Growth of ovarian cancer xenografts causes loss of muscle and bone mass: a new model for the study of cancer cachexia

Background Cachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of all cancer deaths, cachexia is generally under‐studied in OC due to a limited number of pre‐clinical animal models. We aimed to address this...

Full description

Saved in:
Bibliographic Details
Published in:Journal of cachexia, sarcopenia and muscle Vol. 9; no. 4; pp. 685 - 700
Main Authors: Pin, Fabrizio, Barreto, Rafael, Kitase, Yukiko, Mitra, Sumegha, Erne, Carlie E., Novinger, Leah J., Zimmers, Teresa A., Couch, Marion E., Bonewald, Lynda F., Bonetto, Andrea
Format: Journal Article
Language:English
Published: Germany John Wiley & Sons, Inc 01.08.2018
John Wiley and Sons Inc
Wiley
Subjects:
Animal model
Animals
Biomarkers
Body Composition
Bone and Bones - diagnostic imaging
Bone and Bones - pathology
Bone Density
Cachexia - diagnosis
Cachexia - etiology
Cancer cachexia
Cancer therapies
Cell Line, Tumor
Chemotherapy
Cytokines
Disease Models, Animal
Energy Metabolism
ES‐2
Ethanol
Female
Heterografts
Histology
Humans
IL‐6
Laboratory animals
Medical prognosis
Mice
Mitochondria - metabolism
Muscle Strength
Muscular Atrophy - diagnostic imaging
Muscular Atrophy - metabolism
Muscular Atrophy - pathology
Musculoskeletal system
Mutation
Organ Size
Original
Ovarian cancer
Ovarian Neoplasms - complications
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Penicillin
Quality of life
Sarcopenia
Signal Transduction
Skeletal muscle
X-Ray Microtomography
United States > US
Animal model
Cancer cachexia
ES-2
IL-6
Skeletal muscle
Ovarian cancer
ISSN:2190-5991, 2190-6009, 2190-6009
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Abstract Background Cachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of all cancer deaths, cachexia is generally under‐studied in OC due to a limited number of pre‐clinical animal models. We aimed to address this gap by characterizing the cachectic phenotype in a mouse model of OC. Methods Nod SCID gamma mice (n = 6–10) were injected intraperitoneally with 1 × 107 ES‐2 human OC cells to mimic disseminated abdominal disease. Muscle size and strength, as well as bone morphometry, were assessed. Tumour‐derived effects on muscle fibres were investigated in C2C12 myotube cultures. IL‐6 levels were detected in serum and ascites from tumour hosts, as well as in tumour sections. Results In about 2 weeks, ES‐2 cells developed abdominal tumours infiltrating omentum, mesentery, and adjacent organs. The ES‐2 tumours caused severe cachexia with marked loss of body weight (–12%, P < 0.01) and ascites accumulation in the peritoneal cavity (4.7 ± 1.5 mL). Skeletal muscles appeared markedly smaller in the tumour‐bearing mice (approximately –35%, P < 0.001). Muscle loss was accompanied by fibre atrophy, consistent with reduced muscle cross‐sectional area (–34%, P < 0.01) and muscle weakness (–50%, P < 0.001). Body composition assessment by dual‐energy X‐ray absorptiometry revealed decreased bone mineral density (–8%, P < 0.01) and bone mineral content (–19%, P < 0.01), also consistent with reduced trabecular bone in both femurs and vertebrae, as suggested by micro‐CT imaging of bone morphometry. In the ES‐2 mouse model, cachexia was also associated with high tumour‐derived IL‐6 levels in plasma and ascites (26.3 and 279.6 pg/mL, respectively) and with elevated phospho‐STAT3 (+274%, P < 0.001), reduced phospho‐AKT (–44%, P < 0.001) and decreased mitochondrial proteins, as well as with increased protein ubiquitination (+42%, P < 0.001) and expression of ubiquitin ligases in the skeletal muscle of tumour hosts. Similarly, ES‐2 conditioned medium directly induced fibre atrophy in C2C12 mouse myotubes (–16%, P < 0.001), consistent with elevated phospho‐STAT3 (+1.4‐fold, P < 0.001) and altered mitochondrial homoeostasis and metabolism, while inhibition of the IL‐6/STAT3 signalling by means of INCB018424 was sufficient to restore the myotubes size. Conclusions Our results suggest that the development of ES‐2 OC promotes muscle atrophy in both in vivo and in vitro conditions, accompanied by loss of bone mass, enhanced muscle protein catabolism, abnormal mitochondrial homoeostasis, and elevated IL‐6 levels. Therefore, this represents an appropriate model for the study of OC cachexia. Our model will aid in identifying molecular mediators that could be effectively targeted in order to improve muscle wasting associated with OC.
AbstractList BackgroundCachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of all cancer deaths, cachexia is generally under‐studied in OC due to a limited number of pre‐clinical animal models. We aimed to address this gap by characterizing the cachectic phenotype in a mouse model of OC.MethodsNod SCID gamma mice (n = 6–10) were injected intraperitoneally with 1 × 107 ES‐2 human OC cells to mimic disseminated abdominal disease. Muscle size and strength, as well as bone morphometry, were assessed. Tumour‐derived effects on muscle fibres were investigated in C2C12 myotube cultures. IL‐6 levels were detected in serum and ascites from tumour hosts, as well as in tumour sections.ResultsIn about 2 weeks, ES‐2 cells developed abdominal tumours infiltrating omentum, mesentery, and adjacent organs. The ES‐2 tumours caused severe cachexia with marked loss of body weight (–12%, P < 0.01) and ascites accumulation in the peritoneal cavity (4.7 ± 1.5 mL). Skeletal muscles appeared markedly smaller in the tumour‐bearing mice (approximately –35%, P < 0.001). Muscle loss was accompanied by fibre atrophy, consistent with reduced muscle cross‐sectional area (–34%, P < 0.01) and muscle weakness (–50%, P < 0.001). Body composition assessment by dual‐energy X‐ray absorptiometry revealed decreased bone mineral density (–8%, P < 0.01) and bone mineral content (–19%, P < 0.01), also consistent with reduced trabecular bone in both femurs and vertebrae, as suggested by micro‐CT imaging of bone morphometry. In the ES‐2 mouse model, cachexia was also associated with high tumour‐derived IL‐6 levels in plasma and ascites (26.3 and 279.6 pg/mL, respectively) and with elevated phospho‐STAT3 (+274%, P < 0.001), reduced phospho‐AKT (–44%, P < 0.001) and decreased mitochondrial proteins, as well as with increased protein ubiquitination (+42%, P < 0.001) and expression of ubiquitin ligases in the skeletal muscle of tumour hosts. Similarly, ES‐2 conditioned medium directly induced fibre atrophy in C2C12 mouse myotubes (–16%, P < 0.001), consistent with elevated phospho‐STAT3 (+1.4‐fold, P < 0.001) and altered mitochondrial homoeostasis and metabolism, while inhibition of the IL‐6/STAT3 signalling by means of INCB018424 was sufficient to restore the myotubes size.ConclusionsOur results suggest that the development of ES‐2 OC promotes muscle atrophy in both in vivo and in vitro conditions, accompanied by loss of bone mass, enhanced muscle protein catabolism, abnormal mitochondrial homoeostasis, and elevated IL‐6 levels. Therefore, this represents an appropriate model for the study of OC cachexia. Our model will aid in identifying molecular mediators that could be effectively targeted in order to improve muscle wasting associated with OC.
Background Cachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of all cancer deaths, cachexia is generally under‐studied in OC due to a limited number of pre‐clinical animal models. We aimed to address this gap by characterizing the cachectic phenotype in a mouse model of OC. Methods Nod SCID gamma mice (n = 6–10) were injected intraperitoneally with 1 × 107 ES‐2 human OC cells to mimic disseminated abdominal disease. Muscle size and strength, as well as bone morphometry, were assessed. Tumour‐derived effects on muscle fibres were investigated in C2C12 myotube cultures. IL‐6 levels were detected in serum and ascites from tumour hosts, as well as in tumour sections. Results In about 2 weeks, ES‐2 cells developed abdominal tumours infiltrating omentum, mesentery, and adjacent organs. The ES‐2 tumours caused severe cachexia with marked loss of body weight (–12%, P < 0.01) and ascites accumulation in the peritoneal cavity (4.7 ± 1.5 mL). Skeletal muscles appeared markedly smaller in the tumour‐bearing mice (approximately –35%, P < 0.001). Muscle loss was accompanied by fibre atrophy, consistent with reduced muscle cross‐sectional area (–34%, P < 0.01) and muscle weakness (–50%, P < 0.001). Body composition assessment by dual‐energy X‐ray absorptiometry revealed decreased bone mineral density (–8%, P < 0.01) and bone mineral content (–19%, P < 0.01), also consistent with reduced trabecular bone in both femurs and vertebrae, as suggested by micro‐CT imaging of bone morphometry. In the ES‐2 mouse model, cachexia was also associated with high tumour‐derived IL‐6 levels in plasma and ascites (26.3 and 279.6 pg/mL, respectively) and with elevated phospho‐STAT3 (+274%, P < 0.001), reduced phospho‐AKT (–44%, P < 0.001) and decreased mitochondrial proteins, as well as with increased protein ubiquitination (+42%, P < 0.001) and expression of ubiquitin ligases in the skeletal muscle of tumour hosts. Similarly, ES‐2 conditioned medium directly induced fibre atrophy in C2C12 mouse myotubes (–16%, P < 0.001), consistent with elevated phospho‐STAT3 (+1.4‐fold, P < 0.001) and altered mitochondrial homoeostasis and metabolism, while inhibition of the IL‐6/STAT3 signalling by means of INCB018424 was sufficient to restore the myotubes size. Conclusions Our results suggest that the development of ES‐2 OC promotes muscle atrophy in both in vivo and in vitro conditions, accompanied by loss of bone mass, enhanced muscle protein catabolism, abnormal mitochondrial homoeostasis, and elevated IL‐6 levels. Therefore, this represents an appropriate model for the study of OC cachexia. Our model will aid in identifying molecular mediators that could be effectively targeted in order to improve muscle wasting associated with OC.
Cachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of all cancer deaths, cachexia is generally under-studied in OC due to a limited number of pre-clinical animal models. We aimed to address this gap by characterizing the cachectic phenotype in a mouse model of OC.BACKGROUNDCachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of all cancer deaths, cachexia is generally under-studied in OC due to a limited number of pre-clinical animal models. We aimed to address this gap by characterizing the cachectic phenotype in a mouse model of OC.Nod SCID gamma mice (n = 6-10) were injected intraperitoneally with 1 × 107 ES-2 human OC cells to mimic disseminated abdominal disease. Muscle size and strength, as well as bone morphometry, were assessed. Tumour-derived effects on muscle fibres were investigated in C2C12 myotube cultures. IL-6 levels were detected in serum and ascites from tumour hosts, as well as in tumour sections.METHODSNod SCID gamma mice (n = 6-10) were injected intraperitoneally with 1 × 107 ES-2 human OC cells to mimic disseminated abdominal disease. Muscle size and strength, as well as bone morphometry, were assessed. Tumour-derived effects on muscle fibres were investigated in C2C12 myotube cultures. IL-6 levels were detected in serum and ascites from tumour hosts, as well as in tumour sections.In about 2 weeks, ES-2 cells developed abdominal tumours infiltrating omentum, mesentery, and adjacent organs. The ES-2 tumours caused severe cachexia with marked loss of body weight (-12%, P < 0.01) and ascites accumulation in the peritoneal cavity (4.7 ± 1.5 mL). Skeletal muscles appeared markedly smaller in the tumour-bearing mice (approximately -35%, P < 0.001). Muscle loss was accompanied by fibre atrophy, consistent with reduced muscle cross-sectional area (-34%, P < 0.01) and muscle weakness (-50%, P < 0.001). Body composition assessment by dual-energy X-ray absorptiometry revealed decreased bone mineral density (-8%, P < 0.01) and bone mineral content (-19%, P < 0.01), also consistent with reduced trabecular bone in both femurs and vertebrae, as suggested by micro-CT imaging of bone morphometry. In the ES-2 mouse model, cachexia was also associated with high tumour-derived IL-6 levels in plasma and ascites (26.3 and 279.6 pg/mL, respectively) and with elevated phospho-STAT3 (+274%, P < 0.001), reduced phospho-AKT (-44%, P < 0.001) and decreased mitochondrial proteins, as well as with increased protein ubiquitination (+42%, P < 0.001) and expression of ubiquitin ligases in the skeletal muscle of tumour hosts. Similarly, ES-2 conditioned medium directly induced fibre atrophy in C2C12 mouse myotubes (-16%, P < 0.001), consistent with elevated phospho-STAT3 (+1.4-fold, P < 0.001) and altered mitochondrial homoeostasis and metabolism, while inhibition of the IL-6/STAT3 signalling by means of INCB018424 was sufficient to restore the myotubes size.RESULTSIn about 2 weeks, ES-2 cells developed abdominal tumours infiltrating omentum, mesentery, and adjacent organs. The ES-2 tumours caused severe cachexia with marked loss of body weight (-12%, P < 0.01) and ascites accumulation in the peritoneal cavity (4.7 ± 1.5 mL). Skeletal muscles appeared markedly smaller in the tumour-bearing mice (approximately -35%, P < 0.001). Muscle loss was accompanied by fibre atrophy, consistent with reduced muscle cross-sectional area (-34%, P < 0.01) and muscle weakness (-50%, P < 0.001). Body composition assessment by dual-energy X-ray absorptiometry revealed decreased bone mineral density (-8%, P < 0.01) and bone mineral content (-19%, P < 0.01), also consistent with reduced trabecular bone in both femurs and vertebrae, as suggested by micro-CT imaging of bone morphometry. In the ES-2 mouse model, cachexia was also associated with high tumour-derived IL-6 levels in plasma and ascites (26.3 and 279.6 pg/mL, respectively) and with elevated phospho-STAT3 (+274%, P < 0.001), reduced phospho-AKT (-44%, P < 0.001) and decreased mitochondrial proteins, as well as with increased protein ubiquitination (+42%, P < 0.001) and expression of ubiquitin ligases in the skeletal muscle of tumour hosts. Similarly, ES-2 conditioned medium directly induced fibre atrophy in C2C12 mouse myotubes (-16%, P < 0.001), consistent with elevated phospho-STAT3 (+1.4-fold, P < 0.001) and altered mitochondrial homoeostasis and metabolism, while inhibition of the IL-6/STAT3 signalling by means of INCB018424 was sufficient to restore the myotubes size.Our results suggest that the development of ES-2 OC promotes muscle atrophy in both in vivo and in vitro conditions, accompanied by loss of bone mass, enhanced muscle protein catabolism, abnormal mitochondrial homoeostasis, and elevated IL-6 levels. Therefore, this represents an appropriate model for the study of OC cachexia. Our model will aid in identifying molecular mediators that could be effectively targeted in order to improve muscle wasting associated with OC.CONCLUSIONSOur results suggest that the development of ES-2 OC promotes muscle atrophy in both in vivo and in vitro conditions, accompanied by loss of bone mass, enhanced muscle protein catabolism, abnormal mitochondrial homoeostasis, and elevated IL-6 levels. Therefore, this represents an appropriate model for the study of OC cachexia. Our model will aid in identifying molecular mediators that could be effectively targeted in order to improve muscle wasting associated with OC.
Abstract Background Cachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of all cancer deaths, cachexia is generally under‐studied in OC due to a limited number of pre‐clinical animal models. We aimed to address this gap by characterizing the cachectic phenotype in a mouse model of OC. Methods Nod SCID gamma mice (n = 6–10) were injected intraperitoneally with 1 × 107 ES‐2 human OC cells to mimic disseminated abdominal disease. Muscle size and strength, as well as bone morphometry, were assessed. Tumour‐derived effects on muscle fibres were investigated in C2C12 myotube cultures. IL‐6 levels were detected in serum and ascites from tumour hosts, as well as in tumour sections. Results In about 2 weeks, ES‐2 cells developed abdominal tumours infiltrating omentum, mesentery, and adjacent organs. The ES‐2 tumours caused severe cachexia with marked loss of body weight (–12%, P < 0.01) and ascites accumulation in the peritoneal cavity (4.7 ± 1.5 mL). Skeletal muscles appeared markedly smaller in the tumour‐bearing mice (approximately –35%, P < 0.001). Muscle loss was accompanied by fibre atrophy, consistent with reduced muscle cross‐sectional area (–34%, P < 0.01) and muscle weakness (–50%, P < 0.001). Body composition assessment by dual‐energy X‐ray absorptiometry revealed decreased bone mineral density (–8%, P < 0.01) and bone mineral content (–19%, P < 0.01), also consistent with reduced trabecular bone in both femurs and vertebrae, as suggested by micro‐CT imaging of bone morphometry. In the ES‐2 mouse model, cachexia was also associated with high tumour‐derived IL‐6 levels in plasma and ascites (26.3 and 279.6 pg/mL, respectively) and with elevated phospho‐STAT3 (+274%, P < 0.001), reduced phospho‐AKT (–44%, P < 0.001) and decreased mitochondrial proteins, as well as with increased protein ubiquitination (+42%, P < 0.001) and expression of ubiquitin ligases in the skeletal muscle of tumour hosts. Similarly, ES‐2 conditioned medium directly induced fibre atrophy in C2C12 mouse myotubes (–16%, P < 0.001), consistent with elevated phospho‐STAT3 (+1.4‐fold, P < 0.001) and altered mitochondrial homoeostasis and metabolism, while inhibition of the IL‐6/STAT3 signalling by means of INCB018424 was sufficient to restore the myotubes size. Conclusions Our results suggest that the development of ES‐2 OC promotes muscle atrophy in both in vivo and in vitro conditions, accompanied by loss of bone mass, enhanced muscle protein catabolism, abnormal mitochondrial homoeostasis, and elevated IL‐6 levels. Therefore, this represents an appropriate model for the study of OC cachexia. Our model will aid in identifying molecular mediators that could be effectively targeted in order to improve muscle wasting associated with OC.
Cachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of all cancer deaths, cachexia is generally under-studied in OC due to a limited number of pre-clinical animal models. We aimed to address this gap by characterizing the cachectic phenotype in a mouse model of OC. Nod SCID gamma mice (n = 6-10) were injected intraperitoneally with 1 × 10 ES-2 human OC cells to mimic disseminated abdominal disease. Muscle size and strength, as well as bone morphometry, were assessed. Tumour-derived effects on muscle fibres were investigated in C2C12 myotube cultures. IL-6 levels were detected in serum and ascites from tumour hosts, as well as in tumour sections. In about 2 weeks, ES-2 cells developed abdominal tumours infiltrating omentum, mesentery, and adjacent organs. The ES-2 tumours caused severe cachexia with marked loss of body weight (-12%, P < 0.01) and ascites accumulation in the peritoneal cavity (4.7 ± 1.5 mL). Skeletal muscles appeared markedly smaller in the tumour-bearing mice (approximately -35%, P < 0.001). Muscle loss was accompanied by fibre atrophy, consistent with reduced muscle cross-sectional area (-34%, P < 0.01) and muscle weakness (-50%, P < 0.001). Body composition assessment by dual-energy X-ray absorptiometry revealed decreased bone mineral density (-8%, P < 0.01) and bone mineral content (-19%, P < 0.01), also consistent with reduced trabecular bone in both femurs and vertebrae, as suggested by micro-CT imaging of bone morphometry. In the ES-2 mouse model, cachexia was also associated with high tumour-derived IL-6 levels in plasma and ascites (26.3 and 279.6 pg/mL, respectively) and with elevated phospho-STAT3 (+274%, P < 0.001), reduced phospho-AKT (-44%, P < 0.001) and decreased mitochondrial proteins, as well as with increased protein ubiquitination (+42%, P < 0.001) and expression of ubiquitin ligases in the skeletal muscle of tumour hosts. Similarly, ES-2 conditioned medium directly induced fibre atrophy in C2C12 mouse myotubes (-16%, P < 0.001), consistent with elevated phospho-STAT3 (+1.4-fold, P < 0.001) and altered mitochondrial homoeostasis and metabolism, while inhibition of the IL-6/STAT3 signalling by means of INCB018424 was sufficient to restore the myotubes size. Our results suggest that the development of ES-2 OC promotes muscle atrophy in both in vivo and in vitro conditions, accompanied by loss of bone mass, enhanced muscle protein catabolism, abnormal mitochondrial homoeostasis, and elevated IL-6 levels. Therefore, this represents an appropriate model for the study of OC cachexia. Our model will aid in identifying molecular mediators that could be effectively targeted in order to improve muscle wasting associated with OC.
