells to use mitochondrial oxidative metabolism by feeding ketogenic diets that are high in fats and low in glucose and other carbohydrates, would selectively cause metabolic oxidative stress in cancer versus normal cells. Increased metabolic oxidative stress in cancer cells would in turn be predicted to selectively sensitize cancer cells to conventional radiation and chemotherapies. This review summarizes the evidence supporting the hypothesis that ketogenic diets may be safely used as an adjuvant therapy to conventional radiation and chemotherapies and discusses the proposed mechanisms by which ketogenic diets may enhance cancer cell therapeutic responses. Ketogenic diet Oxidative stress Cancer therapy Medicine (General) Biology (General) Sudershan K. Bhatia verfasserin aut Carryn M. Anderson verfasserin aut Julie M. Eichenberger-Gilmore verfasserin aut Zita A. Sibenaller verfasserin aut Kranti A. Mapuskar verfasserin aut Joshua D. Schoenfeld verfasserin aut John M. Buatti verfasserin aut Douglas R. Spitz verfasserin aut Melissa A. Fath verfasserin aut In Redox Biology Elsevier, 2013 2(2014), C, Seite 963-970 (DE-627)735687307 (DE-600)2701011-9 22132317 nnns volume:2 year:2014 number:C pages:963-970 https://doi.org/10.1016/j.redox.2014.08.002 kostenfrei https://doaj.org/article/b33c13805b3e4342821a2e82435b3589 kostenfrei http://www.sciencedirect.com/science/article/pii/S2213231714000925 kostenfrei https://doaj.org/toc/2213-2317 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 2 2014 C 963-970
spelling	10.1016/j.redox.2014.08.002 doi (DE-627)DOAJ035338946 (DE-599)DOAJb33c13805b3e4342821a2e82435b3589 DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Bryan G. Allen verfasserin aut Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2•−and H2O2. It has also been proposed that cancer cells increase glucose and hydroperoxide metabolism to compensate for increased levels of ROS. Given this theoretical construct, it is reasonable to propose that forcing cancer cells to use mitochondrial oxidative metabolism by feeding ketogenic diets that are high in fats and low in glucose and other carbohydrates, would selectively cause metabolic oxidative stress in cancer versus normal cells. Increased metabolic oxidative stress in cancer cells would in turn be predicted to selectively sensitize cancer cells to conventional radiation and chemotherapies. This review summarizes the evidence supporting the hypothesis that ketogenic diets may be safely used as an adjuvant therapy to conventional radiation and chemotherapies and discusses the proposed mechanisms by which ketogenic diets may enhance cancer cell therapeutic responses. Ketogenic diet Oxidative stress Cancer therapy Medicine (General) Biology (General) Sudershan K. Bhatia verfasserin aut Carryn M. Anderson verfasserin aut Julie M. Eichenberger-Gilmore verfasserin aut Zita A. Sibenaller verfasserin aut Kranti A. Mapuskar verfasserin aut Joshua D. Schoenfeld verfasserin aut John M. Buatti verfasserin aut Douglas R. Spitz verfasserin aut Melissa A. Fath verfasserin aut In Redox Biology Elsevier, 2013 2(2014), C, Seite 963-970 (DE-627)735687307 (DE-600)2701011-9 22132317 nnns volume:2 year:2014 number:C pages:963-970 https://doi.org/10.1016/j.redox.2014.08.002 kostenfrei https://doaj.org/article/b33c13805b3e4342821a2e82435b3589 kostenfrei http://www.sciencedirect.com/science/article/pii/S2213231714000925 kostenfrei https://doaj.org/toc/2213-2317 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 2 2014 C 963-970
allfields_unstemmed	10.1016/j.redox.2014.08.002 doi (DE-627)DOAJ035338946 (DE-599)DOAJb33c13805b3e4342821a2e82435b3589 DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Bryan G. Allen verfasserin aut Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2•−and H2O2. It has also been proposed that cancer cells increase glucose and hydroperoxide metabolism to compensate for increased levels of ROS. Given this theoretical construct, it is reasonable to propose that forcing cancer cells to use mitochondrial oxidative metabolism by feeding ketogenic diets that are high in fats and low in glucose and other carbohydrates, would selectively cause metabolic oxidative stress in cancer versus normal cells. Increased metabolic oxidative stress in cancer cells would in turn be predicted to selectively sensitize cancer cells to conventional radiation and chemotherapies. This review summarizes the evidence supporting the hypothesis that ketogenic diets may be safely used as an adjuvant therapy to conventional radiation and chemotherapies and discusses the proposed mechanisms by which ketogenic diets may enhance cancer cell therapeutic responses. Ketogenic diet Oxidative stress Cancer therapy Medicine (General) Biology (General) Sudershan K. Bhatia verfasserin aut Carryn M. Anderson verfasserin aut Julie M. Eichenberger-Gilmore verfasserin aut Zita A. Sibenaller verfasserin aut Kranti A. Mapuskar verfasserin aut Joshua D. Schoenfeld verfasserin aut John M. Buatti verfasserin aut Douglas R. Spitz verfasserin aut Melissa A. Fath verfasserin aut In Redox Biology Elsevier, 2013 2(2014), C, Seite 963-970 (DE-627)735687307 (DE-600)2701011-9 22132317 nnns volume:2 year:2014 number:C pages:963-970 https://doi.org/10.1016/j.redox.2014.08.002 kostenfrei https://doaj.org/article/b33c13805b3e4342821a2e82435b3589 kostenfrei http://www.sciencedirect.com/science/article/pii/S2213231714000925 kostenfrei https://doaj.org/toc/2213-2317 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 2 2014 C 963-970
