PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer

Abstract The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-inter...
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Autor*in:	Glaviano, Antonino [verfasserIn] Foo, Aaron S. C. Lam, Hiu Y. Yap, Kenneth C. H. Jacot, William Jones, Robert H. Eng, Huiyan Nair, Madhumathy G. Makvandi, Pooyan Geoerger, Birgit Kulke, Matthew H. Baird, Richard D. Prabhu, Jyothi S. Carbone, Daniela Pecoraro, Camilla Teh, Daniel B. L. Sethi, Gautam Cavalieri, Vincenzo Lin, Kevin H. Javidi-Sharifi, Nathalie R. Toska, Eneda Davids, Matthew S. Brown, Jennifer R. Diana, Patrizia Stebbing, Justin Fruman, David A. Kumar, Alan P.

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	PI3K/AKT/mTORC pathway Pan PI3K inhibitors Isoform-specific PI3K inhibitors Dual PI3K/mTOR inhibitors AKT inhibitors Allosteric mTOR inhibitors ATP-competitive mTOR inhibitors Bi-steric mTOR inhibitors PDK1 inhibitors Cancer

Anmerkung:	© The Author(s) 2023. corrected publication 2023

Übergeordnetes Werk:	Enthalten in: Molecular cancer - London : Biomed Central, 2002, 22(2023), 1 vom: 18. Aug.
Übergeordnetes Werk:	volume:22 ; year:2023 ; number:1 ; day:18 ; month:08

Links:	Volltext

DOI / URN:	10.1186/s12943-023-01827-6

Katalog-ID:	SPR052795810

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520			\|a Abstract The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-interactions with several other signaling pathways, and dysregulation of signal transduction can predispose to cancer development. The PAM axis is the most frequently activated signaling pathway in human cancer and is often implicated in resistance to anticancer therapies. Dysfunction of components of this pathway such as hyperactivity of PI3K, loss of function of PTEN, and gain-of-function of AKT, are notorious drivers of treatment resistance and disease progression in cancer. In this review we highlight the major dysregulations in the PAM signaling pathway in cancer, and discuss the results of PI3K, AKT and mTOR inhibitors as monotherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy for overcoming treatment resistance. Finally, the major mechanisms of resistance to PAM signaling targeted therapies, including PAM signaling in immunology and immunotherapies are also discussed.
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700	1		\|a Diana, Patrizia \|4 aut
700	1		\|a Stebbing, Justin \|4 aut
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700	1		\|a Kumar, Alan P. \|4 aut
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allfields	10.1186/s12943-023-01827-6 doi (DE-627)SPR052795810 (SPR)s12943-023-01827-6-e DE-627 ger DE-627 rakwb eng Glaviano, Antonino verfasserin aut PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. corrected publication 2023 Abstract The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-interactions with several other signaling pathways, and dysregulation of signal transduction can predispose to cancer development. The PAM axis is the most frequently activated signaling pathway in human cancer and is often implicated in resistance to anticancer therapies. Dysfunction of components of this pathway such as hyperactivity of PI3K, loss of function of PTEN, and gain-of-function of AKT, are notorious drivers of treatment resistance and disease progression in cancer. In this review we highlight the major dysregulations in the PAM signaling pathway in cancer, and discuss the results of PI3K, AKT and mTOR inhibitors as monotherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy for overcoming treatment resistance. Finally, the major mechanisms of resistance to PAM