Author Bonetto, Andrea
Novinger, Leah J.
Kitase, Yukiko
Erne, Carlie E.
Couch, Marion E.
Bonewald, Lynda F.
Pin, Fabrizio
Mitra, Sumegha
Barreto, Rafael
Zimmers, Teresa A.
AuthorAffiliation 1 Department of Anatomy and Cell Biology Indiana University School of Medicine Indianapolis IN 46202 USA
4 Department of Biochemistry and Molecular Biology Indiana University Bloomington IN 47405 USA
7 IUPUI Center for Cachexia Research Innovation and Therapy Indiana University School of Medicine Indianapolis IN 46202 USA
2 Indiana Center for Musculoskeletal Health Indiana University School of Medicine Indianapolis IN 46202 USA
6 Department of Otolaryngology ‐ Head and Neck Surgery Indiana University School of Medicine Indianapolis IN 46202 USA
5 Simon Cancer Center Indiana University School of Medicine Indianapolis IN 46202 USA
3 Department of Surgery Indiana University School of Medicine Indianapolis IN 46202 USA
AuthorAffiliation_xml – name: 6 Department of Otolaryngology ‐ Head and Neck Surgery Indiana University School of Medicine Indianapolis IN 46202 USA
– name: 4 Department of Biochemistry and Molecular Biology Indiana University Bloomington IN 47405 USA
– name: 5 Simon Cancer Center Indiana University School of Medicine Indianapolis IN 46202 USA
– name: 1 Department of Anatomy and Cell Biology Indiana University School of Medicine Indianapolis IN 46202 USA
– name: 3 Department of Surgery Indiana University School of Medicine Indianapolis IN 46202 USA
– name: 7 IUPUI Center for Cachexia Research Innovation and Therapy Indiana University School of Medicine Indianapolis IN 46202 USA
– name: 2 Indiana Center for Musculoskeletal Health Indiana University School of Medicine Indianapolis IN 46202 USA
Author_xml – sequence: 1
  givenname: Fabrizio
  surname: Pin
  fullname: Pin, Fabrizio
  organization: Indiana University School of Medicine
– sequence: 2
  givenname: Rafael
  surname: Barreto
  fullname: Barreto, Rafael
  organization: Indiana University School of Medicine
– sequence: 3
  givenname: Yukiko
  surname: Kitase
  fullname: Kitase, Yukiko
  organization: Indiana University School of Medicine
– sequence: 4
  givenname: Sumegha
  surname: Mitra
  fullname: Mitra, Sumegha
  organization: Indiana University School of Medicine
– sequence: 5
  givenname: Carlie E.
  surname: Erne
  fullname: Erne, Carlie E.
  organization: Indiana University School of Medicine
– sequence: 6
  givenname: Leah J.
  surname: Novinger
  fullname: Novinger, Leah J.
  organization: Indiana University School of Medicine
– sequence: 7
  givenname: Teresa A.
  surname: Zimmers
  fullname: Zimmers, Teresa A.
  organization: Indiana University School of Medicine
– sequence: 8
  givenname: Marion E.
  surname: Couch
  fullname: Couch, Marion E.
  organization: Indiana University School of Medicine
– sequence: 9
  givenname: Lynda F.
  surname: Bonewald
  fullname: Bonewald, Lynda F.
  organization: Indiana University School of Medicine
– sequence: 10
  givenname: Andrea
  orcidid: 0000-0002-3235-1871
  surname: Bonetto
  fullname: Bonetto, Andrea
  email: abonetto@iu.edu
  organization: Indiana University School of Medicine
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30009406$$D View this record in MEDLINE/PubMed
BookMark eNp9ks9vFCEUgCemxv6wF_8AQ-LFNNkKDMMMHpqYjdaaGg_2Tt4wj102M1Bhptv972W7a2MbIxd48L0vD3jHxYEPHoviDaPnjFL-YWXScM54ydiL4ogzRWeSUnWwX1dKscPiNKUVzUNIJiv6qjgsc6AElUfFdBnDelySYEm4g-jAEwPeYCT36MMigh1T3pkSJtKHlLbgMCXTIwHfkTYXQwZI6SMB4nFNhtBhT2yIZFwiSePUbbYpe6cBs8R7B6-Llxb6hKf7-aS4-fL5Zv51dv3j8mr-6XpmJG3YrGZKdhVwrKyQCKw1givDUDQto6rMgeWdYqJipVJYWmoZQFta2VQVF015UlzttF2Alb6NboC40QGcftgIcaEhji5fRhuQkEVcNm0tTGeaymBdcoG8ltZAlV0XO9ft1A7YGfRjhP6J9OmJd0u9CHdaMioYq7Pg_V4Qw68J06gHlwz2PXgMU9Kc1rShZclVRt89Q1dhij6_lOb5vBa0ljJTb_-u6LGUP5-bgbMdYGL-uYj2EWFUb5tHb5tHPzRPhukz2LgRRhe2t3H9v1PYLmXtetz8R66_zX9-3-X8Bg1q1fY
CitedBy_id crossref_primary_10_1016_j_acra_2021_11_011
crossref_primary_10_1016_j_jnutbio_2019_05_010
crossref_primary_10_1016_j_molmet_2024_101976
crossref_primary_10_3390_healthcare7030085
crossref_primary_10_3390_jcm7100359
crossref_primary_10_1007_s12032_025_02621_8
crossref_primary_10_1016_j_beem_2021_101598
crossref_primary_10_1242_dmm_043166
crossref_primary_10_3390_jcm11010087
crossref_primary_10_1096_fj_201802799R
crossref_primary_10_1038_s42003_023_04902_2
crossref_primary_10_1007_s11914_023_00788_5
crossref_primary_10_3390_cells11060990
crossref_primary_10_1152_ajpregu_00035_2025
crossref_primary_10_1186_s13048_021_00772_6
crossref_primary_10_1042_BCJ20201009
crossref_primary_10_1002_jpen_2287
crossref_primary_10_1016_j_jconrel_2023_07_033
crossref_primary_10_1016_j_tem_2024_12_005
crossref_primary_10_3390_cells11030579
crossref_primary_10_1016_j_canlet_2021_06_030
crossref_primary_10_1002_jcsm_12524
crossref_primary_10_3389_fcell_2021_636498
crossref_primary_10_1002_cam4_4416
crossref_primary_10_1210_endocr_bqad176
crossref_primary_10_3389_fcell_2022_861622
crossref_primary_10_3389_fendo_2019_00543
crossref_primary_10_1016_j_clnu_2020_02_017
crossref_primary_10_1016_j_smhs_2024_01_006
crossref_primary_10_1002_jcsm_12489
crossref_primary_10_1002_jcsm_12885
crossref_primary_10_1002_jcsm_12642
crossref_primary_10_1007_s11914_021_00712_9
crossref_primary_10_1002_jbmr_4572
crossref_primary_10_3390_cancers12030595
crossref_primary_10_1002_jcsm_12440
crossref_primary_10_1186_s13045_023_01454_0
crossref_primary_10_1002_smll_202204436
crossref_primary_10_1177_15353702211009213
crossref_primary_10_1002_mco2_70030
crossref_primary_10_1371_journal_pone_0236680
crossref_primary_10_3390_cancers14112808
crossref_primary_10_3390_cells10030516
crossref_primary_10_3390_ijms21239268
crossref_primary_10_1007_s11914_024_00872_4
crossref_primary_10_1002_jcsm_13289
crossref_primary_10_1002_jbmr_4480
crossref_primary_10_1016_j_phanu_2020_100236
crossref_primary_10_1186_s13048_019_0586_1
crossref_primary_10_3389_fnut_2025_1538766
crossref_primary_10_1002_jcsm_12991
crossref_primary_10_3390_diagnostics9040206
crossref_primary_10_3390_ijms22168936
crossref_primary_10_1177_10732748211038445
crossref_primary_10_3389_fcell_2021_690452
crossref_primary_10_3390_cancers11040571
crossref_primary_10_1002_jcsm_12864
crossref_primary_10_1038_s41401_019_0275_z
crossref_primary_10_3390_ijms22031486
crossref_primary_10_1186_s13293_022_00465_9
crossref_primary_10_3390_cells11203305
crossref_primary_10_3389_fcell_2021_719643
crossref_primary_10_1073_pnas_2200215119
crossref_primary_10_1152_ajpcell_00374_2025
crossref_primary_10_1002_jcsm_12388
crossref_primary_10_1186_s12885_021_08518_9
crossref_primary_10_1096_fj_202002257R
crossref_primary_10_3389_fmolb_2023_1158330
crossref_primary_10_3389_fendo_2019_00809
Cites_doi 10.1152/ajpendo.00039.2012
10.1016/j.canlet.2013.08.022
10.3389/fphys.2016.00472
10.1038/nrc2946
10.1038/ncomms3126
10.1097/IGC.0000000000000867
10.1097/MCO.0b013e3283455d45
10.1016/j.ygyno.2016.05.027
10.1016/j.ejca.2014.11.022
10.1016/S1470-2045(02)00821-5
10.1002/art.20963
10.1038/nmeth.2089
10.1093/rheumatology/kei091
10.1155/2014/168407
10.1016/j.ejso.2016.12.016
10.1097/01.AOG.0000227787.24587.d1
10.1016/j.clnu.2012.05.009
10.1056/NEJMoa052985
10.3322/canjclin.49.5.297
10.1067/mob.2000.107092
10.1016/j.ygyno.2006.03.005
10.1016/j.ygyno.2013.03.003
10.18632/oncotarget.9779
10.1002/jcsm.12107
10.1158/0008-5472.CAN-14-0274
10.1371/journal.pone.0169673
10.3346/jkms.2014.29.9.1253
10.1016/j.ymthe.2004.08.013
10.1002/art.22175
10.1016/j.bbrc.2009.12.123
10.1038/ncomms7670
10.1371/journal.pone.0022538
10.1016/j.taap.2010.11.003
10.1158/0008-5472.CAN-09-1257
10.1371/journal.pone.0140403
10.1016/j.clnu.2009.12.004
10.1111/j.1699-0463.1969.tb04520.x
10.18632/oncotarget.6439
10.1097/AOG.0b013e318264f794
10.1016/j.canlet.2010.02.019
10.1016/j.ygyno.2015.05.040
10.1016/j.cyto.2012.01.015
10.1200/JCO.2000.18.7.1570
10.1016/j.cmet.2012.06.011
10.1200/JCO.2002.20.5.1248
10.1093/annonc/mdp605
10.3389/fphys.2016.00679
10.1002/jbmr.141
10.1200/JCO.2007.13.1953
10.1016/j.bbrc.2013.04.087
10.1038/s41598-017-15040-1
10.1210/endo-128-5-2657
10.1158/0008-5472.CAN-04-2102
10.1016/j.ygyno.2007.06.010
10.1056/NEJMoa1002028
10.1186/2044-5040-2-14
10.3322/caac.21442
10.1056/NEJMoa1110352
10.1016/S0092-8674(04)00400-3
10.1371/journal.pone.0072162
10.1002/jcsm.12261
10.1007/s00109-012-0946-4
10.3322/caac.21387
10.1186/1471-2407-11-210
10.1097/01.mco.0000078983.18774.cc
10.1172/JCI116897
10.1038/srep32695
10.1038/sj.ejcn.1602540
10.1634/theoncologist.2012-0416
10.1016/j.bbagen.2012.11.009
10.1038/bonekey.2015.101
10.1016/j.bbi.2012.07.022
10.1016/j.cell.2010.07.011
10.2146/ajhp050045.p1
ContentType Journal Article
Copyright 2018 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders
2018 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders.