allfieldsGer	10.1016/j.redox.2014.08.002 doi (DE-627)DOAJ035338946 (DE-599)DOAJb33c13805b3e4342821a2e82435b3589 DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Bryan G. Allen verfasserin aut Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2•−and H2O2. It has also been proposed that cancer cells increase glucose and hydroperoxide metabolism to compensate for increased levels of ROS. Given this theoretical construct, it is reasonable to propose that forcing cancer cells to use mitochondrial oxidative metabolism by feeding ketogenic diets that are high in fats and low in glucose and other carbohydrates, would selectively cause metabolic oxidative stress in cancer versus normal cells. Increased metabolic oxidative stress in cancer cells would in turn be predicted to selectively sensitize cancer cells to conventional radiation and chemotherapies. This review summarizes the evidence supporting the hypothesis that ketogenic diets may be safely used as an adjuvant therapy to conventional radiation and chemotherapies and discusses the proposed mechanisms by which ketogenic diets may enhance cancer cell therapeutic responses. Ketogenic diet Oxidative stress Cancer therapy Medicine (General) Biology (General) Sudershan K. Bhatia verfasserin aut Carryn M. Anderson verfasserin aut Julie M. Eichenberger-Gilmore verfasserin aut Zita A. Sibenaller verfasserin aut Kranti A. Mapuskar verfasserin aut Joshua D. Schoenfeld verfasserin aut John M. Buatti verfasserin aut Douglas R. Spitz verfasserin aut Melissa A. Fath verfasserin aut In Redox Biology Elsevier, 2013 2(2014), C, Seite 963-970 (DE-627)735687307 (DE-600)2701011-9 22132317 nnns volume:2 year:2014 number:C pages:963-970 https://doi.org/10.1016/j.redox.2014.08.002 kostenfrei https://doaj.org/article/b33c13805b3e4342821a2e82435b3589 kostenfrei http://www.sciencedirect.com/science/article/pii/S2213231714000925 kostenfrei https://doaj.org/toc/2213-2317 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 2 2014 C 963-970
allfieldsSound	10.1016/j.redox.2014.08.002 doi (DE-627)DOAJ035338946 (DE-599)DOAJb33c13805b3e4342821a2e82435b3589 DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Bryan G. Allen verfasserin aut Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2•−and H2O2. It has also been proposed that cancer cells increase glucose and hydroperoxide metabolism to compensate for increased levels of ROS. Given this theoretical construct, it is reasonable to propose that forcing cancer cells to use mitochondrial oxidative metabolism by feeding ketogenic diets that are high in fats and low in glucose and other carbohydrates, would selectively cause metabolic oxidative stress in cancer versus normal cells. Increased metabolic oxidative stress in cancer cells would in turn be predicted to selectively sensitize cancer cells to conventional radiation and chemotherapies. This review summarizes the evidence supporting the hypothesis that ketogenic diets may be safely used as an adjuvant therapy to conventional radiation and chemotherapies and discusses the proposed mechanisms by which ketogenic diets may enhance cancer cell therapeutic responses. Ketogenic diet Oxidative stress Cancer therapy Medicine (General) Biology (General) Sudershan K. Bhatia verfasserin aut Carryn M. Anderson verfasserin aut Julie M. Eichenberger-Gilmore verfasserin aut Zita A. Sibenaller verfasserin aut Kranti A. Mapuskar verfasserin aut Joshua D. Schoenfeld verfasserin aut John M. Buatti verfasserin aut Douglas R. Spitz verfasserin aut Melissa A. Fath verfasserin aut In Redox Biology Elsevier, 2013 2(2014), C, Seite 963-970 (DE-627)735687307 (DE-600)2701011-9 22132317 nnns volume:2 year:2014 number:C pages:963-970 https://doi.org/10.1016/j.redox.2014.08.002 kostenfrei https://doaj.org/article/b33c13805b3e4342821a2e82435b3589 kostenfrei http://www.sciencedirect.com/science/article/pii/S2213231714000925 kostenfrei https://doaj.org/toc/2213-2317 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 2 2014 C 963-970
language	English
source	In Redox Biology 2(2014), C, Seite 963-970 volume:2 year:2014 number:C pages:963-970
sourceStr	In Redox Biology 2(2014), C, Seite 963-970 volume:2 year:2014 number:C pages:963-970
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Ketogenic diet Oxidative stress Cancer therapy Medicine (General) Biology (General)
isfreeaccess_bool	true
