Targeting RAGE prevents muscle wasting and prolongs survival in cancer cachexia
Background Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer‐associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major cli...
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| Published in | Journal of cachexia, sarcopenia and muscle Vol. 11; no. 4; pp. 929 - 946 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Germany
John Wiley & Sons, Inc
01.08.2020
Wiley Open Access/Springer Verlag John Wiley and Sons Inc Wiley |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Background
Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer‐associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major clinical feature of cachexia, leading to weight loss, dampening patients' quality of life, and reducing patients' response to anticancer therapy. RAGE (receptor for advanced glycation end‐products) is a multiligand receptor of the immunoglobulin superfamily and a mediator of muscle regeneration, inflammation, and cancer.
Methods
By using murine models consisting in the injection of colon 26 murine adenocarcinoma (C26‐ADK) or Lewis lung carcinoma (LLC) cells in BALB/c and C57BL/6 or Ager−/− (RAGE‐null) mice, respectively, we investigated the involvement of RAGE signalling in the main features of cancer cachexia, including the inflammatory state. In vitro experiments were performed using myotubes derived from C2C12 myoblasts or primary myoblasts isolated from C57BL/6 wild type and Ager−/− mice treated with the RAGE ligand, S100B (S100 calcium‐binding protein B), TNF (tumor necrosis factor)α±IFN (interferon) γ, and tumour cell‐ or masses‐conditioned media to analyse hallmarks of muscle atrophy. Finally, muscles of wild type and Ager−/− mice were injected with TNFα/IFNγ or S100B in a tumour‐free environment.
Results
We demonstrate that RAGE is determinant to activate signalling pathways leading to muscle protein degradation in the presence of proinflammatory cytokines and/or tumour‐derived cachexia‐inducing factors. We identify the RAGE ligand, S100B, as a novel factor able to induce muscle atrophy per se via a p38 MAPK (p38 mitogen‐activated protein kinase)/myogenin axis and STAT3 (signal transducer and activator of transcription 3)‐dependent MyoD (myoblast determination protein 1) degradation. Lastly, we found that in cancer conditions, an increase in serum levels of tumour‐derived S100B and HMGB1 (high mobility group box 1) occurs leading to chronic activation/overexpression of RAGE, which induces hallmarks of cancer cachexia (i.e. muscle wasting, systemic inflammation, and release of tumour‐derived pro‐cachectic factors). Absence of RAGE in mice translates into reduced serum levels of cachexia‐inducing factors, delayed loss of muscle mass and strength, reduced tumour progression, and increased survival.
Conclusions
RAGE is a molecular determinant in inducing the hallmarks of cancer cachexia, and molecular targeting of RAGE might represent a therapeutic strategy to prevent or counteract the cachectic syndrome. |
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| AbstractList | Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer-associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major clinical feature of cachexia, leading to weight loss, dampening patients' quality of life, and reducing patients' response to anticancer therapy. RAGE (receptor for advanced glycation end-products) is a multiligand receptor of the immunoglobulin superfamily and a mediator of muscle regeneration, inflammation, and cancer.
By using murine models consisting in the injection of colon 26 murine adenocarcinoma (C26-ADK) or Lewis lung carcinoma (LLC) cells in BALB/c and C57BL/6 or Ager
(RAGE-null) mice, respectively, we investigated the involvement of RAGE signalling in the main features of cancer cachexia, including the inflammatory state. In vitro experiments were performed using myotubes derived from C2C12 myoblasts or primary myoblasts isolated from C57BL/6 wild type and Ager
mice treated with the RAGE ligand, S100B (S100 calcium-binding protein B), TNF (tumor necrosis factor)α±IFN (interferon) γ, and tumour cell- or masses-conditioned media to analyse hallmarks of muscle atrophy. Finally, muscles of wild type and Ager
mice were injected with TNFα/IFNγ or S100B in a tumour-free environment.