2018. 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.
Copyright_xml – notice: 2018 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders
– notice: 2018 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders.
– notice: 2018. 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.
DBID 24P
AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
3V.
7X7
7XB
8FI
8FJ
8FK
ABUWG
AFKRA
AZQEC
BENPR
CCPQU
DWQXO
FYUFA
GHDGH
K9.
M0S
PHGZM
PHGZT
PIMPY
PJZUB
PKEHL
PPXIY
PQEST
PQQKQ
PQUKI
PRINS
7X8
5PM
DOA
DOI 10.1002/jcsm.12311
DatabaseName Wiley Open Access Journals
CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
ProQuest Central (Corporate)
ProQuest Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest Central UK/Ireland
ProQuest Central Essentials
ProQuest Central
ProQuest One Community College
ProQuest Central
Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Health & Medical Complete (Alumni)
Health & Medical Collection (Alumni Edition)
ProQuest Central Premium
ProQuest One Academic
ProQuest Publicly Available Content
ProQuest Health & Medical Research Collection
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic (retired)
ProQuest One Academic UKI Edition
ProQuest Central China
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Publicly Available Content Database
ProQuest One Academic Middle East (New)
ProQuest Central Essentials
ProQuest One Academic Eastern Edition
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
ProQuest One Health & Nursing
ProQuest Central China
ProQuest Hospital Collection (Alumni)
ProQuest Central
ProQuest Health & Medical Complete
ProQuest Health & Medical Research Collection
Health Research Premium Collection
ProQuest One Academic UKI Edition
Health and Medicine Complete (Alumni Edition)
ProQuest Central Korea
ProQuest Central (New)
ProQuest One Academic
ProQuest One Academic (New)
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList Publicly Available Content Database

MEDLINE - Academic

MEDLINE
Database_xml – sequence: 1
  dbid: 24P
  name: Wiley Online Library Open Access
  url: https://authorservices.wiley.com/open-science/open-access/browse-journals.html
  sourceTypes: Publisher
– sequence: 2
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 3
  dbid: NPM
  name: PubMed
  url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 4
  dbid: PIMPY
  name: Publicly Available Content Database
  url: http://search.proquest.com/publiccontent
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
DocumentTitleAlternate ES‐2 cells cause cachexia in vivo
EISSN 2190-6009
EndPage 700
ExternalDocumentID oai_doaj_org_article_ca6a145268b74cdc85ce7324e276fca5
PMC6104117
30009406
10_1002_jcsm_12311
JCSM12311
Genre article
Research Support, U.S. Gov't, Non-P.H.S
Research Support, Non-U.S. Gov't
Journal Article
Research Support, N.I.H., Extramural
GeographicLocations United States--US
GeographicLocations_xml – name: United States--US
GrantInformation_xml – fundername: Veterans Administration
  funderid: I01BX002764‐01A1
– fundername: Department of Surgery and the Department of Otolaryngology – Head&Neck Surgery at Indiana University
  funderid: R21CA190028
– fundername: Cancer Center at Indiana University School of Medicine
– fundername: Commonwealth of Pennsylvania Health Research Formula Fund
  funderid: 080‐37038‐AI0801; 2012F‐RFA67‐16
– fundername: National Institutes of Health
  funderid: R01CA122596; R01CA194593; 1PO1AG039355
– fundername: V Foundation for Cancer Research
  funderid: V2017‐021
– fundername: Indiana University Simon Cancer Center
– fundername: IU Simon Cancer Center Support Grant
  funderid: P30CA082709
– fundername: NCI NIH HHS
  grantid: R01 CA122596
– fundername: NCI NIH HHS
  grantid: R01 CA194593
– fundername: Commonwealth of Pennsylvania Health Research Formula Fund
  grantid: 080‐37038‐AI0801; 2012F‐RFA67‐16
– fundername: Veterans Administration
  grantid: I01BX002764‐01A1
– fundername: Department of Surgery and the Department of Otolaryngology – Head&Neck Surgery at Indiana University
  grantid: R21CA190028
– fundername: IU Simon Cancer Center Support Grant
  grantid: P30CA082709
– fundername: V Foundation for Cancer Research
  grantid: V2017‐021
– fundername: National Institutes of Health
  grantid: R01CA122596; R01CA194593; 1PO1AG039355
GroupedDBID ---
0R~
1OC
24P
2VQ
4.4
40G
53G
5VS
7X7
8FI
8FJ
AAHHS
AAKDD
AAZKR
ABUWG
ACCFJ
ACCMX
ACXQS
ADBBV
ADINQ
ADKYN
ADPDF
ADRAZ
ADZMN
ADZOD
AEEZP
AENEX
AEQDE
AFKRA
AHBYD
AHSBF
AIWBW
AJBDE
ALIPV
ALMA_UNASSIGNED_HOLDINGS
ALUQN
AMKLP
AOIJS
AVUZU
AZFZN
BAWUL
BCNDV
BENPR
BPHCQ
BVXVI
CCPQU
DIK
EBS
EJD
EMOBN
FYUFA
GROUPED_DOAJ
GX1
H13
HMCUK
HYE
IAO
IHR
INH
ITC
KQ8
M48
M~E
O9-
OK1
OVD
OVEED
PIMPY
PQQKQ
PROAC
RPM
RSV
SMD
SOJ
U2A
UKHRP
WIN
ZOVNA
AAFWJ
AAMMB
AAYXX
AEFGJ
AFFHD
AFPKN
AGXDD
AIDQK
AIDYY
CITATION
PHGZM
PHGZT
CGR
CUY
CVF
ECM
EIF
NPM
3V.
7XB
8FK
AZQEC
DWQXO
K9.
PJZUB
PKEHL
PPXIY
PQEST
PQUKI
PRINS
7X8
PUEGO
5PM
ID FETCH-LOGICAL-c6081-7196d5a2e5f46ea1bc429c1e48b1093429f2d91451399e3f0f1aab3f68552483
IEDL.DBID DOA
ISICitedReferencesCount 75
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000442345000007&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 2190-5991
2190-6009
IngestDate Tue Oct 14 19:07:15 EDT 2025
Tue Nov 04 01:54:09 EST 2025
Fri Sep 05 11:58:51 EDT 2025
Tue Oct 07 07:13:10 EDT 2025
Mon Jul 21 06:04:27 EDT 2025
Sat Nov 29 04:06:37 EST 2025
Tue Nov 18 21:23:51 EST 2025
Wed Jan 22 16:54:48 EST 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 4
Keywords Animal model
Cancer cachexia
ES-2
IL-6
Skeletal muscle
Ovarian cancer
Language English
License Attribution-NonCommercial
2018 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders.
