Cited by 319Nutrition and Health in AgingMuscle Physiology and DisordersMuscle metabolism and nutrition

Muscle wasting in cancer cachexia: clinical implications, diagnosis, and emerging treatment strategies

Dodson, Shontelle, Baracos, Vickie E., Jatoi, Aminah, Evans, William J., Cella, David, Dalton, James T., Steiner, Mitchell S.·2011·Annual Review of Medicine

Abstract

Cancer cachexia is a complex metabolic condition characterized by loss of skeletal muscle. Common clinical manifestations include muscle wasting, anemia, reduced caloric intake, and altered immune function, which contribute to increased disability, fatigue, diminished quality of life, and reduced survival. The prevalence of cachexia and the impact of this disorder on the patient and family underscore the need for effective management strategies. Dietary supplementation and appetite stimulation alone are inadequate to reverse the underlying metabolic abnormalities of cancer cachexia and have limited long-term impact on patient quality of life and survival. Therapies that can increase muscle mass and physical performance may be a promising option; however, there are currently no drugs approved for the prevention or treatment of cancer cachexia. Several agents are in clinical development, including anabolic agents, such as selective androgen receptor modulators and drugs targeting inflammatory cytokines that promote skeletal muscle catabolism.

Integrity signals

Registry

Crossref · 10.1146/annurev-med-061509-131248

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83 of 83 references verified0 citation errors · 0 not checkable

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  • Tumour-induced inflammation can increase production of tumour necrosis factor alpha, interleukin 6, interferon gamma, and other cytokines, resulting in increased protein catabolism, decreased protein anabolism, insulin resistance, and lipolysis.

    “Tumour-induced inflammation can lead to increased production of tumour necrosis factor alpha, interleukin 6, interferon gamma, and other cytokines, which results in increased protein catabolism, decreased protein anabolism, insulin resistance, and lipolysis.115”

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Authors
Dodson, S., Baracos, V. E., Jatoi, A., Evans, W. J., Cella, D., Dalton, J. T., & Steiner, M. S.
Affiliations
  • GTx (United States) (US)
  • University of Alberta (CA)
  • Mayo Clinic (US)
  • GlaxoSmithKline (United States) (US)
  • Robert H. Lurie Comprehensive Cancer Center of Northwestern University (US)
Venue
Annual Review of Medicine
Published
2011-02-18
Volume
62
Issue
1
Pages
265-279
ISSN
  • 0066-4219 (ISSN-L)
  • 1545-326X
OpenAlex
W2121063540
Cited by
319
References
83
Citations by year
2026: 2 · 2025: 15 · 2024: 15 · 2023: 16 · 2022: 22 · 2021: 22 · 2020: 23 · 2019: 17 · 2018: 21 · 2017: 19 · 2016: 19 · 2015: 26 · 2014: 31 · 2013: 19 · 2012: 34
FWCI
2.17
Type
journal article
Language
en
Open access
closed
Locations
  • Annual Review of Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
Keywords
cancer cachexia, muscle atrophy, skeletal muscle atrophy, anemia, energy intake, immune function, quality of life, survival, dietary supplementation, appetite stimulation, muscle mass, physical performance, anabolic agents, selective androgen receptor modulators, inflammatory cytokines, skeletal muscle catabolism, cachexia treatment
MeSH terms
Cachexia, Clinical Trials as Topic, Energy Metabolism, Female, Humans, Male, Muscular Atrophy, Neoplasms, Quality of Life, Cytokines, Muscle, Skeletal, Anabolic Agents

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