We demonstrate that RAGE is determinant to activate signalling pathways leading to muscle protein degradation in the presence of proinflammatory cytokines and/or tumour-derived cachexia-inducing factors. We identify the RAGE ligand, S100B, as a novel factor able to induce muscle atrophy per se via a p38 MAPK (p38 mitogen-activated protein kinase)/myogenin axis and STAT3 (signal transducer and activator of transcription 3)-dependent MyoD (myoblast determination protein 1) degradation. Lastly, we found that in cancer conditions, an increase in serum levels of tumour-derived S100B and HMGB1 (high mobility group box 1) occurs leading to chronic activation/overexpression of RAGE, which induces hallmarks of cancer cachexia (i.e. muscle wasting, systemic inflammation, and release of tumour-derived pro-cachectic factors). Absence of RAGE in mice translates into reduced serum levels of cachexia-inducing factors, delayed loss of muscle mass and strength, reduced tumour progression, and increased survival.
RAGE is a molecular determinant in inducing the hallmarks of cancer cachexia, and molecular targeting of RAGE might represent a therapeutic strategy to prevent or counteract the cachectic syndrome. Background Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer‐associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major clinical feature of cachexia, leading to weight loss, dampening patients' quality of life, and reducing patients' response to anticancer therapy. RAGE (receptor for advanced glycation end‐products) is a multiligand receptor of the immunoglobulin superfamily and a mediator of muscle regeneration, inflammation, and cancer. Methods By using murine models consisting in the injection of colon 26 murine adenocarcinoma (C26‐ADK) or Lewis lung carcinoma (LLC) cells in BALB/c and C57BL/6 or Ager−/− (RAGE‐null) mice, respectively, we investigated the involvement of RAGE signalling in the main features of cancer cachexia, including the inflammatory state. In vitro experiments were performed using myotubes derived from C2C12 myoblasts or primary myoblasts isolated from C57BL/6 wild type and Ager−/− mice treated with the RAGE ligand, S100B (S100 calcium‐binding protein B), TNF (tumor necrosis factor)α±IFN (interferon) γ, and tumour cell‐ or masses‐conditioned media to analyse hallmarks of muscle atrophy. Finally, muscles of wild type and Ager−/− mice were injected with TNFα/IFNγ or S100B in a tumour‐free environment. Results We demonstrate that RAGE is determinant to activate signalling pathways leading to muscle protein degradation in the presence of proinflammatory cytokines and/or tumour‐derived cachexia‐inducing factors. We identify the RAGE ligand, S100B, as a novel factor able to induce muscle atrophy per se via a p38 MAPK (p38 mitogen‐activated protein kinase)/myogenin axis and STAT3 (signal transducer and activator of transcription 3)‐dependent MyoD (myoblast determination protein 1) degradation. Lastly, we found that in cancer conditions, an increase in serum levels of tumour‐derived S100B and HMGB1 (high mobility group box 1) occurs leading to chronic activation/overexpression of RAGE, which induces hallmarks of cancer cachexia (i.e. muscle wasting, systemic inflammation, and release of tumour‐derived pro‐cachectic factors). Absence of RAGE in mice translates into reduced serum levels of cachexia‐inducing factors, delayed loss of muscle mass and strength, reduced tumour progression, and increased survival. Conclusions RAGE is a molecular determinant in inducing the hallmarks of cancer cachexia, and molecular targeting of RAGE might represent a therapeutic strategy to prevent or counteract the cachectic syndrome. BackgroundCachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer‐associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major clinical feature of cachexia, leading to weight loss, dampening patients' quality of life, and reducing patients' response to anticancer therapy. RAGE (receptor for advanced glycation end‐products) is a multiligand receptor of the immunoglobulin superfamily and a mediator of muscle regeneration, inflammation, and cancer.MethodsBy using murine models consisting in the injection of colon 26 murine adenocarcinoma (C26‐ADK) or Lewis lung carcinoma (LLC) cells in BALB/c and C57BL/6 or Ager−/− (RAGE‐null) mice, respectively, we investigated the involvement