This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c6081-7196d5a2e5f46ea1bc429c1e48b1093429f2d91451399e3f0f1aab3f68552483
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ORCID 0000-0002-3235-1871
OpenAccessLink https://doaj.org/article/ca6a145268b74cdc85ce7324e276fca5
PMID 30009406
PQID 2329740766
PQPubID 4370305
PageCount 16
ParticipantIDs doaj_primary_oai_doaj_org_article_ca6a145268b74cdc85ce7324e276fca5
pubmedcentral_primary_oai_pubmedcentral_nih_gov_6104117
proquest_miscellaneous_2070803329
proquest_journals_2329740766
pubmed_primary_30009406
crossref_primary_10_1002_jcsm_12311
crossref_citationtrail_10_1002_jcsm_12311
wiley_primary_10_1002_jcsm_12311_JCSM12311
PublicationCentury 2000
PublicationDate August 2018
PublicationDateYYYYMMDD 2018-08-01
PublicationDate_xml – month: 08
  year: 2018
  text: August 2018
PublicationDecade 2010
PublicationPlace Germany
PublicationPlace_xml – name: Germany
– name: Heidelberg
– name: Hoboken
PublicationTitle Journal of cachexia, sarcopenia and muscle
PublicationTitleAlternate J Cachexia Sarcopenia Muscle
PublicationYear 2018
Publisher John Wiley & Sons, Inc
John Wiley and Sons Inc
Wiley
Publisher_xml – name: John Wiley & Sons, Inc
– name: John Wiley and Sons Inc
– name: Wiley
References 2010; 10
2017; 7
2012; 120
2004; 64
2017; 8
2007; 107
2013; 4
2012; 366
1999; 49
2017; 43
2013; 129
1991; 51
1969; 77
2011; 11
2010; 142
2014; 29
2012; 16
2011; 14
2012; 58
2013; 8
2016; 142
2013; 18
2010; 21
2000; 18
2006; 63
2010; 25
2015; 138
2010; 29
2013; 435
2003; 6
2008; 26
2007; 61
2010; 391
2015; 12
2009; 69
2015; 6
2013; 1830
2015; 4
2006; 54
2015; 51
2017; 27
2008; 18
2017; 67
2015; 10
2013; 91
2010; 363
2002; 3
2014; 2014
2013; 341
2011; 250
2011; 6
2012; 303
2006; 354
2018; 68
2001; 21
2006; 157
2004; 10
2016; 6
2016; 7
2012; 2
2006; 108
2006; 45
2002; 20
2013; 32
1993; 92
2013; 34
2013; 30
2017; 12
2000; 183
2005; 52
2010; 295
2014; 74
1991; 128
2004; 117
2006; 103
2012; 9
e_1_2_8_28_1
e_1_2_8_47_1
e_1_2_8_26_1
e_1_2_8_49_1
e_1_2_8_68_1
Ottanelli S (e_1_2_8_75_1) 2015; 12
e_1_2_8_3_1
e_1_2_8_81_1
e_1_2_8_5_1
e_1_2_8_7_1
e_1_2_8_9_1
e_1_2_8_43_1
e_1_2_8_66_1
e_1_2_8_22_1
e_1_2_8_45_1
e_1_2_8_64_1
e_1_2_8_62_1
e_1_2_8_41_1
e_1_2_8_60_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_59_1
e_1_2_8_15_1
e_1_2_8_38_1
e_1_2_8_57_1
Gadducci A (e_1_2_8_20_1) 2001; 21
e_1_2_8_70_1
e_1_2_8_32_1
e_1_2_8_55_1
e_1_2_8_78_1
e_1_2_8_11_1
e_1_2_8_34_1
e_1_2_8_53_1
e_1_2_8_76_1
e_1_2_8_51_1
e_1_2_8_74_1
e_1_2_8_72_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
e_1_2_8_48_1
e_1_2_8_69_1
Lau DH (e_1_2_8_52_1) 1991; 51
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_67_1
e_1_2_8_23_1
e_1_2_8_44_1
e_1_2_8_65_1
e_1_2_8_63_1
e_1_2_8_40_1
e_1_2_8_61_1
Kanabrocki EL (e_1_2_8_30_1) 2006; 157
e_1_2_8_18_1
e_1_2_8_39_1
Damrauer JS (e_1_2_8_24_1) 2008; 18
e_1_2_8_14_1
e_1_2_8_35_1
e_1_2_8_16_1
e_1_2_8_37_1
e_1_2_8_58_1
e_1_2_8_79_1
Zhang M (e_1_2_8_80_1) 2013; 34
e_1_2_8_10_1
e_1_2_8_31_1
e_1_2_8_56_1
e_1_2_8_77_1
e_1_2_8_12_1
e_1_2_8_33_1
e_1_2_8_54_1
e_1_2_8_73_1
e_1_2_8_50_1
e_1_2_8_71_1
References_xml – volume: 91
  start-page: 357
  year: 2013
  end-page: 368
  article-title: Platinum‐resistance in ovarian cancer cells is mediated by IL‐6 secretion via the increased expression of its target cIAP‐2
  publication-title: J Mol Med
– volume: 4
  year: 2015
  article-title: Assessment of muscle mass and strength in mice
  publication-title: Bonekey Rep
– volume: 103
  start-page: 247
  year: 2006
  end-page: 252
  article-title: Body weight and composition changes in ovarian cancer patients during adjuvant chemotherapy
  publication-title: Gynecol Oncol
– volume: 10
  start-page: 803
  year: 2010
  end-page: 808
  article-title: The genesis and evolution of high‐grade serous ovarian cancer
  publication-title: Nat Rev Cancer
– volume: 4
  year: 2013
  article-title: Evaluating cell lines as tumour models by comparison of genomic profiles
  publication-title: Nat Commun
– volume: 68
  start-page: 7
  year: 2018
  end-page: 30
  article-title: Cancer statistics, 2018
  publication-title: CA Cancer J Clin
– volume: 51
  start-page: 400
  year: 2015
  end-page: 408
  article-title: Bone mineral density and fractures after risk‐reducing salpingo‐oophorectomy in women at increased risk for breast and ovarian cancer
  publication-title: Eur J Cancer
– volume: 18
  start-page: 139
  year: 2008
  end-page: 148
  article-title: Chemotherapy‐induced muscle wasting: association with NF‐kB and cancer cachexia
  publication-title: Basic Applied Myology
– volume: 67
  start-page: 7
  year: 2017
  end-page: 30
  article-title: Cancer statistics, 2017
  publication-title: CA Cancer J Clin
– volume: 21
  start-page: 1594
  year: 2010
  end-page: 1598
  article-title: Low body mass index and sarcopenia associated with dose‐limiting toxicity of sorafenib in patients with renal cell carcinoma
  publication-title: Ann Oncol
– volume: 303
  start-page: E410
  year: 2012
  end-page: E421
  article-title: JAK/STAT3 pathway inhibition blocks skeletal muscle wasting downstream of IL‐6 and in experimental cancer cachexia
  publication-title: Am J Physiol Endocrinol Metab
– volume: 43
  start-page: 717
  year: 2017
  end-page: 724
  article-title: The influence of sarcopenia on survival and surgical complications in ovarian cancer patients undergoing primary debulking surgery
  publication-title: Eur J Surg Oncol
– volume: 9
  start-page: 671
  year: 2012
  end-page: 675
  article-title: NIH Image to ImageJ: 25 years of image analysis
  publication-title: Nat Methods
– volume: 6
  year: 2015
  article-title: Regulation of autophagy and the ubiquitin‐proteasome system by the FoxO transcriptional network during muscle atrophy
  publication-title: Nat Commun
– volume: 58
  start-page: 133
  year: 2012
  end-page: 147
  article-title: Inflammation and ovarian cancer
  publication-title: Cytokine
– volume: 10
  year: 2015
  article-title: Skeletal muscle depletion and markers for cancer cachexia are strong prognostic factors in epithelial ovarian cancer
  publication-title: PLoS One
– volume: 129
  start-page: 548
  year: 2013
  end-page: 553
  article-title: Nutritional status, CT body composition measures and survival in ovarian cancer
  publication-title: Gynecol Oncol
– volume: 3
  start-page: 513
  year: 2002
  article-title: Bone metastasis from epithelial ovarian carcinoma
  publication-title: Lancet Oncol
– volume: 128
  start-page: 2657
  year: 1991
  end-page: 2659
  article-title: Chinese hamster ovarian cells transfected with the murine interleukin‐6 gene cause hypercalcemia as well as cachexia, leukocytosis and thrombocytosis in tumor‐bearing nude mice
  publication-title: Endocrinology
– volume: 52
  start-page: 833
  year: 2005
  end-page: 840
  article-title: A two‐year prospective controlled study of bone mass and bone turnover in children with early juvenile idiopathic arthritis
  publication-title: Arthritis Rheum
– volume: 18
  start-page: 1570
  year: 2000
  end-page: 1593
  article-title: Osteoporosis due to cancer treatment: pathogenesis and management
  publication-title: J Clin Oncol Off J Am Soc Clin Oncol
– volume: 142
  start-page: 311
  year: 2016
  end-page: 316
  article-title: Muscle composition measured by CT scan is a measurable predictor of overall survival in advanced ovarian cancer
  publication-title: Gynecol Oncol
– volume: 117
  start-page: 399
  year: 2004
  end-page: 412
  article-title: Foxo transcription factors induce the atrophy‐related ubiquitin ligase atrogin‐1 and cause skeletal muscle atrophy
  publication-title: Cell
– volume: 51
  start-page: 5181
  year: 1991
  end-page: 5187
  article-title: Multifactorial mechanisms associated with broad cross‐resistance of ovarian carcinoma cells selected by cyanomorpholino doxorubicin
  publication-title: Cancer Res
– volume: 7
  year: 2017
  article-title: Differential bone loss in mouse models of colon cancer cachexia
  publication-title: Front Physiol
– volume: 107
  start-page: 260
  year: 2007
  end-page: 265
  article-title: Weight change during chemotherapy as a potential prognostic factor for stage III epithelial ovarian carcinoma: a Gynecologic Oncology Group study
  publication-title: Gynecol Oncol
– volume: 435
  start-page: 188
  year: 2013
  end-page: 194
  article-title: Silencing of the STAT3 signaling pathway reverses the inherent and induced chemoresistance of human ovarian cancer cells
  publication-title: Biochem Biophys Res Commun
– volume: 69
  start-page: 9192
  year: 2009
  end-page: 9201
  article-title: Epithelial‐to‐mesenchymal transition and ovarian tumor progression induced by tissue transglutaminase
  publication-title: Cancer Res
– volume: 1830
  start-page: 2770
  year: 2013
  end-page: 2778
  article-title: Mitochondrial and sarcoplasmic reticulum abnormalities in cancer cachexia: altered energetic efficiency?
