A single chemotherapy administration induces muscle atrophy, mitochondrial alterations and apoptosis in breast cancer patients

Background Breast cancer patients are commonly treated with sequential administrations of epirubicin–cyclophosphamide (EC) and paclitaxel (TAX). The chronic effect of this treatment induces skeletal muscle alterations, but the specific effect of each chemotherapy agent is unknown. This study aimed t...

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Veröffentlicht in:	Journal of cachexia, sarcopenia and muscle Jg. 15; H. 1; S. 292 - 305
Hauptverfasser:	Mallard, Joris, Hucteau, Elyse, Bender, Laura, Moinard‐Butot, Fabien, Rochelle, Emma, Boutonnet, Lauréline, Grandperrin, Antoine, Schott, Roland, Pflumio, Carole, Trensz, Philippe, Kalish‐Weindling, Michal, Charles, Anne‐Laure, Gény, Bernard, Favret, Fabrice, Pivot, Xavier, Hureau, Thomas J., Pagano, Allan F.
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	Germany John Wiley & Sons, Inc 01.02.2024 Wiley Open Access/Springer Verlag Wiley
Schlagworte:	Anthracycline‐cyclophosphamide Apoptosis Biopsy Breast cancer Cancer Cancer therapies Cell cycle Chemotherapy Homeostasis Life Sciences Mitochondria Mitochondrial respiration Muscle biopsies Musculoskeletal system Reactive oxygen species Respiration Skeletal muscle deconditioning Taxanes Mitochondrial respiration Mitochondria Muscle biopsies Anthracycline-cyclophosphamide Skeletal muscle deconditioning Taxanes metabolism pathology
ISSN:	2190-5991, 2190-6009, 2190-6009
Online-Zugang:	Volltext
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Abstract	Background Breast cancer patients are commonly treated with sequential administrations of epirubicin–cyclophosphamide (EC) and paclitaxel (TAX). The chronic effect of this treatment induces skeletal muscle alterations, but the specific effect of each chemotherapy agent is unknown. This study aimed to investigate the effect of EC or TAX administration on skeletal muscle homeostasis in breast cancer patients. Methods Twenty early breast cancer patients undergoing EC followed by TAX chemotherapies were included. Two groups of 10 women were established and performed vastus lateralis skeletal muscle biopsies either before the first administration (pre) of EC (50 ± 14 years) or TAX (50 ± 16 years) and 4 days later (post). Mitochondrial respiratory capacity recording, reactive oxygen species production, western blotting and histological analyses were performed. Results Decrease in muscle fibres cross‐sectional area was only observed post‐EC (−25%; P < 0.001), associated with a reduction in mitochondrial respiratory capacity for the complex I (CI)‐linked substrate state (−32%; P = 0.001), oxidative phosphorylation (OXPHOS) by CI (−35%; P = 0.002), CI&CII (−26%; P = 0.022) and CII (−24%; P = 0.027). If H2O2 production was unchanged post‐EC, an increase was observed post‐TAX for OXPHOS by CII (+25%; P = 0.022). We found a decrease in makers of mitochondrial content, as shown post‐EC by a decrease in the protein levels of citrate synthase (−53%; P < 0.001) and VDAC (−39%; P < 0.001). Despite no changes in markers of mitochondrial fission, a decrease in the expression of a marker of mitochondrial inner‐membrane fusion was found post‐EC (OPA1; −60%; P < 0.001). We explored markers of mitophagy and found reductions post‐EC in the protein levels of PINK1 (−63%; P < 0.001) and Parkin (−56%; P = 0.005), without changes post‐TAX. An increasing trend in Bax protein level was found post‐EC (+96%; P = 0.068) and post‐TAX (+77%; P = 0.073), while the Bcl‐2 level was decreased only post‐EC (−52%; P = 0.007). If an increasing trend in TUNEL‐positive signal was observed post‐EC (+68%; P = 0.082), upregulation was highlighted post‐TAX (+86%; P < 0.001), suggesting activation of the apoptosis process. Conclusions We demonstrated that a single administration of EC induced, in only 4 days, skeletal muscle atrophy and mitochondrial alterations in breast cancer patients. These alterations were characterized by reductions in mitochondrial function and content as well as impairment of mitochondrial dynamics and an increase in apoptosis. TAX administration did not worsen these alterations as this group had already received EC during the preceding weeks. However, it resulted in an increased apoptosis, likely in response to the increased H2O2 production.