of RAGE signalling in the main features of cancer cachexia, including the inflammatory state. In vitro experiments were performed using myotubes derived from C2C12 myoblasts or primary myoblasts isolated from C57BL/6 wild type and Ager−/− mice treated with the RAGE ligand, S100B (S100 calcium‐binding protein B), TNF (tumor necrosis factor)α±IFN (interferon) γ, and tumour cell‐ or masses‐conditioned media to analyse hallmarks of muscle atrophy. Finally, muscles of wild type and Ager−/− mice were injected with TNFα/IFNγ or S100B in a tumour‐free environment.ResultsWe demonstrate that RAGE is determinant to activate signalling pathways leading to muscle protein degradation in the presence of proinflammatory cytokines and/or tumour‐derived cachexia‐inducing factors. We identify the RAGE ligand, S100B, as a novel factor able to induce muscle atrophy per se via a p38 MAPK (p38 mitogen‐activated protein kinase)/myogenin axis and STAT3 (signal transducer and activator of transcription 3)‐dependent MyoD (myoblast determination protein 1) degradation. Lastly, we found that in cancer conditions, an increase in serum levels of tumour‐derived S100B and HMGB1 (high mobility group box 1) occurs leading to chronic activation/overexpression of RAGE, which induces hallmarks of cancer cachexia (i.e. muscle wasting, systemic inflammation, and release of tumour‐derived pro‐cachectic factors). Absence of RAGE in mice translates into reduced serum levels of cachexia‐inducing factors, delayed loss of muscle mass and strength, reduced tumour progression, and increased survival.ConclusionsRAGE is a molecular determinant in inducing the hallmarks of cancer cachexia, and molecular targeting of RAGE might represent a therapeutic strategy to prevent or counteract the cachectic syndrome. Background Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer-associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major clinical feature of cachexia, leading to weight loss, dampening patients' quality of life, and reducing patients' response to anticancer therapy. RAGE (receptor for advanced glycation end-products) is a multiligand receptor of the immunoglobulin superfamily and a mediator of muscle regeneration, inflammation, and cancer. Methods By using murine models consisting in the injection of colon 26 murine adenocarcinoma (C26-ADK) or Lewis lung carcinoma (LLC) cells in BALB/c and C57BL/6 or Ager À/À (RAGE-null) mice, respectively, we investigated the involvement of RAGE signalling in the main features of cancer cachexia, including the inflammatory state. In vitro experiments were performed using myotubes derived from C2C12 myoblasts or primary myoblasts isolated from C57BL/6 wild type and Ager À/À mice treated with the RAGE ligand, S100B (S100 calcium-binding protein B), TNF (tumor necrosis factor)α±IFN (interferon) γ, and tumour cell-or masses-conditioned media to analyse hallmarks of muscle atrophy. Finally, muscles of wild type and Ager À/ À mice were injected with TNFα/IFNγ or S100B in a tumour-free environment. Results We demonstrate that RAGE is determinant to activate signalling pathways leading to muscle protein degradation in the presence of proinflammatory cytokines and/or tumour-derived cachexia-inducing factors. We identify the RAGE ligand, S100B, as a novel factor able to induce muscle atrophy per se via a p38 MAPK (p38 mitogen-activated protein kinase)/myogenin axis and STAT3 (signal transducer and activator of transcription 3)-dependent MyoD (myoblast determination protein 1) degradation. Lastly, we found that in cancer conditions, an increase in serum levels of tumour-derived S100B and HMGB1 (high mobility group box 1) occurs leading to chronic activation/overexpression of RAGE, which induces hallmarks of cancer cachexia (i.e. muscle wasting, systemic inflammation, and release of tumour-derived pro-cachectic factors). Absence of RAGE in mice translates into reduced serum levels of cachexia-inducing factors, delayed loss of muscle mass and strength, reduced tumour progression, and increased survival. Conclusions RAGE is a molecular determinant in inducing the hallmarks of cancer cachexia, and molecular targeting of RAGE might represent a therapeutic strategy to prevent or counteract the cachectic syndrome. Abstract Background Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer‐associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major