  publication-title: Biochim Biophys Acta
– volume: 63
  start-page: 419
  year: 2006
  end-page: 430
  article-title: Cancer‐treatment‐induced bone loss, part 1
  publication-title: Am J Health Syst Pharm
– volume: 6
  year: 2011
  article-title: STAT3 activation in skeletal muscle links muscle wasting and the acute phase response in cancer cachexia
  publication-title: PLoS One
– volume: 2
  start-page: 14
  year: 2012
  article-title: IL‐6 regulation on skeletal muscle mitochondrial remodeling during cancer cachexia in the ApcMin/+ mouse
  publication-title: Skelet Muscle
– volume: 108
  start-page: 361
  year: 2006
  end-page: 368
  article-title: Clinical behavior of stage II‐IV low‐grade serous carcinoma of the ovary
  publication-title: Obstet Gynecol
– volume: 27
  start-page: 223
  year: 2017
  end-page: 232
  article-title: Sarcopenia in advanced serous ovarian cancer
  publication-title: International Journal of Gynecological Cancer: Official Journal of the International Gynecological Cancer Society
– volume: 49
  start-page: 297
  year: 1999
  end-page: 320
  article-title: Epithelial ovarian cancer: prevention, diagnosis, and treatment
  publication-title: CA Cancer J Clin
– volume: 18
  start-page: 423
  year: 2013
  end-page: 429
  article-title: A study to evaluate the cause of bone demineralization in gynecological cancer survivors
  publication-title: Oncologist
– volume: 138
  start-page: 372
  year: 2015
  end-page: 377
  article-title: In vivo tumor growth of high‐grade serous ovarian cancer cell lines
  publication-title: Gynecol Oncol
– volume: 7
  start-page: 43442
  year: 2016
  end-page: 43460
  article-title: Chemotherapy‐related cachexia is associated with mitochondrial depletion and the activation of ERK1/2 and p38 MAPKs
  publication-title: Oncotarget
– volume: 8
  year: 2013
  article-title: Type‐specific cell line models for type‐specific ovarian cancer research
  publication-title: PLoS One
– volume: 61
  start-page: 642
  year: 2007
  end-page: 646
  article-title: Malnutrition among gynaecological cancer patients
  publication-title: Eur J Clin Nutr
– volume: 7
  year: 2017
  article-title: ACVR2B/Fc counteracts chemotherapy‐induced loss of muscle and bone mass
  publication-title: Sci Rep
– volume: 16
  start-page: 153
  year: 2012
  end-page: 166
  article-title: Cancer cachexia: mediators, signaling, and metabolic pathways
  publication-title: Cell Metab
– volume: 250
  start-page: 312
  year: 2011
  end-page: 321
  article-title: Cisplatin triggers atrophy of skeletal C2C12 myotubes via impairment of Akt signalling pathway and subsequent increment activity of proteasome and autophagy systems
  publication-title: Toxicol Appl Pharmacol
– volume: 2014
  start-page: 168407
  year: 2014
  end-page: 168407
  article-title: Inflammation based regulation of cancer cachexia
  publication-title: Biomed Res Int
– volume: 391
  start-page: 1548
  year: 2010
  end-page: 1554
  article-title: Acute inhibition of myostatin‐family proteins preserves skeletal muscle in mouse models of cancer cachexia
  publication-title: Biochem Biophys Res Commun
– volume: 295
  start-page: 110
  year: 2010
  end-page: 123
  article-title: Autocrine production of interleukin‐6 confers cisplatin and paclitaxel resistance in ovarian cancer cells
  publication-title: Cancer Lett
– volume: 7
  start-page: 458
  year: 2016
  end-page: 466
  article-title: Loss of skeletal muscle during neoadjuvant chemotherapy is related to decreased survival in ovarian cancer patients
  publication-title: J Cachexia Sarcopenia Muscle
– volume: 64
  start-page: 8193
  year: 2004
  end-page: 8198
  article-title: Regulation of protein catabolism by muscle‐specific and cytokine‐inducible ubiquitin ligase E3alpha‐II during cancer cachexia
  publication-title: Cancer Res
– volume: 7
  year: 2016
  article-title: Cancer and chemotherapy contribute to muscle loss by activating common signaling pathways
  publication-title: Front Physiol
– volume: 354
  start-page: 34
  year: 2006
  end-page: 43
  article-title: Intraperitoneal cisplatin and paclitaxel in ovarian cancer
  publication-title: N Engl J Med
– volume: 142
  start-page: 531
  year: 2010
  end-page: 543
  article-title: Reversal of cancer cachexia and muscle wasting by ActRIIB antagonism leads to prolonged survival
  publication-title: Cell
– volume: 12
  year: 2017
  article-title: Elevated bone turnover markers after risk‐reducing salpingo‐oophorectomy in women at increased risk for breast and ovarian cancer
  publication-title: PLoS One
– volume: 363
  start-page: 1117
  year: 2010
  end-page: 1127
  article-title: Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis
  publication-title: N Engl J Med
– volume: 34
  start-page: 1270
  year: 2013
  end-page: 1273
  article-title: Bone metastasis from ovarian cancer. Clinical analysis of 26 cases
  publication-title: Saudi Med J
– volume: 120
  start-page: 612
  year: 2012
  end-page: 618
  article-title: Ten‐year relative survival for epithelial ovarian cancer
  publication-title: Obstet Gynecol
– volume: 8
  start-page: 1081
  year: 2017
  end-page: 1083
  article-title: Ethical guidelines for publishing in the Journal of Cachexia, Sarcopenia and Muscle: update 2017
  publication-title: J Cachexia Sarcopenia Muscle
– volume: 77
  start-page: 758
  year: 1969
  end-page: 760
  article-title: Heterotransplantation of a human malignant tumour to "Nude" mice
  publication-title: Acta Pathol Microbiol Scand
– volume: 92
  start-page: 2783
  year: 1993
  end-page: 2789
  article-title: Tumor necrosis factor‐alpha mediates changes in tissue protein turnover in a rat cancer cachexia model
  publication-title: J Clin Invest
– volume: 74
  start-page: 6980
  year: 2014
  end-page: 6990
  article-title: Patient‐derived ovarian tumor xenografts recapitulate human clinicopathology and genetic alterations
  publication-title: Cancer Res
– volume: 14
  start-page: 250
  year: 2011
  end-page: 254
  article-title: Two faces of drug therapy in cancer: drug‐related lean tissue loss and its adverse consequences to survival and toxicity
  publication-title: Curr Opin Clin Nutr Metab Care
– volume: 183
  start-page: 956
  year: 2000
  end-page: 963
  article-title: Magnetic resonance imaging in an experimental model of human ovarian cancer demonstrating altered microvascular permeability after inhibition of vascular endothelial growth factor
  publication-title: Am J Obstet Gynecol
– volume: 30
  start-page: S126
  year: 2013
  end-page: S134
  article-title: Cortisol and inflammatory processes in ovarian cancer patients following primary treatment: relationships with depression, fatigue, and disability
  publication-title: Brain Behav Immun
– volume: 25
  start-page: 1468
  year: 2010
  end-page: 1486
  article-title: Guidelines for assessment of bone microstructure in rodents using micro‐computed tomography
  publication-title: J Bone Miner Res
– volume: 366
  start-page: 610
  year: 2012
  end-page: 618
  article-title: Paraneoplastic thrombocytosis in ovarian cancer
  publication-title: N Engl J Med
– volume: 32
  start-page: 65
  year: 2013
  end-page: 72
  article-title: Nutritional status, cachexia and survival in patients with advanced colorectal carcinoma. Different assessment criteria for nutritional status provide unequal results
  publication-title: Clin Nutr
– volume: 29
  start-page: 154
  year: 2010
  end-page: 159
  article-title: Consensus definition of sarcopenia, cachexia and pre‐cachexia: joint document elaborated by Special Interest Groups (SIG) “cachexia‐anorexia in chronic wasting diseases” and “nutrition in geriatrics”
  publication-title: Clin Nutr
– volume: 26
  start-page: 83
  year: 2008
  end-page: 89
  article-title: Tumor residual after surgical cytoreduction in prediction of clinical outcome in stage IV epithelial ovarian cancer: a Gynecologic Oncology Group study
  publication-title: J Clin Oncol Off J Am Soc Clin Oncol
– volume: 341
  start-page: 231
  year: 2013
  end-page: 239
  article-title: Abrogation of constitutive Stat3 activity circumvents cisplatin resistant ovarian cancer
  publication-title: Cancer Lett
– volume: 20
  start-page: 1248
  year: 2002
  end-page: 1259
  article-title: Survival effect of maximal cytoreductive surgery for advanced ovarian carcinoma during the platinum era: a meta‐analysis