AbstractList	BackgroundBreast cancer patients are commonly treated with sequential administrations of epirubicin–cyclophosphamide (EC) and paclitaxel (TAX). The chronic effect of this treatment induces skeletal muscle alterations, but the specific effect of each chemotherapy agent is unknown. This study aimed to investigate the effect of EC or TAX administration on skeletal muscle homeostasis in breast cancer patients.MethodsTwenty early breast cancer patients undergoing EC followed by TAX chemotherapies were included. Two groups of 10 women were established and performed vastus lateralis skeletal muscle biopsies either before the first administration (pre) of EC (50 ± 14 years) or TAX (50 ± 16 years) and 4 days later (post). Mitochondrial respiratory capacity recording, reactive oxygen species production, western blotting and histological analyses were performed.ResultsDecrease in muscle fibres cross-sectional area was only observed post-EC (−25%; P < 0.001), associated with a reduction in mitochondrial respiratory capacity for the complex I (CI)-linked substrate state (−32%; P = 0.001), oxidative phosphorylation (OXPHOS) by CI (−35%; P = 0.002), CI&CII (−26%; P = 0.022) and CII (−24%; P = 0.027). If H2O2 production was unchanged post-EC, an increase was observed post-TAX for OXPHOS by CII (+25%; P = 0.022). We found a decrease in makers of mitochondrial content, as shown post-EC by a decrease in the protein levels of citrate synthase (−53%; P < 0.001) and VDAC (−39%; P < 0.001). Despite no changes in markers of mitochondrial fission, a decrease in the expression of a marker of mitochondrial inner-membrane fusion was found post-EC (OPA1; −60%; P < 0.001). We explored markers of mitophagy and found reductions post-EC in the protein levels of PINK1 (−63%; P < 0.001) and Parkin (−56%; P = 0.005), without changes post-TAX. An increasing trend in Bax protein level was found post-EC (+96%; P = 0.068) and post-TAX (+77%; P = 0.073), while the Bcl-2 level was decreased only post-EC (−52%; P = 0.007). If an increasing trend in TUNEL-positive signal was observed post-EC (+68%; P = 0.082), upregulation was highlighted post-TAX (+86%; P < 0.001), suggesting activation of the apoptosis process.ConclusionsWe demonstrated that a single administration of EC induced, in only 4 days, skeletal muscle atrophy and mitochondrial alterations in breast cancer patients. These alterations were characterized by reductions in mitochondrial function and content as well as impairment of mitochondrial dynamics and an increase in apoptosis. TAX administration did not worsen these alterations as this group had already received EC during the preceding weeks. However, it resulted in an increased apoptosis, likely in response to the increased H2O2 production. Breast cancer patients are commonly treated with sequential administrations of epirubicin-cyclophosphamide (EC) and paclitaxel (TAX). The chronic effect of this treatment induces skeletal muscle alterations, but the specific effect of each chemotherapy agent is unknown. This study aimed to investigate the effect of EC or TAX administration on skeletal muscle homeostasis in breast cancer patients.BACKGROUNDBreast cancer patients are commonly treated with sequential administrations of epirubicin-cyclophosphamide (EC) and paclitaxel (TAX). The chronic effect of this treatment induces skeletal muscle alterations, but the specific effect of each chemotherapy agent is unknown. This study aimed to investigate the effect of EC or TAX administration on skeletal muscle homeostasis in breast cancer patients.Twenty early breast cancer patients undergoing EC followed by TAX chemotherapies were included. Two groups of 10 women were established and performed vastus lateralis skeletal muscle biopsies either before the first administration (pre) of EC (50 ± 14 years) or TAX (50 ± 16 years) and 4 days later (post). Mitochondrial respiratory capacity