signaling targeted therapies, including PAM signaling in immunology and immunotherapies are also discussed. PI3K/AKT/mTORC pathway (dpeaa)DE-He213 Pan PI3K inhibitors (dpeaa)DE-He213 Isoform-specific PI3K inhibitors (dpeaa)DE-He213 Dual PI3K/mTOR inhibitors (dpeaa)DE-He213 AKT inhibitors (dpeaa)DE-He213 Allosteric mTOR inhibitors (dpeaa)DE-He213 ATP-competitive mTOR inhibitors (dpeaa)DE-He213 Bi-steric mTOR inhibitors (dpeaa)DE-He213 PDK1 inhibitors (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 Foo, Aaron S. C. aut Lam, Hiu Y. aut Yap, Kenneth C. H. aut Jacot, William aut Jones, Robert H. aut Eng, Huiyan aut Nair, Madhumathy G. aut Makvandi, Pooyan aut Geoerger, Birgit aut Kulke, Matthew H. aut Baird, Richard D. aut Prabhu, Jyothi S. aut Carbone, Daniela aut Pecoraro, Camilla aut Teh, Daniel B. L. aut Sethi, Gautam aut Cavalieri, Vincenzo aut Lin, Kevin H. aut Javidi-Sharifi, Nathalie R. aut Toska, Eneda aut Davids, Matthew S. aut Brown, Jennifer R. aut Diana, Patrizia aut Stebbing, Justin aut Fruman, David A. aut Kumar, Alan P. aut Enthalten in Molecular cancer London : Biomed Central, 2002 22(2023), 1 vom: 18. Aug. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:22 year:2023 number:1 day:18 month:08 https://dx.doi.org/10.1186/s12943-023-01827-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2023 1 18 08
spelling	10.1186/s12943-023-01827-6 doi (DE-627)SPR052795810 (SPR)s12943-023-01827-6-e DE-627 ger DE-627 rakwb eng Glaviano, Antonino verfasserin aut PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. corrected publication 2023 Abstract The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-interactions with several other signaling pathways, and dysregulation of signal transduction can predispose to cancer development. The PAM axis is the most frequently activated signaling pathway in human cancer and is often implicated in resistance to anticancer therapies. Dysfunction of components of this pathway such as hyperactivity of PI3K, loss of function of PTEN, and gain-of-function of AKT, are notorious drivers of treatment resistance and disease progression in cancer. In this review we highlight the major dysregulations in the PAM signaling pathway in cancer, and discuss the results of PI3K, AKT and mTOR inhibitors as monotherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy for overcoming treatment resistance. Finally, the major mechanisms of resistance to PAM signaling targeted therapies, including PAM signaling in immunology and immunotherapies are also discussed. PI3K/AKT/mTORC pathway (dpeaa)DE-He213 Pan PI3K inhibitors (dpeaa)DE-He213 Isoform-specific PI3K inhibitors (dpeaa)DE-He213 Dual PI3K/mTOR inhibitors (dpeaa)DE-He213 AKT inhibitors (dpeaa)DE-He213 Allosteric mTOR inhibitors (dpeaa)DE-He213 ATP-competitive mTOR inhibitors (dpeaa)DE-He213 Bi-steric mTOR inhibitors (dpeaa)DE-He213 PDK1 inhibitors (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 Foo, Aaron S. C. aut Lam, Hiu Y. aut Yap, Kenneth C. H. aut Jacot, William aut Jones, Robert H. aut Eng, Huiyan aut Nair, Madhumathy G. aut Makvandi, Pooyan aut Geoerger, Birgit aut Kulke, Matthew H. aut Baird, Richard D. aut Prabhu, Jyothi S. aut Carbone, Daniela aut Pecoraro, Camilla aut Teh, Daniel B. L. aut Sethi, Gautam aut Cavalieri, Vincenzo aut Lin, Kevin H. aut Javidi-Sharifi, Nathalie R. aut Toska, Eneda aut Davids, Matthew S. aut Brown, Jennifer R. aut Diana, Patrizia aut Stebbing, Justin aut Fruman, David A. aut Kumar, Alan P. aut Enthalten in Molecular cancer London : Biomed Central, 2002 22(2023), 1 vom: 18. Aug. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:22 year:2023 number:1 day:18 month:08 https://dx.doi.org/10.1186/s12943-023-01827-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2023 1 18 08
