The association of body composition phenotypes before chemotherapy with epithelial ovarian cancer mortality.


Journal

Journal of the National Cancer Institute
ISSN: 1460-2105
Titre abrégé: J Natl Cancer Inst
Pays: United States
ID NLM: 7503089

Informations de publication

Date de publication:
28 May 2024
Historique:
received: 23 02 2024
revised: 17 04 2024
accepted: 11 05 2024
medline: 28 5 2024
pubmed: 28 5 2024
entrez: 27 5 2024
Statut: aheadofprint

Résumé

The association of body composition with epithelial ovarian carcinoma (EOC) mortality is poorly understood. To date, evidence suggests high adiposity associates with decreased mortality (an obesity paradox), but the impact of muscle on this association has not been investigated. Herein, we define associations of muscle and adiposity joint-exposure body composition phenotypes with EOC mortality. Body composition from 500 women in The Body Composition and Epithelial Ovarian Cancer Survival Study was dichotomized as normal/low skeletal muscle index (SMI), a proxy for sarcopenia and high/low adiposity. Four phenotypes were classified as fit/reference (normal SMI/low adiposity; 16.2%), overweight/obese (normal SMI/high adiposity; 51.2%), sarcopenia/overweight-obese (low SMI/high adiposity; 15.6%), and sarcopenia/cachexia (low SMI/low adiposity; 17%). We used multivariable Cox models to estimate associations of each phenotype with mortality for EOC overall and high-grade serous ovarian carcinoma (HGSOC). Overweight/obesity was associated with up to 51% and 104% increased mortality in EOC and HGSOC (HR = 1.51, 95% CI: 1.05-2.19 and HR = 2.04, 95% CI: 1.29-3.21). Sarcopenia/overweight-obesity was associated with up to 66% and 67% increased mortality in EOC and HGSOC (HR = 1.66, 95% CI: 1.13-2.45 and HR = 1.67, 95% CI: 1.05-2.68). Sarcopenia/cachexia was associated with up to 73% and 109% increased mortality in EOC and HGSOC (HR = 1.73, 95% CI: 1.14-2.63 and HR = 2.09, 95% CI: 1.25-3.50). Overweight/obesity, sarcopenia/overweight-obesity and sarcopenia/cachexia phenotypes were each associated with increased mortality in EOC and HGSOC. Exercise and dietary interventions could be leveraged as ancillary treatment strategies for improving outcomes in the most fatal gynecological malignancy with no previously established modifiable prognostic factors.

Sections du résumé

BACKGROUND BACKGROUND
The association of body composition with epithelial ovarian carcinoma (EOC) mortality is poorly understood. To date, evidence suggests high adiposity associates with decreased mortality (an obesity paradox), but the impact of muscle on this association has not been investigated. Herein, we define associations of muscle and adiposity joint-exposure body composition phenotypes with EOC mortality.
METHODS METHODS
Body composition from 500 women in The Body Composition and Epithelial Ovarian Cancer Survival Study was dichotomized as normal/low skeletal muscle index (SMI), a proxy for sarcopenia and high/low adiposity. Four phenotypes were classified as fit/reference (normal SMI/low adiposity; 16.2%), overweight/obese (normal SMI/high adiposity; 51.2%), sarcopenia/overweight-obese (low SMI/high adiposity; 15.6%), and sarcopenia/cachexia (low SMI/low adiposity; 17%). We used multivariable Cox models to estimate associations of each phenotype with mortality for EOC overall and high-grade serous ovarian carcinoma (HGSOC).
RESULTS RESULTS
Overweight/obesity was associated with up to 51% and 104% increased mortality in EOC and HGSOC (HR = 1.51, 95% CI: 1.05-2.19 and HR = 2.04, 95% CI: 1.29-3.21). Sarcopenia/overweight-obesity was associated with up to 66% and 67% increased mortality in EOC and HGSOC (HR = 1.66, 95% CI: 1.13-2.45 and HR = 1.67, 95% CI: 1.05-2.68). Sarcopenia/cachexia was associated with up to 73% and 109% increased mortality in EOC and HGSOC (HR = 1.73, 95% CI: 1.14-2.63 and HR = 2.09, 95% CI: 1.25-3.50).
CONCLUSIONS CONCLUSIONS
Overweight/obesity, sarcopenia/overweight-obesity and sarcopenia/cachexia phenotypes were each associated with increased mortality in EOC and HGSOC. Exercise and dietary interventions could be leveraged as ancillary treatment strategies for improving outcomes in the most fatal gynecological malignancy with no previously established modifiable prognostic factors.

Identifiants

pubmed: 38802116
pii: 7682147
doi: 10.1093/jnci/djae112
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© The Author(s) 2024. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Auteurs

Evan W Davis (EW)

Department of Cancer Prevention and Control, Roswell Park Comprehensive Cancer Center, Buffalo, 14263, NY, USA.

Kristopher Attwood (K)

Department of Biostatistics and Bioinformatics, Roswell Park Comprehensive Cancer Center, Buffalo, 14263, NY, USA.

Joseph Prunier (J)

Lake Erie College of Osteopathic Medicine, Elmira, 14901, NY, USA.

Gyorgy Paragh (G)

Department of Dermatology, Roswell Park Comprehensive Cancer Center, Buffalo, 14263, NY, USA.

Janine M Joseph (JM)

Department of Cancer Prevention and Control, Roswell Park Comprehensive Cancer Center, Buffalo, 14263, NY, USA.

André Klein (A)

Department of Research Information Technology, Roswell Park Comprehensive Cancer Center, Buffalo, 14263, NY, USA.

Charles Roche (C)

Department of Diagnostic Radiology, Roswell Park Comprehensive Cancer Center, Buffalo, 14263, NY, USA.

Nancy Barone (N)

Department of Cancer Prevention and Control, Roswell Park Comprehensive Cancer Center, Buffalo, 14263, NY, USA.

John Lewis Etter (JL)

Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, 14623, NY, USA.

Andrew D Ray (AD)

Department of Cancer Prevention and Control, Roswell Park Comprehensive Cancer Center, Buffalo, 14263, NY, USA.
Department of Rehabilitation, Roswell Park Comprehensive Cancer Center, Buffalo, 14263, NY, USA.

Britton Trabert (B)

Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, 84112, UT, USA.
Huntsman Cancer Institute at the University of Utah, Cancer Control and Population Sciences, Salt Lake City, 84112, UT, USA.

Matthew B Schabath (MB)

Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, 33612, FL, USA.

Lauren C Peres (LC)

Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, 33612, FL, USA.

Rikki Cannioto (R)

Department of Cancer Prevention and Control, Roswell Park Comprehensive Cancer Center, Buffalo, 14263, NY, USA.

Classifications MeSH