recording, reactive oxygen species production, western blotting and histological analyses were performed.METHODSTwenty early breast cancer patients undergoing EC followed by TAX chemotherapies were included. Two groups of 10 women were established and performed vastus lateralis skeletal muscle biopsies either before the first administration (pre) of EC (50 ± 14 years) or TAX (50 ± 16 years) and 4 days later (post). Mitochondrial respiratory capacity recording, reactive oxygen species production, western blotting and histological analyses were performed.Decrease in muscle fibres cross-sectional area was only observed post-EC (-25%; P < 0.001), associated with a reduction in mitochondrial respiratory capacity for the complex I (CI)-linked substrate state (-32%; P = 0.001), oxidative phosphorylation (OXPHOS) by CI (-35%; P = 0.002), CI&CII (-26%; P = 0.022) and CII (-24%; P = 0.027). If H2 O2 production was unchanged post-EC, an increase was observed post-TAX for OXPHOS by CII (+25%; P = 0.022). We found a decrease in makers of mitochondrial content, as shown post-EC by a decrease in the protein levels of citrate synthase (-53%; P < 0.001) and VDAC (-39%; P < 0.001). Despite no changes in markers of mitochondrial fission, a decrease in the expression of a marker of mitochondrial inner-membrane fusion was found post-EC (OPA1; -60%; P < 0.001). We explored markers of mitophagy and found reductions post-EC in the protein levels of PINK1 (-63%; P < 0.001) and Parkin (-56%; P = 0.005), without changes post-TAX. An increasing trend in Bax protein level was found post-EC (+96%; P = 0.068) and post-TAX (+77%; P = 0.073), while the Bcl-2 level was decreased only post-EC (-52%; P = 0.007). If an increasing trend in TUNEL-positive signal was observed post-EC (+68%; P = 0.082), upregulation was highlighted post-TAX (+86%; P < 0.001), suggesting activation of the apoptosis process.RESULTSDecrease in muscle fibres cross-sectional area was only observed post-EC (-25%; P < 0.001), associated with a reduction in mitochondrial respiratory capacity for the complex I (CI)-linked substrate state (-32%; P = 0.001), oxidative phosphorylation (OXPHOS) by CI (-35%; P = 0.002), CI&CII (-26%; P = 0.022) and CII (-24%; P = 0.027). If H2 O2 production was unchanged post-EC, an increase was observed post-TAX for OXPHOS by CII (+25%; P = 0.022). We found a decrease in makers of mitochondrial content, as shown post-EC by a decrease in the protein levels of citrate synthase (-53%; P < 0.001) and VDAC (-39%; P < 0.001). Despite no changes in markers of mitochondrial fission, a decrease in the expression of a marker of mitochondrial inner-membrane fusion was found post-EC (OPA1; -60%; P < 0.001). We explored markers of mitophagy and found reductions post-EC in the protein levels of PINK1 (-63%; P < 0.001) and Parkin (-56%; P = 0.005), without changes post-TAX. An increasing trend in Bax protein level was found post-EC (+96%; P = 0.068) and post-TAX (+77%; P = 0.073), while the Bcl-2 level was decreased only post-EC (-52%; P = 0.007). If an increasing trend in TUNEL-positive signal was observed post-EC (+68%; P = 0.082), upregulation was highlighted post-TAX (+86%; P < 0.001), suggesting activation of the apoptosis process.We demonstrated that a single administration of EC induced, in only 4 days, skeletal muscle atrophy and mitochondrial alterations in breast cancer patients. These alterations were characterized by reductions in mitochondrial function and content as well as impairment of mitochondrial dynamics and an increase in apoptosis. TAX administration did not worsen these alterations as this group had already received EC during the preceding weeks. However, it resulted in an increased apoptosis, likely in response to the increased H2 O2 production.CONCLUSIONSWe demonstrated that a single administration of EC induced, in only 4 days, skeletal muscle atrophy and mitochondrial