clinical feature of cachexia, leading to weight loss, dampening patients' quality of life, and reducing patients' response to anticancer therapy. RAGE (receptor for advanced glycation end‐products) is a multiligand receptor of the immunoglobulin superfamily and a mediator of muscle regeneration, inflammation, and cancer. Methods By using murine models consisting in the injection of colon 26 murine adenocarcinoma (C26‐ADK) or Lewis lung carcinoma (LLC) cells in BALB/c and C57BL/6 or Ager−/− (RAGE‐null) mice, respectively, we investigated the involvement of RAGE signalling in the main features of cancer cachexia, including the inflammatory state. In vitro experiments were performed using myotubes derived from C2C12 myoblasts or primary myoblasts isolated from C57BL/6 wild type and Ager−/− mice treated with the RAGE ligand, S100B (S100 calcium‐binding protein B), TNF (tumor necrosis factor)α±IFN (interferon) γ, and tumour cell‐ or masses‐conditioned media to analyse hallmarks of muscle atrophy. Finally, muscles of wild type and Ager−/− mice were injected with TNFα/IFNγ or S100B in a tumour‐free environment. Results We demonstrate that RAGE is determinant to activate signalling pathways leading to muscle protein degradation in the presence of proinflammatory cytokines and/or tumour‐derived cachexia‐inducing factors. We identify the RAGE ligand, S100B, as a novel factor able to induce muscle atrophy per se via a p38 MAPK (p38 mitogen‐activated protein kinase)/myogenin axis and STAT3 (signal transducer and activator of transcription 3)‐dependent MyoD (myoblast determination protein 1) degradation. Lastly, we found that in cancer conditions, an increase in serum levels of tumour‐derived S100B and HMGB1 (high mobility group box 1) occurs leading to chronic activation/overexpression of RAGE, which induces hallmarks of cancer cachexia (i.e. muscle wasting, systemic inflammation, and release of tumour‐derived pro‐cachectic factors). Absence of RAGE in mice translates into reduced serum levels of cachexia‐inducing factors, delayed loss of muscle mass and strength, reduced tumour progression, and increased survival. Conclusions RAGE is a molecular determinant in inducing the hallmarks of cancer cachexia, and molecular targeting of RAGE might represent a therapeutic strategy to prevent or counteract the cachectic syndrome. Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer-associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major clinical feature of cachexia, leading to weight loss, dampening patients' quality of life, and reducing patients' response to anticancer therapy. RAGE (receptor for advanced glycation end-products) is a multiligand receptor of the immunoglobulin superfamily and a mediator of muscle regeneration, inflammation, and cancer.BACKGROUNDCachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer-associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major clinical feature of cachexia, leading to weight loss, dampening patients' quality of life, and reducing patients' response to anticancer therapy. RAGE (receptor for advanced glycation end-products) is a multiligand receptor of the immunoglobulin superfamily and a mediator of muscle regeneration, inflammation, and cancer.By using murine models consisting in the injection of colon 26 murine adenocarcinoma (C26-ADK) or Lewis lung carcinoma (LLC) cells in BALB/c and C57BL/6 or Ager-/- (RAGE-null) mice, respectively, we investigated the involvement of RAGE signalling in the main features of cancer cachexia, including the inflammatory state. In vitro experiments were performed using myotubes derived from C2C12 myoblasts or primary myoblasts isolated from C57BL/6 wild type and Ager-/- mice treated with the RAGE ligand, S100B (S100 calcium-binding protein B), TNF (tumor necrosis factor)α±IFN (interferon) γ, and tumour cell- or masses-conditioned media to analyse hallmarks of muscle atrophy. Finally, muscles of wild type and Ager-/- mice were injected with TNFα/IFNγ or S100B in a tumour-free environment.METHODSBy using murine models consisting in the injection of colon 26 murine adenocarcinoma (C26-ADK) or Lewis lung carcinoma (LLC) cells in BALB/c and C57BL/6 or Ager-/- (RAGE-null) mice, respectively, we investigated the involvement of RAGE signalling in the main features of cancer cachexia, including the