Abstract
Cancer is a life-threatening disease that has plagued humans for centuries. The vast majority of cancer-related mortality results from metastasis. Indeed, the invasive growth of metastatic cancer cells in vital organs causes fatal organ dysfunction, but metastasis-related deaths also result from cachexia, a debilitating wasting syndrome characterized by an involuntary loss of skeletal muscle mass and function. In fact, about 80% of metastatic cancer patients suffer from cachexia, which often renders them too weak to tolerate standard doses of anticancer therapies and makes them susceptible to death from cardiac and respiratory failure. The goals of this review are to highlight important findings that help explain how cancer-induced systemic changes drive the development of cachexia and to discuss unmet challenges and potential therapeutic strategies targeting cachexia to improve the quality of life and survival of cancer patients.
Highlights
With disease progression, cancers induce systemic changes in tissues such as the bone, liver, adipose tissue, and skeletal muscles (Argiles et al 2018, Kaplan et al 2006, McAllister & Weinberg 2010)
A cachexia diagnosis in cancer patients has become increasingly difficult in the current age of obesity, where the loss of muscle mass can be masked by fat gain (Esfandiari et al 2014)
Great strides have been achieved in the field of cancer-associated cachexia due to mechanistic studies that have identified how muscle and fat cells respond to Tumor-induced systemic factors (TISFs) and perturbed signaling pathways; the great majority of experimental studies designed for treating cachexia have performed poorly in over 100 clinical trials
Summary
Cancers induce systemic changes in tissues such as the bone, liver, adipose tissue, and skeletal muscles (Argiles et al 2018, Kaplan et al 2006, McAllister & Weinberg 2010) These changes perturb tissue homeostasis and create a metabolic imbalance in the host. Possibilities include tumor-derived factors, metabolites from a secondary organ that is indirectly impacted by the tumor, or perhaps circulating factors derived from the altered immune system (Fearon et al 2012) It is unclear whether there exists a master regulator of cachexia or whether unique combinations of already-identified mediators, which may differ depending on the type and stage of cancer, drive cachexia. We discuss advances in cancer-associated cachexia research in light of these questions and highlight the challenges and promising areas of research
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