alterations in breast cancer patients. These alterations were characterized by reductions in mitochondrial function and content as well as impairment of mitochondrial dynamics and an increase in apoptosis. TAX administration did not worsen these alterations as this group had already received EC during the preceding weeks. However, it resulted in an increased apoptosis, likely in response to the increased H2 O2 production. Background Breast cancer patients are commonly treated with sequential administrations of epirubicin–cyclophosphamide (EC) and paclitaxel (TAX). The chronic effect of this treatment induces skeletal muscle alterations, but the specific effect of each chemotherapy agent is unknown. This study aimed to investigate the effect of EC or TAX administration on skeletal muscle homeostasis in breast cancer patients. Methods Twenty early breast cancer patients undergoing EC followed by TAX chemotherapies were included. Two groups of 10 women were established and performed vastus lateralis skeletal muscle biopsies either before the first administration (pre) of EC (50 ± 14 years) or TAX (50 ± 16 years) and 4 days later (post). Mitochondrial respiratory capacity recording, reactive oxygen species production, western blotting and histological analyses were performed. Results Decrease in muscle fibres cross-sectional area was only observed post-EC (−25%; P < 0.001), associated with a reduction in mitochondrial respiratory capacity for the complex I (CI)-linked substrate state (−32%; P = 0.001), oxidative phosphorylation (OXPHOS) by CI (−35%; P = 0.002), CI&CII (−26%; P = 0.022) and CII (−24%; P = 0.027). If H2O2 production was unchanged post-EC, an increase was observed post-TAX for OXPHOS by CII (+25%; P = 0.022). We found a decrease in makers of mitochondrial content, as shown post-EC by a decrease in the protein levels of citrate synthase (−53%; P < 0.001) and VDAC (−39%; P < 0.001). Despite no changes in markers of mitochondrial fission, a decrease in the expression of a marker of mitochondrial inner-membrane fusion was found post-EC (OPA1; −60%; P < 0.001). We explored markers of mitophagy and found reductions post-EC in the protein levels of PINK1 (−63%; P < 0.001) and Parkin (−56%; P = 0.005), without changes post-TAX. An increasing trend in Bax protein level was found post-EC (+96%; P = 0.068) and post-TAX (+77%; P = 0.073), while the Bcl-2 level was decreased only post-EC (−52%; P = 0.007). If an increasing trend in TUNEL-positive signal was observed post-EC (+68%; P = 0.082), upregulation was highlighted post-TAX (+86%; P < 0.001), suggesting activation of the apoptosis process. Conclusions We demonstrated that a single administration of EC induced, in only 4 days, skeletal muscle atrophy and mitochondrial alterations in breast cancer patients. These alterations were characterized by reductions in mitochondrial function and content as well as impairment of mitochondrial dynamics and an increase in apoptosis. TAX administration did not worsen these alterations as this group had already received EC during the preceding weeks. However, it resulted in an increased apoptosis, likely in response to the increased H2O2 production. Abstract Background Breast cancer patients are commonly treated with sequential administrations of epirubicin–cyclophosphamide (EC) and paclitaxel (TAX). The chronic effect of this treatment induces skeletal muscle alterations, but the specific effect of each chemotherapy agent is unknown. This study aimed to investigate the effect of EC or TAX administration on skeletal muscle homeostasis in breast cancer patients. Methods Twenty early breast cancer patients undergoing EC followed by TAX chemotherapies were included. Two groups of 10 women were established and performed vastus lateralis skeletal muscle biopsies either before the first administration (pre) of EC (50 ± 14 years) or TAX (50 ± 16 years) and 4 days later (post). Mitochondrial respiratory capacity recording, reactive oxygen species production, western blotting and histological analyses were performed. Results Decrease in muscle fibres cross‐sectional area was only observed post‐EC (−25%; P < 0.001), associated with a reduction in mitochondrial respiratory capacity for the complex I (CI)‐linked substrate state (−32%; P = 0.001), oxidative phosphorylation (OXPHOS) by CI (−35%; P = 0.002), CI&CII (−26%; P = 0.022) and CII (−24%; P = 0.027). If H2O2 production was unchanged post‐EC, an increase was observed post‐TAX for OXPHOS by CII (+25%; P = 0.022). We found a decrease in makers of mitochondrial content, as shown post‐EC by a decrease in the protein levels of citrate synthase (−53%; P < 0.001) and VDAC (−39%; P < 0.001). Despite no changes in markers of mitochondrial fission, a decrease in the expression of a marker of mitochondrial inner‐membrane fusion was found post‐EC (OPA1; −60%; P < 0.001). We explored markers of mitophagy and found reductions post‐EC in the protein levels of PINK1 (−63%; P < 0.001) and Parkin (−56%; P = 0.005), without changes post‐TAX. An increasing trend in Bax protein level was found post‐EC (+96%; P = 0.068) and post‐TAX (+77%; P = 0.073), while the Bcl‐2 level was decreased only post‐EC (−52%; P = 0.007). If an increasing trend in TUNEL‐positive signal was observed post‐EC (+68%; P = 0.082), upregulation was highlighted post‐TAX (+86%; P < 0.001), suggesting activation of the apoptosis process. Conclusions We demonstrated that a single administration of EC induced, in only 4 days, skeletal muscle atrophy and mitochondrial alterations in breast cancer patients. These alterations were characterized by reductions in mitochondrial function and content as well as impairment of mitochondrial dynamics and an increase in apoptosis. TAX administration did not worsen these alterations as this group had already received EC during the preceding weeks. However, it resulted in an increased apoptosis, likely in response to the increased H2O2 production. Background Breast cancer patients are commonly treated with sequential administrations of epirubicin–cyclophosphamide (EC) and paclitaxel (TAX). The chronic effect of this treatment induces skeletal muscle alterations, but the specific effect of each chemotherapy agent is unknown. This study aimed to investigate the effect of EC or TAX administration on skeletal muscle homeostasis in breast cancer patients. Methods Twenty early breast cancer patients undergoing EC followed by TAX chemotherapies were included. Two groups of 10 women were established and performed vastus lateralis skeletal muscle biopsies either before the first administration (pre) of EC (50 ± 14 years) or TAX (50 ± 16 years) and 4 days later (post). Mitochondrial respiratory capacity recording, reactive oxygen species production, western blotting and histological analyses were performed. Results Decrease in muscle fibres cross‐sectional area was only observed post‐EC (−25%; P < 0.001), associated with a reduction in mitochondrial respiratory capacity for the complex I (CI)‐linked substrate state (−32%; P = 0.001), oxidative phosphorylation (OXPHOS) by CI (−35%; P = 0.002), CI&CII (−26%; P = 0.022) and CII (−24%; P = 0.027). If H2O2 production was unchanged post‐EC, an increase was observed post‐TAX for OXPHOS by CII (+25%; P = 0.022). We found a decrease in makers of mitochondrial content, as shown post‐EC by a decrease in the protein levels of citrate synthase (−53%; P < 0.001) and VDAC (−39%; P < 0.001). Despite no changes in markers of mitochondrial fission, a decrease in the expression of a marker of mitochondrial inner‐membrane fusion was found post‐EC (OPA1; −60%; P < 0.001). We explored markers of mitophagy and found reductions post‐EC in the protein levels of PINK1 (−63%; P < 0.001) and Parkin (−56%; P = 0.005), without changes post‐TAX. An increasing trend in Bax protein