allfields_unstemmed	10.1186/s12943-023-01827-6 doi (DE-627)SPR052795810 (SPR)s12943-023-01827-6-e DE-627 ger DE-627 rakwb eng Glaviano, Antonino verfasserin aut PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. corrected publication 2023 Abstract The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-interactions with several other signaling pathways, and dysregulation of signal transduction can predispose to cancer development. The PAM axis is the most frequently activated signaling pathway in human cancer and is often implicated in resistance to anticancer therapies. Dysfunction of components of this pathway such as hyperactivity of PI3K, loss of function of PTEN, and gain-of-function of AKT, are notorious drivers of treatment resistance and disease progression in cancer. In this review we highlight the major dysregulations in the PAM signaling pathway in cancer, and discuss the results of PI3K, AKT and mTOR inhibitors as monotherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy for overcoming treatment resistance. Finally, the major mechanisms of resistance to PAM signaling targeted therapies, including PAM signaling in immunology and immunotherapies are also discussed. PI3K/AKT/mTORC pathway (dpeaa)DE-He213 Pan PI3K inhibitors (dpeaa)DE-He213 Isoform-specific PI3K inhibitors (dpeaa)DE-He213 Dual PI3K/mTOR inhibitors (dpeaa)DE-He213 AKT inhibitors (dpeaa)DE-He213 Allosteric mTOR inhibitors (dpeaa)DE-He213 ATP-competitive mTOR inhibitors (dpeaa)DE-He213 Bi-steric mTOR inhibitors (dpeaa)DE-He213 PDK1 inhibitors (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 Foo, Aaron S. C. aut Lam, Hiu Y. aut Yap, Kenneth C. H. aut Jacot, William aut Jones, Robert H. aut Eng, Huiyan aut Nair, Madhumathy G. aut Makvandi, Pooyan aut Geoerger, Birgit aut Kulke, Matthew H. aut Baird, Richard D. aut Prabhu, Jyothi S. aut Carbone, Daniela aut Pecoraro, Camilla aut Teh, Daniel B. L. aut Sethi, Gautam aut Cavalieri, Vincenzo aut Lin, Kevin H. aut Javidi-Sharifi, Nathalie R. aut Toska, Eneda aut Davids, Matthew S. aut Brown, Jennifer R. aut Diana, Patrizia aut Stebbing, Justin aut Fruman, David A. aut Kumar, Alan P. aut Enthalten in Molecular cancer London : Biomed Central, 2002 22(2023), 1 vom: 18. Aug. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:22 year:2023 number:1 day:18 month:08 https://dx.doi.org/10.1186/s12943-023-01827-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2023 1 18 08
allfieldsGer	10.1186/s12943-023-01827-6 doi (DE-627)SPR052795810 (SPR)s12943-023-01827-6-e DE-627 ger DE-627 rakwb eng Glaviano, Antonino verfasserin aut PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. corrected publication 2023 Abstract The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-interactions with several other signaling pathways, and dysregulation of signal transduction can predispose to cancer development. The PAM axis is the most frequently activated signaling pathway in human cancer and is often implicated in resistance to anticancer therapies. Dysfunction of components of this pathway such as hyperactivity of PI3K, loss of function of PTEN, and gain-of-function of AKT, are notorious drivers of treatment resistance and disease progression in cancer. In this review we highlight the major dysregulations in the PAM signaling pathway in cancer, and discuss the results of PI3K, AKT and mTOR inhibitors as monotherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy for overcoming treatment resistance. Finally, the major mechanisms of resistance to PAM signaling targeted