  publication-title: J Clin Oncol Off J Am Soc Clin Oncol
– volume: 12
  start-page: 116
  year: 2015
  end-page: 129
  article-title: Prevention and treatment of bone fragility in cancer patient
  publication-title: Clin Cases Miner Bone Metab
– volume: 11
  year: 2011
  article-title: Prognostic significance of IL‐6 and IL‐8 ascites levels in ovarian cancer patients
  publication-title: BMC Cancer
– volume: 6
  year: 2016
  article-title: Systemic blockade of ACVR2B ligands prevents chemotherapy‐induced muscle wasting by restoring muscle protein synthesis without affecting oxidative capacity or atrogenes
  publication-title: Sci Rep
– volume: 29
  start-page: 1253
  year: 2014
  end-page: 1259
  article-title: Sarcopenia as a useful predictor for long‐term mortality in cirrhotic patients with ascites
  publication-title: J Korean Med Sci
– volume: 6
  start-page: 401
  year: 2003
  end-page: 406
  article-title: Cytokines in the pathogenesis of cancer cachexia
  publication-title: Curr Opin Clin Nutr Metab Care
– volume: 45
  start-page: 11
  year: 2006
  end-page: 19
  article-title: The pathophysiology of the growth plate in juvenile idiopathic arthritis
  publication-title: Rheumatology (Oxford)
– volume: 10
  start-page: 1032
  year: 2004
  end-page: 1042
  article-title: Characterization of intraperitoneal, orthotopic, and metastatic xenograft models of human ovarian cancer
  publication-title: Mol Ther
– volume: 157
  start-page: 349
  year: 2006
  end-page: 354
  article-title: Chronotherapy of ovarian cancer: effect on blood variables and serum cytokines. A case report
  publication-title: Clin Ter
– volume: 21
  start-page: 2941
  year: 2001
  end-page: 2947
  article-title: Malnutrition and cachexia in ovarian cancer patients: pathophysiology and management
  publication-title: Anticancer Res
– volume: 54
  start-page: 3551
  year: 2006
  end-page: 3563
  article-title: Impaired skeletal development in interleukin‐6‐transgenic mice: a model for the impact of chronic inflammation on the growing skeletal system
  publication-title: Arthritis Rheum
– volume: 6
  start-page: 43202
  year: 2015
  end-page: 43215
  article-title: Combination of exercise training and erythropoietin prevents cancer‐induced muscle alterations
  publication-title: Oncotarget
– ident: e_1_2_8_16_1
  doi: 10.1152/ajpendo.00039.2012
– ident: e_1_2_8_63_1
  doi: 10.1016/j.canlet.2013.08.022
– ident: e_1_2_8_64_1
  doi: 10.3389/fphys.2016.00472
– ident: e_1_2_8_4_1
  doi: 10.1038/nrc2946
– ident: e_1_2_8_5_1
  doi: 10.1038/ncomms3126
– ident: e_1_2_8_17_1
  doi: 10.1097/IGC.0000000000000867
– ident: e_1_2_8_27_1
  doi: 10.1097/MCO.0b013e3283455d45
– volume: 51
  start-page: 5181
  year: 1991
  ident: e_1_2_8_52_1
  article-title: Multifactorial mechanisms associated with broad cross‐resistance of ovarian carcinoma cells selected by cyanomorpholino doxorubicin
  publication-title: Cancer Res
– ident: e_1_2_8_35_1
  doi: 10.1016/j.ygyno.2016.05.027
– ident: e_1_2_8_73_1
  doi: 10.1016/j.ejca.2014.11.022
– ident: e_1_2_8_79_1
  doi: 10.1016/S1470-2045(02)00821-5
– ident: e_1_2_8_71_1
  doi: 10.1002/art.20963
– volume: 18
  start-page: 139
  year: 2008
  ident: e_1_2_8_24_1
  article-title: Chemotherapy‐induced muscle wasting: association with NF‐kB and cancer cachexia
  publication-title: Basic Applied Myology
– ident: e_1_2_8_41_1
  doi: 10.1038/nmeth.2089
– ident: e_1_2_8_70_1
  doi: 10.1093/rheumatology/kei091
– ident: e_1_2_8_58_1
  doi: 10.1155/2014/168407
– ident: e_1_2_8_36_1
  doi: 10.1016/j.ejso.2016.12.016
– ident: e_1_2_8_3_1
  doi: 10.1097/01.AOG.0000227787.24587.d1
– volume: 34
  start-page: 1270
  year: 2013
  ident: e_1_2_8_80_1
  article-title: Bone metastasis from ovarian cancer. Clinical analysis of 26 cases
  publication-title: Saudi Med J
– ident: e_1_2_8_26_1
  doi: 10.1016/j.clnu.2012.05.009
– ident: e_1_2_8_11_1
  doi: 10.1056/NEJMoa052985
– ident: e_1_2_8_18_1
  doi: 10.3322/canjclin.49.5.297
– ident: e_1_2_8_54_1
  doi: 10.1067/mob.2000.107092
– ident: e_1_2_8_23_1
  doi: 10.1016/j.ygyno.2006.03.005
– ident: e_1_2_8_33_1
  doi: 10.1016/j.ygyno.2013.03.003
– ident: e_1_2_8_25_1
  doi: 10.18632/oncotarget.9779
– ident: e_1_2_8_51_1
  doi: 10.1002/jcsm.12107
– ident: e_1_2_8_56_1
  doi: 10.1158/0008-5472.CAN-14-0274
– ident: e_1_2_8_74_1
  doi: 10.1371/journal.pone.0169673
– ident: e_1_2_8_32_1
  doi: 10.3346/jkms.2014.29.9.1253
– ident: e_1_2_8_38_1
  doi: 10.1016/j.ymthe.2004.08.013
– ident: e_1_2_8_72_1
  doi: 10.1002/art.22175
– ident: e_1_2_8_48_1
  doi: 10.1016/j.bbrc.2009.12.123
– ident: e_1_2_8_45_1
  doi: 10.1038/ncomms7670
– ident: e_1_2_8_15_1
  doi: 10.1371/journal.pone.0022538
– ident: e_1_2_8_43_1
  doi: 10.1016/j.taap.2010.11.003
– ident: e_1_2_8_55_1
  doi: 10.1158/0008-5472.CAN-09-1257
– ident: e_1_2_8_34_1
  doi: 10.1371/journal.pone.0140403
– ident: e_1_2_8_46_1
  doi: 10.1016/j.clnu.2009.12.004
– ident: e_1_2_8_53_1
  doi: 10.1111/j.1699-0463.1969.tb04520.x
– ident: e_1_2_8_65_1
  doi: 10.18632/oncotarget.6439
– ident: e_1_2_8_8_1
  doi: 10.1097/AOG.0b013e318264f794
– ident: e_1_2_8_62_1
  doi: 10.1016/j.canlet.2010.02.019
– ident: e_1_2_8_57_1
  doi: 10.1016/j.ygyno.2015.05.040
– ident: e_1_2_8_19_1
  doi: 10.1016/j.cyto.2012.01.015
– ident: e_1_2_8_77_1
  doi: 10.1200/JCO.2000.18.7.1570
– ident: e_1_2_8_47_1
  doi: 10.1016/j.cmet.2012.06.011
– ident: e_1_2_8_9_1
  doi: 10.1200/JCO.2002.20.5.1248
– ident: e_1_2_8_28_1
  doi: 10.1093/annonc/mdp605
– ident: e_1_2_8_68_1
  doi: 10.3389/fphys.2016.00679
– ident: e_1_2_8_42_1
  doi: 10.1002/jbmr.141
– ident: e_1_2_8_10_1
  doi: 10.1200/JCO.2007.13.1953
– ident: e_1_2_8_12_1
  doi: 10.1016/j.bbrc.2013.04.087
– ident: e_1_2_8_49_1
  doi: 10.1038/s41598-017-15040-1
– ident: e_1_2_8_69_1
  doi: 10.1210/endo-128-5-2657
– ident: e_1_2_8_67_1
  doi: 10.1158/0008-5472.CAN-04-2102
– ident: e_1_2_8_21_1
  doi: 10.1016/j.ygyno.2007.06.010
– ident: e_1_2_8_37_1
  doi: 10.1056/NEJMoa1002028
– ident: e_1_2_8_66_1
  doi: 10.1186/2044-5040-2-14
– volume: 21
  start-page: 2941
  year: 2001
  ident: e_1_2_8_20_1
  article-title: Malnutrition and cachexia in ovarian cancer patients: pathophysiology and management
  publication-title: Anticancer Res
– ident: e_1_2_8_2_1
  doi: 10.3322/caac.21442
– ident: e_1_2_8_13_1
  doi: 10.1056/NEJMoa1110352
– ident: e_1_2_8_44_1
  doi: 10.1016/S0092-8674(04)00400-3
– ident: e_1_2_8_6_1
  doi: 10.1371/journal.pone.0072162
– ident: e_1_2_8_81_1
  doi: 10.1002/jcsm.12261
– ident: e_1_2_8_29_1
  doi: 10.1007/s00109-012-0946-4
– ident: e_1_2_8_7_1
  doi: 10.3322/caac.21387
– volume: 12
  start-page: 116
  year: 2015
  ident: e_1_2_8_75_1
  article-title: Prevention and treatment of bone fragility in cancer patient
  publication-title: Clin Cases Miner Bone Metab
– volume: 157
  start-page: 349
  year: 2006
  ident: e_1_2_8_30_1
  article-title: Chronotherapy of ovarian cancer: effect on blood variables and serum cytokines. A case report
  publication-title: Clin Ter
– ident: e_1_2_8_14_1
  doi: 10.1186/1471-2407-11-210
– ident: e_1_2_8_59_1
  doi: 10.1097/01.mco.0000078983.18774.cc
– ident: e_1_2_8_60_1
  doi: 10.1172/JCI116897
– ident: e_1_2_8_50_1
  doi: 10.1038/srep32695
– ident: e_1_2_8_22_1
  doi: 10.1038/sj.ejcn.1602540
– ident: e_1_2_8_76_1
  doi: 10.1634/theoncologist.2012-0416
– ident: e_1_2_8_39_1
  doi: 10.1016/j.bbagen.2012.11.009
– ident: e_1_2_8_40_1
  doi: 10.1038/bonekey.2015.101
– ident: e_1_2_8_61_1
  doi: 10.1016/j.bbi.2012.07.022
– ident: e_1_2_8_31_1
  doi: 10.1016/j.cell.2010.07.011
– ident: e_1_2_8_78_1
  doi: 10.2146/ajhp050045.p1
SSID ssj0000461650
Score 2.436248
Snippet Background Cachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of...
Cachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of all cancer...
BackgroundCachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one third of...
Abstract Background Cachexia frequently occurs in women with advanced ovarian cancer (OC), along with enhanced inflammation. Despite being responsible for one...
SourceID doaj
pubmedcentral
proquest
pubmed
crossref
wiley
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 685
SubjectTerms Animal model
Animals
Biomarkers
Body Composition
Bone and Bones - diagnostic imaging
Bone and Bones - pathology
Bone Density
Cachexia - diagnosis
Cachexia - etiology