level was found post‐EC (+96%; P = 0.068) and post‐TAX (+77%; P = 0.073), while the Bcl‐2 level was decreased only post‐EC (−52%; P = 0.007). If an increasing trend in TUNEL‐positive signal was observed post‐EC (+68%; P = 0.082), upregulation was highlighted post‐TAX (+86%; P < 0.001), suggesting activation of the apoptosis process. Conclusions We demonstrated that a single administration of EC induced, in only 4 days, skeletal muscle atrophy and mitochondrial alterations in breast cancer patients. These alterations were characterized by reductions in mitochondrial function and content as well as impairment of mitochondrial dynamics and an increase in apoptosis. TAX administration did not worsen these alterations as this group had already received EC during the preceding weeks. However, it resulted in an increased apoptosis, likely in response to the increased H2O2 production. Breast cancer patients are commonly treated with sequential administrations of epirubicin-cyclophosphamide (EC) and paclitaxel (TAX). The chronic effect of this treatment induces skeletal muscle alterations, but the specific effect of each chemotherapy agent is unknown. This study aimed to investigate the effect of EC or TAX administration on skeletal muscle homeostasis in breast cancer patients. Twenty early breast cancer patients undergoing EC followed by TAX chemotherapies were included. Two groups of 10 women were established and performed vastus lateralis skeletal muscle biopsies either before the first administration (pre) of EC (50 ± 14 years) or TAX (50 ± 16 years) and 4 days later (post). Mitochondrial respiratory capacity recording, reactive oxygen species production, western blotting and histological analyses were performed. Decrease in muscle fibres cross-sectional area was only observed post-EC (-25%; P < 0.001), associated with a reduction in mitochondrial respiratory capacity for the complex I (CI)-linked substrate state (-32%; P = 0.001), oxidative phosphorylation (OXPHOS) by CI (-35%; P = 0.002), CI&CII (-26%; P = 0.022) and CII (-24%; P = 0.027). If H O production was unchanged post-EC, an increase was observed post-TAX for OXPHOS by CII (+25%; P = 0.022). We found a decrease in makers of mitochondrial content, as shown post-EC by a decrease in the protein levels of citrate synthase (-53%; P < 0.001) and VDAC (-39%; P < 0.001). Despite no changes in markers of mitochondrial fission, a decrease in the expression of a marker of mitochondrial inner-membrane fusion was found post-EC (OPA1; -60%; P < 0.001). We explored markers of mitophagy and found reductions post-EC in the protein levels of PINK1 (-63%; P < 0.001) and Parkin (-56%; P = 0.005), without changes post-TAX. An increasing trend in Bax protein level was found post-EC (+96%; P = 0.068) and post-TAX (+77%; P = 0.073), while the Bcl-2 level was decreased only post-EC (-52%; P = 0.007). If an increasing trend in TUNEL-positive signal was observed post-EC (+68%; P = 0.082), upregulation was highlighted post-TAX (+86%; P < 0.001), suggesting activation of the apoptosis process. We demonstrated that a single administration of EC induced, in only 4 days, skeletal muscle atrophy and mitochondrial alterations in breast cancer patients. These alterations were characterized by reductions in mitochondrial function and content as well as impairment of mitochondrial dynamics and an increase in apoptosis. TAX administration did not worsen these alterations as this group had already received EC during the preceding weeks. However, it resulted in an increased apoptosis, likely in response to the increased H O production.
Author	Hucteau, Elyse Charles, Anne‐Laure Grandperrin, Antoine Rochelle, Emma Gény, Bernard Favret, Fabrice Boutonnet, Lauréline Pflumio, Carole Pagano, Allan F. Trensz, Philippe Bender, Laura Pivot, Xavier Schott, Roland Mallard, Joris Moinard‐Butot, Fabien Kalish‐Weindling, Michal Hureau, Thomas J.