container_title	Redox Biology
authorswithroles_txt_mv	Bryan G. Allen @@aut@@ Sudershan K. Bhatia @@aut@@ Carryn M. Anderson @@aut@@ Julie M. Eichenberger-Gilmore @@aut@@ Zita A. Sibenaller @@aut@@ Kranti A. Mapuskar @@aut@@ Joshua D. Schoenfeld @@aut@@ John M. Buatti @@aut@@ Douglas R. Spitz @@aut@@ Melissa A. Fath @@aut@@
publishDateDaySort_date	2014-01-01T00:00:00Z
hierarchy_top_id	735687307
id	DOAJ035338946
language_de	englisch
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callnumber-first	R - Medicine
author	Bryan G. Allen
spellingShingle	Bryan G. Allen misc R5-920 misc QH301-705.5 misc Ketogenic diet misc Oxidative stress misc Cancer therapy misc Medicine (General) misc Biology (General) Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism
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topic_title	R5-920 QH301-705.5 Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism Ketogenic diet Oxidative stress Cancer therapy
topic	misc R5-920 misc QH301-705.5 misc Ketogenic diet misc Oxidative stress misc Cancer therapy misc Medicine (General) misc Biology (General)
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title	Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism
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title_full	Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism
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title_sort	ketogenic diets as an adjuvant cancer therapy: history and potential mechanism
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title_auth	Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism
abstract	Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2•−and H2O2. It has also been proposed that cancer cells increase glucose and hydroperoxide metabolism to compensate for increased levels of ROS. Given this theoretical construct, it is reasonable to propose that forcing cancer cells to use mitochondrial oxidative metabolism by feeding ketogenic diets that are high in fats and low in glucose and other carbohydrates, would selectively cause metabolic oxidative stress in cancer versus normal cells. Increased metabolic oxidative stress in cancer cells would in turn be predicted to selectively sensitize cancer cells to conventional radiation and chemotherapies. This review summarizes the evidence supporting the hypothesis that ketogenic diets may be safely used as an adjuvant therapy to conventional radiation and chemotherapies and discusses the proposed mechanisms by which ketogenic diets may enhance cancer cell therapeutic responses.
abstractGer	Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2•−and H2O2. It has also been proposed that cancer cells increase glucose and hydroperoxide metabolism to compensate for increased levels of ROS. Given this theoretical construct, it is reasonable to propose that forcing cancer cells to use mitochondrial oxidative metabolism by feeding ketogenic diets that are high in fats and low in glucose and other carbohydrates, would selectively cause metabolic oxidative stress in cancer versus normal cells. Increased metabolic oxidative stress in cancer cells would in turn be predicted to selectively sensitize cancer cells to conventional radiation and chemotherapies. This review summarizes the evidence supporting the hypothesis that ketogenic diets may be safely used as an adjuvant therapy to conventional radiation and chemotherapies and discusses the proposed mechanisms by which ketogenic diets may enhance cancer cell therapeutic responses.
abstract_unstemmed	Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2•−and H2O2. It has also been proposed that cancer cells increase glucose and hydroperoxide metabolism to compensate for increased levels of ROS. Given this theoretical construct, it is reasonable to propose that forcing cancer cells to use mitochondrial oxidative metabolism by feeding ketogenic diets that are high in fats and low in glucose and other carbohydrates, would selectively cause metabolic oxidative stress in cancer versus normal cells. Increased metabolic oxidative stress in cancer cells would in turn be predicted to selectively sensitize cancer cells to conventional radiation and chemotherapies. This review summarizes the evidence supporting the hypothesis that ketogenic diets may be safely used as an adjuvant therapy to conventional radiation and chemotherapies and discusses the proposed mechanisms by which ketogenic diets may enhance cancer cell therapeutic responses.
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title_short	Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism
url	https://doi.org/10.1016/j.redox.2014.08.002 https://doaj.org/article/b33c13805b3e4342821a2e82435b3589 http://www.sciencedirect.com/science/article/pii/S2213231714000925 https://doaj.org/toc/2213-2317
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Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism

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