therapies, including PAM signaling in immunology and immunotherapies are also discussed. PI3K/AKT/mTORC pathway (dpeaa)DE-He213 Pan PI3K inhibitors (dpeaa)DE-He213 Isoform-specific PI3K inhibitors (dpeaa)DE-He213 Dual PI3K/mTOR inhibitors (dpeaa)DE-He213 AKT inhibitors (dpeaa)DE-He213 Allosteric mTOR inhibitors (dpeaa)DE-He213 ATP-competitive mTOR inhibitors (dpeaa)DE-He213 Bi-steric mTOR inhibitors (dpeaa)DE-He213 PDK1 inhibitors (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 Foo, Aaron S. C. aut Lam, Hiu Y. aut Yap, Kenneth C. H. aut Jacot, William aut Jones, Robert H. aut Eng, Huiyan aut Nair, Madhumathy G. aut Makvandi, Pooyan aut Geoerger, Birgit aut Kulke, Matthew H. aut Baird, Richard D. aut Prabhu, Jyothi S. aut Carbone, Daniela aut Pecoraro, Camilla aut Teh, Daniel B. L. aut Sethi, Gautam aut Cavalieri, Vincenzo aut Lin, Kevin H. aut Javidi-Sharifi, Nathalie R. aut Toska, Eneda aut Davids, Matthew S. aut Brown, Jennifer R. aut Diana, Patrizia aut Stebbing, Justin aut Fruman, David A. aut Kumar, Alan P. aut Enthalten in Molecular cancer London : Biomed Central, 2002 22(2023), 1 vom: 18. Aug. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:22 year:2023 number:1 day:18 month:08 https://dx.doi.org/10.1186/s12943-023-01827-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2023 1 18 08
allfieldsSound	10.1186/s12943-023-01827-6 doi (DE-627)SPR052795810 (SPR)s12943-023-01827-6-e DE-627 ger DE-627 rakwb eng Glaviano, Antonino verfasserin aut PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. corrected publication 2023 Abstract The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-interactions with several other signaling pathways, and dysregulation of signal transduction can predispose to cancer development. The PAM axis is the most frequently activated signaling pathway in human cancer and is often implicated in resistance to anticancer therapies. Dysfunction of components of this pathway such as hyperactivity of PI3K, loss of function of PTEN, and gain-of-function of AKT, are notorious drivers of treatment resistance and disease progression in cancer. In this review we highlight the major dysregulations in the PAM signaling pathway in cancer, and discuss the results of PI3K, AKT and mTOR inhibitors as monotherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy for overcoming treatment resistance. Finally, the major mechanisms of resistance to PAM signaling targeted therapies, including PAM signaling in immunology and immunotherapies are also discussed. PI3K/AKT/mTORC pathway (dpeaa)DE-He213 Pan PI3K inhibitors (dpeaa)DE-He213 Isoform-specific PI3K inhibitors (dpeaa)DE-He213 Dual PI3K/mTOR inhibitors (dpeaa)DE-He213 AKT inhibitors (dpeaa)DE-He213 Allosteric mTOR inhibitors (dpeaa)DE-He213 ATP-competitive mTOR inhibitors (dpeaa)DE-He213 Bi-steric mTOR inhibitors (dpeaa)DE-He213 PDK1 inhibitors (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 Foo, Aaron S. C. aut Lam, Hiu Y. aut Yap, Kenneth C. H. aut Jacot, William aut Jones, Robert H. aut Eng, Huiyan aut Nair, Madhumathy G. aut Makvandi, Pooyan aut Geoerger, Birgit aut Kulke, Matthew H. aut Baird, Richard D. aut Prabhu, Jyothi S. aut Carbone, Daniela aut Pecoraro, Camilla aut Teh, Daniel B. L. aut Sethi, Gautam aut Cavalieri, Vincenzo aut Lin, Kevin H. aut Javidi-Sharifi, Nathalie R. aut Toska, Eneda aut Davids, Matthew S. aut Brown, Jennifer R. aut Diana, Patrizia aut Stebbing, Justin aut Fruman, David A. aut Kumar, Alan P. aut Enthalten in Molecular cancer London : Biomed Central, 2002 22(2023), 1 vom: 18. Aug. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:22 year:2023 number:1 day:18 month:08 https://dx.doi.org/10.1186/s12943-023-01827-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2023 1 18 08