Author_xml	– sequence: 1 givenname: Joris orcidid: 0009-0009-0890-3136 surname: Mallard fullname: Mallard, Joris email: j.mallard@icans.eu organization: Institut de Cancérologie Strasbourg Europe (ICANS) – sequence: 2 givenname: Elyse surname: Hucteau fullname: Hucteau, Elyse organization: Institut de Cancérologie Strasbourg Europe (ICANS) – sequence: 3 givenname: Laura surname: Bender fullname: Bender, Laura organization: Institut de Cancérologie Strasbourg Europe (ICANS) – sequence: 4 givenname: Fabien surname: Moinard‐Butot fullname: Moinard‐Butot, Fabien organization: Institut de Cancérologie Strasbourg Europe (ICANS) – sequence: 5 givenname: Emma surname: Rochelle fullname: Rochelle, Emma organization: University of Strasbourg – sequence: 6 givenname: Lauréline surname: Boutonnet fullname: Boutonnet, Lauréline organization: University of Strasbourg – sequence: 7 givenname: Antoine surname: Grandperrin fullname: Grandperrin, Antoine organization: University of Strasbourg – sequence: 8 givenname: Roland surname: Schott fullname: Schott, Roland organization: Institut de Cancérologie Strasbourg Europe (ICANS) – sequence: 9 givenname: Carole surname: Pflumio fullname: Pflumio, Carole organization: Institut de Cancérologie Strasbourg Europe (ICANS) – sequence: 10 givenname: Philippe surname: Trensz fullname: Trensz, Philippe organization: Institut de Cancérologie Strasbourg Europe (ICANS) – sequence: 11 givenname: Michal surname: Kalish‐Weindling fullname: Kalish‐Weindling, Michal organization: Institut de Cancérologie Strasbourg Europe (ICANS) – sequence: 12 givenname: Anne‐Laure surname: Charles fullname: Charles, Anne‐Laure organization: University of Strasbourg – sequence: 13 givenname: Bernard surname: Gény fullname: Gény, Bernard organization: University Hospital of Strasbourg – sequence: 14 givenname: Fabrice surname: Favret fullname: Favret, Fabrice organization: University of Strasbourg – sequence: 15 givenname: Xavier surname: Pivot fullname: Pivot, Xavier organization: Institut de Cancérologie Strasbourg Europe (ICANS) – sequence: 16 givenname: Thomas J. surname: Hureau fullname: Hureau, Thomas J. organization: University of Strasbourg – sequence: 17 givenname: Allan F. surname: Pagano fullname: Pagano, Allan F. organization: University of Strasbourg
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Copyright	2024 The Authors. published by Wiley Periodicals LLC. 2024 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by Wiley Periodicals LLC. 2024. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. licence_http://creativecommons.org/publicdomain/zero
Copyright_xml	– notice: 2024 The Authors. published by Wiley Periodicals LLC. – notice: 2024 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by Wiley Periodicals LLC. – notice: 2024. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: licence_http://creativecommons.org/publicdomain/zero
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Snippet	Background Breast cancer patients are commonly treated with sequential administrations of epirubicin–cyclophosphamide (EC) and paclitaxel (TAX). The chronic... Breast cancer patients are commonly treated with sequential administrations of epirubicin-cyclophosphamide (EC) and paclitaxel (TAX). The chronic effect of... BackgroundBreast cancer patients are commonly treated with sequential administrations of epirubicin–cyclophosphamide (EC) and paclitaxel (TAX). The chronic... Background Breast cancer patients are commonly treated with sequential administrations of epirubicin–cyclophosphamide (EC) and paclitaxel (TAX). The chronic... Abstract Background Breast cancer patients are commonly treated with sequential administrations of epirubicin–cyclophosphamide (EC) and paclitaxel (TAX). The...
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SubjectTerms	Anthracycline‐cyclophosphamide Apoptosis Biopsy Breast cancer Cancer Cancer therapies Cell cycle Chemotherapy Homeostasis Life Sciences Mitochondria Mitochondrial respiration Muscle biopsies Musculoskeletal system Reactive oxygen species Respiration Skeletal muscle deconditioning Taxanes
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Title	A single chemotherapy administration induces muscle atrophy, mitochondrial alterations and apoptosis in breast cancer patients
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