inflammatory state. In vitro experiments were performed using myotubes derived from C2C12 myoblasts or primary myoblasts isolated from C57BL/6 wild type and Ager-/- mice treated with the RAGE ligand, S100B (S100 calcium-binding protein B), TNF (tumor necrosis factor)α±IFN (interferon) γ, and tumour cell- or masses-conditioned media to analyse hallmarks of muscle atrophy. Finally, muscles of wild type and Ager-/- mice were injected with TNFα/IFNγ or S100B in a tumour-free environment.We demonstrate that RAGE is determinant to activate signalling pathways leading to muscle protein degradation in the presence of proinflammatory cytokines and/or tumour-derived cachexia-inducing factors. We identify the RAGE ligand, S100B, as a novel factor able to induce muscle atrophy per se via a p38 MAPK (p38 mitogen-activated protein kinase)/myogenin axis and STAT3 (signal transducer and activator of transcription 3)-dependent MyoD (myoblast determination protein 1) degradation. Lastly, we found that in cancer conditions, an increase in serum levels of tumour-derived S100B and HMGB1 (high mobility group box 1) occurs leading to chronic activation/overexpression of RAGE, which induces hallmarks of cancer cachexia (i.e. muscle wasting, systemic inflammation, and release of tumour-derived pro-cachectic factors). Absence of RAGE in mice translates into reduced serum levels of cachexia-inducing factors, delayed loss of muscle mass and strength, reduced tumour progression, and increased survival.RESULTSWe demonstrate that RAGE is determinant to activate signalling pathways leading to muscle protein degradation in the presence of proinflammatory cytokines and/or tumour-derived cachexia-inducing factors. We identify the RAGE ligand, S100B, as a novel factor able to induce muscle atrophy per se via a p38 MAPK (p38 mitogen-activated protein kinase)/myogenin axis and STAT3 (signal transducer and activator of transcription 3)-dependent MyoD (myoblast determination protein 1) degradation. Lastly, we found that in cancer conditions, an increase in serum levels of tumour-derived S100B and HMGB1 (high mobility group box 1) occurs leading to chronic activation/overexpression of RAGE, which induces hallmarks of cancer cachexia (i.e. muscle wasting, systemic inflammation, and release of tumour-derived pro-cachectic factors). Absence of RAGE in mice translates into reduced serum levels of cachexia-inducing factors, delayed loss of muscle mass and strength, reduced tumour progression, and increased survival.RAGE is a molecular determinant in inducing the hallmarks of cancer cachexia, and molecular targeting of RAGE might represent a therapeutic strategy to prevent or counteract the cachectic syndrome.CONCLUSIONSRAGE is a molecular determinant in inducing the hallmarks of cancer cachexia, and molecular targeting of RAGE might represent a therapeutic strategy to prevent or counteract the cachectic syndrome. |
| Author | Sorci, Guglielmo Salvadori, Laura Sagheddu, Roberta Chiappalupi, Sara Romani, Luigina Coletti, Dario Riuzzi, Francesca Vukasinovic, Aleksandra Renga, Giorgia Donato, Rosario |
| AuthorAffiliation | 3 CNRS UMR 8256, INSERM ERL U1164, Biological Adaptation and Aging B2A Sorbonne Université Paris France 4 Interuniversity Institute of Myology Perugia Italy 2 Department of Anatomical, Histological, Forensic and Orthopedic Sciences Sapienza University of Rome Rome Italy 5 Centro Universitario di Ricerca sulla Genomica Funzionale University of Perugia Perugia Italy 1 Department of Experimental Medicine University of Perugia Perugia Italy |
| AuthorAffiliation_xml | – name: 3 CNRS UMR 8256, INSERM ERL U1164, Biological Adaptation and Aging B2A Sorbonne Université Paris France – name: 1 Department of Experimental Medicine University of Perugia Perugia Italy – name: 5 Centro Universitario di Ricerca sulla Genomica Funzionale University of Perugia Perugia Italy – name: 4 Interuniversity Institute of Myology Perugia Italy – name: 2 Department of Anatomical, Histological, Forensic and Orthopedic Sciences Sapienza University of Rome Rome Italy |