Cancer cachexia
Cancer therapies
Cell Line, Tumor
Chemotherapy
Cytokines
Disease Models, Animal
Energy Metabolism
ES‐2
Ethanol
Female
Heterografts
Histology
Humans
IL‐6
Laboratory animals
Medical prognosis
Mice
Mitochondria - metabolism
Muscle Strength
Muscular Atrophy - diagnostic imaging
Muscular Atrophy - metabolism
Muscular Atrophy - pathology
Musculoskeletal system
Mutation
Organ Size
Original
Ovarian cancer
Ovarian Neoplasms - complications
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Penicillin
Quality of life
Sarcopenia
Signal Transduction
Skeletal muscle
X-Ray Microtomography
SummonAdditionalLinks – databaseName: ProQuest Publicly Available Content
  dbid: PIMPY
  link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZgi1AvvB-BgozgAlLYOA_HywVBRXmIrVaiQuUU-Um36iZls6n685lxvIEVVU_cdpNJZGfG48_x5PsIecGY1MJNRKxMlsV5wVwMOE7FQkqnMs5T7VUUvn8t9_fF4eFkFj6PbkNZ5Ton-kTdsz1j3TYk4bFpNL4xHwMOACAMa3D-9vRXjBpSuNcaBDWuki0k3hIjsjX7PJ39GN65ILk496KtKX5BXQA2GhhL0_GxbhevIZEztjFHeSr_i_Dnv2WUf8NbPz_t3fy_PbtFbgScSt_1gXWbXLH1HXJ9Gnbi75LuI6zfV0e0cbQ5g_W2rKnGAFrSc1tjyZdbtXCka21LT6CTaLjoWrgXlbWhqqktXQBwf0MlBWRPvSIPBQRNAZFST3qLl4R7aqSdPp_Le-Rg78PB7qc4SDjEmgPYiEsY4KaQqS1czq1kSsP8p5nNhUIeK_jjUjNBtWAASjZziWNSqsxxURRpLrL7ZFRDgx4SahMlLFeaG1MiJb5wwkonDTwto1VSROTl2meVDvTmqLJxUvXEzGmF_q28fyPyfLA97Uk9LrR6j64fLJCI2x9olj-rMK4rLblkKNMuVJlro0WhbQkg1aYld1pCs3bWTq9CdmirPz6OyLPhNIxr3KyRtW06sIFcLJIMLCPyoI-zoSWZLwhN4OpyIwI3mrp5pp4fee5wQMs5Y2VEXvlYvaT71Zfdb1P_69HlfXhMtgFFir4qcoeMVsvOPiHX9Nlq3i6fhjH4G8hJQfo
  priority: 102
  providerName: ProQuest
– databaseName: Wiley Open Access Journals
  dbid: 24P
  link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3da9UwFA9jivgyv13dlIi-KNQ1SZvkDl90OEXcGDhkbyVJE3fHbjtub8f-fM9JezsvDkF8a5OTkI9zkl--foeQ14wZp8NEp7YSIs0LFlLAcTbVxgQrpOQuelH48U0dHuqTk8nRGnm_fAvT80OMG25oGXG8RgM3tt25Jg09c-3sHYy7-LD3FmNCo-MGnh-NOyxIJS6ji1aO76ULQEIjPynfuU6-MiNF4v6b0OaflyZ_B7NxNtq_93_1uE82BhRKP_Rq84Cs-fohuXMwnLM_It1nWJ0vTmkTaHMJq2lTU4fqMadXvsYLXWHRQkjX-paeQ6VQcNa1kBc1dUVtU3s6A1i-Sw0F3E6jvx0K-JgC3qSR0haTDHk6JJW-mprH5Hj_0_Hel3Rw0JA6CVAiVWC-VWG4L0IuvWHWwezmmM-1RZYq-Am8mqAvYIBBXoQsMGOsCFIXBc-1eELWayjQJqE-s9pL62RVKSS810F7E0zFJ6pyNisS8mbZR6UbyMvRh8Z52dMu8xKbsYzNmJBXo-xFT9lxo9RH7OpRAmm2Y0Az_1kOVls6Iw1DJ-zaqtxVThfOK4CgnisZnIFibS8VpRxsvy0Bo8IiLVNSJuTlGA1Wi0cxpvZNBzIw0upMgGRCnvZ6NZZExOueGaRWKxq3UtTVmHp6GpnBAQvnjKmEvI0a95fql1_3vh_Er2f_IrxF7gJi1P0NyG2yvph3_jm57S4X03b-ItrfLyq9M5E
  priority: 102
  providerName: Wiley-Blackwell
Title Growth of ovarian cancer xenografts causes loss of muscle and bone mass: a new model for the study of cancer cachexia
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjcsm.12311
https://www.ncbi.nlm.nih.gov/pubmed/30009406
https://www.proquest.com/docview/2329740766
https://www.proquest.com/docview/2070803329
https://pubmed.ncbi.nlm.nih.gov/PMC6104117
https://doaj.org/article/ca6a145268b74cdc85ce7324e276fca5
Volume 9
WOSCitedRecordID wos000442345000007&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVAON
  databaseName: DOAJ Directory of Open Access Journals
  customDbUrl:
  eissn: 2190-6009
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0000461650
  issn: 2190-5991
  databaseCode: DOA
  dateStart: 20100101
  isFulltext: true
  titleUrlDefault: https://www.doaj.org/
  providerName: Directory of Open Access Journals
– providerCode: PRVPQU
  databaseName: Health & Medical Collection
  customDbUrl:
  eissn: 2190-6009
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0000461650
  issn: 2190-5991
  databaseCode: 7X7
  dateStart: 20100901
  isFulltext: true
  titleUrlDefault: https://search.proquest.com/healthcomplete
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: ProQuest Central
  customDbUrl:
  eissn: 2190-6009
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0000461650
  issn: 2190-5991
  databaseCode: BENPR
  dateStart: 20100901
  isFulltext: true
  titleUrlDefault: https://www.proquest.com/central
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: Publicly Available Content Database
  customDbUrl:
  eissn: 2190-6009
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0000461650
  issn: 2190-5991
  databaseCode: PIMPY
  dateStart: 20100901
  isFulltext: true
  titleUrlDefault: http://search.proquest.com/publiccontent
  providerName: ProQuest
– providerCode: PRVWIB
  databaseName: Wiley Free Archive
  customDbUrl:
  eissn: 2190-6009
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0000461650
  issn: 2190-5991
  databaseCode: WIN
  dateStart: 20100101
  isFulltext: true
  titleUrlDefault: https://onlinelibrary.wiley.com
  providerName: Wiley-Blackwell
– providerCode: PRVWIB
  databaseName: Wiley Online Library Open Access
  customDbUrl:
  eissn: 2190-6009
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0000461650
  issn: 2190-5991
  databaseCode: 24P
  dateStart: 20100101
  isFulltext: true
  titleUrlDefault: https://authorservices.wiley.com/open-science/open-access/browse-journals.html
  providerName: Wiley-Blackwell
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3fb9MwED7BQIgXxG8CozKCF5DCYiexXd7YtMEQrSKYoDxFtmNrRWuKmmban8_ZyaJWTPDCixXHF-viO9uflct3AK8oVUa6sYx1laZxllMXI47TsVTK6ZRzZkIWhW-fxXQqZ7NxsZHqy8eEdfTA3cDtGcUV9XmwpRaZqYzMjRWIAiwT3BkV2EsR9WwcpsIanHHKQ3pW5v-VzhEFDdykbO-naRZvccmmdGs3CqT9VyHNPwMmN4Fs2ImO7sKdHkKS953q9-Care_DrUn_kfwBtB_waL0-JUtHlud4FFY1Md62K3Jhax-N5dYN3mkb25Az1MoLLtoG-yKqrohe1pYsEFO_I4og6CYhWQ5BcEsQLJLAR-sf6fs0nhH6Yq4ewsnR4cnBx7jPrhAbjjggFjj3qlwxm7uMW0W1wa3JUJtJ7SmmsOJYNfaJfBHD2NQljiqlU8dlnrNMpo9gp0aFngCxiZaWa8OrSni2eumkVU5VbCwqo5M8gteXg1yannncJ8A4KzvOZFZ6g5TBIBG8HGR_dXwbV0rte1sNEp4jO9xAzyl7zyn_5TkR7F5auuwnblMiwMQTViI4j-DF0IxTzn9HUbVdtiiDy6RMUpSM4HHnGIMmaYjVTPBpseUyW6put9Tz00DrjUA2o1RE8CY4119ev_x08HUSrp7-j4F4BrcRBsourHEXdtar1j6Hm-Z8PW9WI7jOsgJLMROhlCO4sX84Lb6MwpTDWnE8KX5g7fvx9Dc0wC5f
linkProvider Directory of Open Access Journals
linkToHtml http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1bb9MwFLbGQMAL90thgBHwAFJYnYvtIiEEg7GxdkKiQn2zbMdmRWsymnYbP4r_yDlOGqiY9rYH3nI5sezkXL6TnHyHkKeMaSt9T0YmT5IozZiPAMeZSGrtTcJ5bEMXha99sbsrR6Pe5xXya_EvDJZVLnxicNR5afEd-TpEfoC-kHXzNwc_IuwahV9XFy00arXYcT-PIGWrXm-_h-f7LI43Pww3tqKmq0BkOcS_SIDO5ZmOXeZT7jQzFlyyZS6VBqmVYMfHeQ8b2ELsdonveqa1STyXWRanMoFhz5HzICawgkyMRPtKB7nLeegJG-MP2hlAr5YQNV7_bqvJS4gTjC2FwNAp4CR4-2-V5t_oOYS_zav_2Y27Rq40OJu-rQ3jOllxxQ1ycdBUEtwk84_T8mi2R0tPy0MNVlhQiwYwpceuwJI1P6vgyLxyFd2Hu4iCk3kFY1Fd5NSUhaMTSDxeUU0hM6GhoxCFDIACoqaBtBcvaca0SJt9PNa3yPAs1nybrBYwobuEuq6RjhvL81wgpb_00mmvc3g4uTXdrEOeL5RC2YaeHbuE7KuaWDpWqEAqKFCHPGllD2pSkhOl3qFutRJIJB4OlNNvqvFLymquGbaZl0akNrcys04AyHax4N5qmNbaQqtU490q9UelOuRxexr8En5s0oUr5yADsUR2E5DskDu1IrczSUJBaxeuFksqvjTV5TPFeC9wnwPaTxkTHfIiGMMpy1efNr4Mwta909fwiFzaGg76qr-9u3OfXAZELOsKzzWyOpvO3QNywR7OxtX0YTB3StQZW8lvYLGOCQ
linkToPdf http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1bb9MwFD4aA028cL8UBhgBDyCF1rnYLhJCsDEY26pJm1DfLNuxWdGajKbdxk_j33HspIGKaW974C2XE8tOzjU5-T6A55QqI1xfRDpPkijNqIswj9ORUMrphLHYBBaFr9t8MBDDYX93CX7N_4XxbZVznxgcdV4a_468i5EfU1-sulnXNW0Ru-sb745-RJ5Byn9pndNp1CqyZX-eYPlWvd1cx2f9Io43Pu6vfY4ahoHIMIyFEUf9yzMV28ylzCqqDbpnQ20qtIdZwh0X531PZotx3Cau56hSOnFMZFmcigSHvQSXeZJwzxrBh7x9veNxzFngh439z9oZpmEtOGrc_W6q8WuMGZQuhMPAGnBWqvtvx-bfmXQIhRvX_-ObeAOuNfk3eV8bzE1YssUtWNlpOgxuw-zTpDyZHpDSkfJYoXUWxHjDmJBTW_hWNjet8MisshU5xDvqBcezCsciqsiJLgtLxliQvCGKYMVCAtMQwcqAYKZNApivv6QZ03g47dORugP7F7Hmu7Bc4ITuA7E9LSzThuU591D_wgmrnMrxQeVG97IOvJwriDQNbLtnDzmUNeB0LL0yyaBMHXjWyh7VYCVnSn3wetZKeIDxcKCcfJONv5JGMUU9_bzQPDW5EZmxHJNvG3PmjMJprc41TDZer5J_1KsDT9vT6K_8RyhV2HKGMhhjRC9ByQ7cq5W6nUkSGl17eDVfUPeFqS6eKUYHARMdq4CUUt6BV8Ewzlm-_LK2txO2Hpy_hiewgsYhtzcHWw_hKibKom78XIXl6WRmH8EVczwdVZPHwfIJyAs2kt906Za9
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Growth+of+ovarian+cancer+xenografts+causes+loss+of+muscle+and+bone+mass%3A+a+new+model+for+the+study+of+cancer+cachexia&rft.jtitle=Journal+of+cachexia%2C+sarcopenia+and+muscle&rft.au=Pin%2C+Fabrizio&rft.au=Barreto%2C+Rafael&rft.au=Kitase%2C+Yukiko&rft.au=Mitra%2C+Sumegha&rft.date=2018-08-01&rft.pub=John+Wiley+and+Sons+Inc&rft.issn=2190-5991&rft.eissn=2190-6009&rft.volume=9&rft.issue=4&rft.spage=685&rft.epage=700&rft_id=info:doi/10.1002%2Fjcsm.12311&rft_id=info%3Apmid%2F30009406&rft.externalDocID=PMC6104117
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2190-5991&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2190-5991&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2190-5991&client=summon