language	English
source	Enthalten in Molecular cancer 22(2023), 1 vom: 18. Aug. volume:22 year:2023 number:1 day:18 month:08
sourceStr	Enthalten in Molecular cancer 22(2023), 1 vom: 18. Aug. volume:22 year:2023 number:1 day:18 month:08
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	PI3K/AKT/mTORC pathway Pan PI3K inhibitors Isoform-specific PI3K inhibitors Dual PI3K/mTOR inhibitors AKT inhibitors Allosteric mTOR inhibitors ATP-competitive mTOR inhibitors Bi-steric mTOR inhibitors PDK1 inhibitors Cancer
isfreeaccess_bool	true
container_title	Molecular cancer
authorswithroles_txt_mv	Glaviano, Antonino @@aut@@ Foo, Aaron S. C. @@aut@@ Lam, Hiu Y. @@aut@@ Yap, Kenneth C. H. @@aut@@ Jacot, William @@aut@@ Jones, Robert H. @@aut@@ Eng, Huiyan @@aut@@ Nair, Madhumathy G. @@aut@@ Makvandi, Pooyan @@aut@@ Geoerger, Birgit @@aut@@ Kulke, Matthew H. @@aut@@ Baird, Richard D. @@aut@@ Prabhu, Jyothi S. @@aut@@ Carbone, Daniela @@aut@@ Pecoraro, Camilla @@aut@@ Teh, Daniel B. L. @@aut@@ Sethi, Gautam @@aut@@ Cavalieri, Vincenzo @@aut@@ Lin, Kevin H. @@aut@@ Javidi-Sharifi, Nathalie R. @@aut@@ Toska, Eneda @@aut@@ Davids, Matthew S. @@aut@@ Brown, Jennifer R. @@aut@@ Diana, Patrizia @@aut@@ Stebbing, Justin @@aut@@ Fruman, David A. @@aut@@ Kumar, Alan P. @@aut@@
publishDateDaySort_date	2023-08-18T00:00:00Z
hierarchy_top_id	355987619
id	SPR052795810
language_de	englisch
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author	Glaviano, Antonino
spellingShingle	Glaviano, Antonino misc PI3K/AKT/mTORC pathway misc Pan PI3K inhibitors misc Isoform-specific PI3K inhibitors misc Dual PI3K/mTOR inhibitors misc AKT inhibitors misc Allosteric mTOR inhibitors misc ATP-competitive mTOR inhibitors misc Bi-steric mTOR inhibitors misc PDK1 inhibitors misc Cancer PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer
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topic_title	PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer PI3K/AKT/mTORC pathway (dpeaa)DE-He213 Pan PI3K inhibitors (dpeaa)DE-He213 Isoform-specific PI3K inhibitors (dpeaa)DE-He213 Dual PI3K/mTOR inhibitors (dpeaa)DE-He213 AKT inhibitors (dpeaa)DE-He213 Allosteric mTOR inhibitors (dpeaa)DE-He213 ATP-competitive mTOR inhibitors (dpeaa)DE-He213 Bi-steric mTOR inhibitors (dpeaa)DE-He213 PDK1 inhibitors (dpeaa)DE-He213 Cancer (dpeaa)DE-He213
topic	misc PI3K/AKT/mTORC pathway misc Pan PI3K inhibitors misc Isoform-specific PI3K inhibitors misc Dual PI3K/mTOR inhibitors misc AKT inhibitors misc Allosteric mTOR inhibitors misc ATP-competitive mTOR inhibitors misc Bi-steric mTOR inhibitors misc PDK1 inhibitors misc Cancer
topic_unstemmed	misc PI3K/AKT/mTORC pathway misc Pan PI3K inhibitors misc Isoform-specific PI3K inhibitors misc Dual PI3K/mTOR inhibitors misc AKT inhibitors misc Allosteric mTOR inhibitors misc ATP-competitive mTOR inhibitors misc Bi-steric mTOR inhibitors misc PDK1 inhibitors misc Cancer
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title	PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer
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author_browse	Glaviano, Antonino Foo, Aaron S. C. Lam, Hiu Y. Yap, Kenneth C. H. Jacot, William Jones, Robert H. Eng, Huiyan Nair, Madhumathy G. Makvandi, Pooyan Geoerger, Birgit Kulke, Matthew H. Baird, Richard D. Prabhu, Jyothi S. Carbone, Daniela Pecoraro, Camilla Teh, Daniel B. L. Sethi, Gautam Cavalieri, Vincenzo Lin, Kevin H. Javidi-Sharifi, Nathalie R. Toska, Eneda Davids, Matthew S. Brown, Jennifer R. Diana, Patrizia Stebbing, Justin Fruman, David A. Kumar, Alan P.
