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. 2020 Dec;2(4):177-185.
doi: 10.1016/j.smhs.2020.10.003. Epub 2020 Dec 3.

Development and progression of cancer cachexia: Perspectives from bench to bedside

Seongkyun Lim  1 , Jacob L Brown  2 , Tyrone A Washington  3 , Nicholas P Greene  1
Affiliations

Development and progression of cancer cachexia: Perspectives from bench to bedside

Seongkyun Lim et al. Sports Med Health Sci. 2020 Dec.

Abstract

Cancer cachexia (CC) is a devastating syndrome characterized by weight loss, reduced fat mass and muscle mass that affects approximately 80% of cancer patients and is responsible for 22%-30% of cancer-associated deaths. Understanding underlying mechanisms for the development of CC are crucial to advance therapies to treat CC and improve cancer outcomes. CC is a multi-organ syndrome that results in extensive skeletal muscle and adipose tissue wasting; however, CC can impair other organs such as the liver, heart, brain, and bone as well. A considerable amount of CC research focuses on changes that occur within the muscle, but cancer-related impairments in other organ systems are understudied. Furthermore, metabolic changes in organ systems other than muscle may contribute to CC. Therefore, the purpose of this review is to address degenerative mechanisms which occur during CC from a whole-body perspective. Outlining the information known about metabolic changes that occur in response to cancer is necessary to develop and enhance therapies to treat CC. As much of the current evidences in CC are from pre-clinical models we should note the majority of the data reviewed here are from preclinical models.

Keywords: Lewis lung carcinoma; Mitochondrial dysfunction; Muscle atrophy; Protein turnover; Tumor-bearing mouse.

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Conflict of interest statement

Conflict of interest The authors declare no financial or other conflicts of interest that could influence the interpretations of this work.

Figures

Fig. 1
Fig. 1
Summary of alterations previously demonstrated in non-skeletal muscle tissues during cancer cachexia.
See this image and copyright information in PMC

References

    1. Ferlay J., Soerjomataram I., Dikshit R., et al. Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012. Int J Canc. Mar 1 2015;136(5):E359–E386. doi: 10.1002/ijc.29210. - DOI - PubMed
    1. Bray F., Ferlay J., Soerjomataram I., Siegel R.L., Torre L.A., Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA A Cancer J Clin. 2018;68(6):394–424. doi: 10.3322/caac.21492. - DOI - PubMed
    1. Fearon Kenneth C.H., Glass David J., Guttridge Denis C. Cancer cachexia: mediators, signaling, and metabolic pathways. Cell Metabol. 8/8/2012;16(2):153–166. doi: 10.1016/j.cmet.2012.06.011. - DOI - PubMed
    1. Onesti J.K., Guttridge D.C. Inflammation based regulation of cancer cachexia. BioMed Res Int. 2014;2014:168407. doi: 10.1155/2014/16840710.1155/2014/168407. - DOI - PMC - PubMed
    1. Smith B.D., Smith G.L., Hurria A., Hortobagyi G.N., Buchholz T.A. Future of cancer incidence in the United States: burdens upon an aging, changing nation. J Clin Oncol : Off. J. Am. Soc. Clin. Oncol. Jun 10 2009;27(17):2758–2765. doi: 10.1200/jco.2008.20.8983. - DOI - PubMed