| Author_xml | – sequence: 1 givenname: Sara orcidid: 0000-0001-8377-0665 surname: Chiappalupi fullname: Chiappalupi, Sara organization: Interuniversity Institute of Myology – sequence: 2 givenname: Guglielmo orcidid: 0000-0002-1973-9679 surname: Sorci fullname: Sorci, Guglielmo organization: University of Perugia – sequence: 3 givenname: Aleksandra orcidid: 0000-0001-8275-0099 surname: Vukasinovic fullname: Vukasinovic, Aleksandra organization: Interuniversity Institute of Myology – sequence: 4 givenname: Laura orcidid: 0000-0001-9409-2046 surname: Salvadori fullname: Salvadori, Laura organization: Interuniversity Institute of Myology – sequence: 5 givenname: Roberta surname: Sagheddu fullname: Sagheddu, Roberta organization: Interuniversity Institute of Myology – sequence: 6 givenname: Dario orcidid: 0000-0001-7373-1953 surname: Coletti fullname: Coletti, Dario organization: Sorbonne Université – sequence: 7 givenname: Giorgia orcidid: 0000-0002-9762-6493 surname: Renga fullname: Renga, Giorgia organization: University of Perugia – sequence: 8 givenname: Luigina orcidid: 0000-0002-1356-525X surname: Romani fullname: Romani, Luigina organization: University of Perugia – sequence: 9 givenname: Rosario orcidid: 0000-0002-9608-4506 surname: Donato fullname: Donato, Rosario email: rosario.donato@unipg.it organization: University of Perugia – sequence: 10 givenname: Francesca orcidid: 0000-0001-7908-3379 surname: Riuzzi fullname: Riuzzi, Francesca email: francesca.riuzzi@unipg.it organization: Interuniversity Institute of Myology |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32159297$$D View this record in MEDLINE/PubMed https://hal.sorbonne-universite.fr/hal-03714899$$DView record in HAL |
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| ContentType | Journal Article |
| Copyright | 2020 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders 2020 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders. 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Distributed under a Creative Commons Attribution 4.0 International License |
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| References | 2017; 7 2015; 15 2013; 4 2012; 287 2011; 2 2013; 1 2000; 4 2019; 10 2004; 24 2015; 54 2010; 143 2016; 10 2013; 123 2016; 54 2011; 30 2014; 192 2011; 4 2012; 125 2011; 3 2018; 49 2018; 27 2017; 9 2018; 69 2017; 117 1993; 364 2016; 5 2018; 9 2014; 127 2016; 6 1833; 2013 2005; 19 2004; 114 2018; 4 2004; 113 2018; 215 2013; 13 2011; 91 2014; 14 2014; 35 2016; 238 2014; 19 2009; 185 2014; 74 2012; 21 2013; 190 2016; 22 e_1_2_8_28_1 e_1_2_8_24_1 e_1_2_8_47_1 e_1_2_8_26_1 e_1_2_8_49_1 e_1_2_8_3_1 e_1_2_8_5_1 e_1_2_8_7_1 e_1_2_8_9_1 e_1_2_8_20_1 e_1_2_8_43_1 e_1_2_8_22_1 e_1_2_8_45_1 e_1_2_8_41_1 e_1_2_8_17_1 e_1_2_8_19_1 e_1_2_8_13_1 e_1_2_8_36_1 e_1_2_8_15_1 e_1_2_8_38_1 e_1_2_8_32_1 e_1_2_8_34_1 e_1_2_8_30_1 e_1_2_8_29_1 e_1_2_8_25_1 e_1_2_8_46_1 e_1_2_8_27_1 Schiaffino S (e_1_2_8_48_1) 2015; 15 e_1_2_8_2_1 e_1_2_8_4_1 e_1_2_8_6_1 e_1_2_8_8_1 e_1_2_8_21_1 e_1_2_8_42_1 e_1_2_8_23_1 e_1_2_8_44_1 e_1_2_8_40_1 e_1_2_8_18_1 e_1_2_8_39_1 e_1_2_8_14_1 e_1_2_8_35_1 e_1_2_8_16_1 e_1_2_8_37_1 Sorci G (e_1_2_8_11_1) 1833; 2013 e_1_2_8_10_1 e_1_2_8_31_1 e_1_2_8_12_1 e_1_2_8_33_1 e_1_2_8_50_1 |
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| Snippet | Background
Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer‐associated deaths,... Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer-associated deaths, is still a... BackgroundCachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer‐associated deaths, is... Background Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer-associated deaths,... Abstract Background Cachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer‐associated... |
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| SubjectTerms | Antibodies Atrophy Autophagy Cancer Cancer cachexia Cell adhesion & migration Cell culture Cytokines HMGB1 Inflammation Kinases Life Sciences Ligands Lung cancer Medical prognosis Muscle atrophy Musculoskeletal system Myogenin Original Physiology Proteins RAGE S100B Tumor necrosis factor-TNF Tumors |
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| Title | Targeting RAGE prevents muscle wasting and prolongs survival in cancer cachexia |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjcsm.12561 https://www.ncbi.nlm.nih.gov/pubmed/32159297 https://www.proquest.com/docview/2434702626 https://www.proquest.com/docview/2376234261 https://hal.sorbonne-universite.fr/hal-03714899 https://pubmed.ncbi.nlm.nih.gov/PMC7432590 https://doaj.org/article/68ef8c1500fa417db41e5ed1caf3470d |
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