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title_sort	pi3k/akt/mtor signaling transduction pathway and targeted therapies in cancer
title_auth	PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer
abstract	Abstract The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-interactions with several other signaling pathways, and dysregulation of signal transduction can predispose to cancer development. The PAM axis is the most frequently activated signaling pathway in human cancer and is often implicated in resistance to anticancer therapies. Dysfunction of components of this pathway such as hyperactivity of PI3K, loss of function of PTEN, and gain-of-function of AKT, are notorious drivers of treatment resistance and disease progression in cancer. In this review we highlight the major dysregulations in the PAM signaling pathway in cancer, and discuss the results of PI3K, AKT and mTOR inhibitors as monotherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy for overcoming treatment resistance. Finally, the major mechanisms of resistance to PAM signaling targeted therapies, including PAM signaling in immunology and immunotherapies are also discussed. © The Author(s) 2023. corrected publication 2023
abstractGer	Abstract The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-interactions with several other signaling pathways, and dysregulation of signal transduction can predispose to cancer development. The PAM axis is the most frequently activated signaling pathway in human cancer and is often implicated in resistance to anticancer therapies. Dysfunction of components of this pathway such as hyperactivity of PI3K, loss of function of PTEN, and gain-of-function of AKT, are notorious drivers of treatment resistance and disease progression in cancer. In this review we highlight the major dysregulations in the PAM signaling pathway in cancer, and discuss the results of PI3K, AKT and mTOR inhibitors as monotherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy for overcoming treatment resistance. Finally, the major mechanisms of resistance to PAM signaling targeted therapies, including PAM signaling in immunology and immunotherapies are also discussed. © The Author(s) 2023. corrected publication 2023
abstract_unstemmed	Abstract The PI3K/AKT/mTOR (PAM) signaling pathway is a highly conserved signal transduction network in eukaryotic cells that promotes cell survival, cell growth, and cell cycle progression. Growth factor signalling to transcription factors in the PAM axis is highly regulated by multiple cross-interactions with several other signaling pathways, and dysregulation of signal transduction can predispose to cancer development. The PAM axis is the most frequently activated signaling pathway in human cancer and is often implicated in resistance to anticancer therapies. Dysfunction of components of this pathway such as hyperactivity of PI3K, loss of function of PTEN, and gain-of-function of AKT, are notorious drivers of treatment resistance and disease progression in cancer. In this review we highlight the major dysregulations in the PAM signaling pathway in cancer, and discuss the results of PI3K, AKT and mTOR inhibitors as monotherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy for overcoming treatment resistance. Finally, the major mechanisms of resistance to PAM signaling targeted therapies, including PAM signaling in immunology and immunotherapies are also discussed. © The Author(s) 2023. corrected publication 2023
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title_short	PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer
url	https://dx.doi.org/10.1186/s12943-023-01827-6
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author2	Foo, Aaron S. C. Lam, Hiu Y. Yap, Kenneth C. H. Jacot, William Jones, Robert H. Eng, Huiyan Nair, Madhumathy G. Makvandi, Pooyan Geoerger, Birgit Kulke, Matthew H. Baird, Richard D. Prabhu, Jyothi S. Carbone, Daniela Pecoraro, Camilla Teh, Daniel B. L. Sethi, Gautam Cavalieri, Vincenzo Lin, Kevin H. Javidi-Sharifi, Nathalie R. Toska, Eneda Davids, Matthew S. Brown, Jennifer R. Diana, Patrizia Stebbing, Justin Fruman, David A. Kumar, Alan P.
author2Str	Foo, Aaron S. C. Lam, Hiu Y. Yap, Kenneth C. H. Jacot, William Jones, Robert H. Eng, Huiyan Nair, Madhumathy G. Makvandi, Pooyan Geoerger, Birgit Kulke, Matthew H. Baird, Richard D. Prabhu, Jyothi S. Carbone, Daniela Pecoraro, Camilla Teh, Daniel B. L. Sethi, Gautam Cavalieri, Vincenzo Lin, Kevin H. Javidi-Sharifi, Nathalie R. Toska, Eneda Davids, Matthew S. Brown, Jennifer R. Diana, Patrizia Stebbing, Justin Fruman, David A. Kumar, Alan P.
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PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer

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