The Latest Treatments for Cancer Cachexia: An Overview

Watanabe, Hayato; Oshima, Takashi

doi:10.21873/anticanres.16188

Cited by 16 publications

(20 citation statements)

References 76 publications

(90 reference statements)

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“…Selective and safe control of the interconnected pathways of appetite, satiety, nausea, and emesis has become a therapeutic objective. Hundreds of millions of patients worldwide suffer from a range of disorders that could be treated with novel medicines that impact these processes 10,11 . Therapies that suppress appetite or stimulate satiety may help treat obesity and type 2 diabetes by curbing food intake and reducing weight.…”

Section: Mainmentioning

confidence: 99%

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Identification and characterization of human GDF15 knockouts

Gurtan,

Khalid,

Koch

et al. 2024

Preprint

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Growth differentiation factor 15 (GDF15) is a secreted protein that regulates food intake, body weight, and stress responses in pre-clinical models1. The physiological function of GDF15 in humans remains unclear. Pharmacologically, GDF15 agonism in humans caused nausea without accompanying weight loss2, and the effect of GDF15 antagonism is being tested in clinical trials to treat cachexia and anorexia. Human genetics point to a role for GDF15 in hyperemesis gravidarum, but the safety or impact of complete GDF15 loss, particularly during pregnancy, is unknown3-7. Here, we characterize GDF15 loss-of-function carriers (LOF), including 5 homozygous null carriers (knockouts) from 75,018 participants enrolled in the Pakistan Genomic Resource (PGR)8,9. We tested for the association of GDF15 LOF with 97 quantitative traits and binary outcomes. Further, 3 additional knockouts and 59 heterozygous carriers were identified in recall-by-genotype (RBG) studies accompanied by recruitment of family members. GDF15 knockouts ranged in age from 31 to 75 years, were fertile, and showed no consistent overt metabolic dysfunction. Collectively, our data indicate that: (i) complete GDF15 loss is compatible with life and fertility, (ii) chronic therapeutic inhibition of GDF15 may be tolerated, and (iii) GDF15 modulation may not significantly impact body weight or metabolic syndrome.

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Section: Mainmentioning

confidence: 99%

“…GLP1 receptor agonists, for example, reduce body weight in humans through appetite suppression and improved metabolic control 10 . Conversely, therapeutics that increase appetite or suppress nausea and emesis may treat disorders such as anorexia, cachexia, hyperemesis gravidarum, and associated sequelae 11 .…”

Section: Mainmentioning

confidence: 99%

Identification and characterization of human GDF15 knockouts

Gurtan,

Khalid,

Koch

et al. 2024

Preprint

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“…1 ) [ 13 , 15 ]. The loss of weight and muscle mass can be attributed to several factors such as decreased food intake, anorexia, insulin resistance, and low levels of anabolic hormones [ 6 ]. The involvement of the neuroendocrine system in cachexia and the role of the hypothalamus, pituitary gland, and adrenal gland in controlling appetite have recently gained attention in cancer cachexia study [ 16 – 21 ].…”

Section: Cancer Cachexia As a Multi-organ Syndromementioning

confidence: 99%

“…Cachexia is a syndrome characterized by weight and muscle loss (with or without adipose tissue loss) that cannot be entirely reversed by conventional nutritional support. It often occurs as a result of an underlying illness, which can induce various physiological changes including inflammation, loss of appetite or anorexia, low levels of testosterone and other anabolic hormones, and anemia [ 5 , 6 ]. These underlying illnesses can include cancer, kidney disease, heart failure, neurological disease, chronic obstructive pulmonary disease, and AIDS, among others [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Cancer cachexia: molecular mechanisms and treatment strategies

et al. 2023

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Muscle wasting is a consequence of physiological changes or a pathology characterized by increased catabolic activity that leads to progressive loss of skeletal muscle mass and strength. Numerous diseases, including cancer, organ failure, infection, and aging-associated diseases, are associated with muscle wasting. Cancer cachexia is a multifactorial syndrome characterized by loss of skeletal muscle mass, with or without the loss of fat mass, resulting in functional impairment and reduced quality of life. It is caused by the upregulation of systemic inflammation and catabolic stimuli, leading to inhibition of protein synthesis and enhancement of muscle catabolism. Here, we summarize the complex molecular networks that regulate muscle mass and function. Moreover, we describe complex multi-organ roles in cancer cachexia. Although cachexia is one of the main causes of cancer-related deaths, there are still no approved drugs for cancer cachexia. Thus, we compiled recent ongoing pre-clinical and clinical trials and further discussed potential therapeutic approaches for cancer cachexia.

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“…Steroids, in particular corticosteroids, to reduce systemic inflammation and megestrol acetate for appetite stimulation often provide short-term improvement. Similarly, anamorelin hydrochloride, an orally administered drug with ghrelin-like effects, can be used to stimulate appetite [22]. Other potential treatment options include physical exercise, targeted acupuncture, nutrition therapy, as well as enteral and parenteral nutrition.…”

Section: Introductionmentioning

confidence: 99%

Relevance of Dietary Supplement Use in Gastrointestinal-Cancer-Associated Cachexia

Yoon,

Grundmann

2023

Nutrients

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Cancer cachexia is a multi-organ syndrome with unintentional weight loss, sarcopenia, and systemic inflammation. Gastrointestinal (GI) cancer patients are more susceptible to cachexia development due to impaired nutrient absorption and digestion. Given the widespread availability and relatively low cost of dietary supplements, we examined the evidence and effects of fish oil (omega-3 fatty acids), melatonin, probiotics, and green tea for managing symptoms of GI cancer cachexia. A literature review of four specific supplements was conducted using PubMed, Google Scholar, and CINAHL without a date restriction. Of 4621 available literature references, 26 articles were eligible for review. Fish oil decreased C-reactive protein and maintained CD4+ cell count, while melatonin indicated inconsistent findings on managing cachexia, but was well-tolerated. Probiotics decreased serum pro-inflammatory biomarkers and increased the tolerability of chemotherapy by reducing side effects. Green tea preparations and extracts showed a decreased risk of developing various cancers and did not impact tumor growth, survival, or adverse effects. Among these four supplements, probiotics are most promising for further research in preventing systemic inflammation and maintaining adequate absorption of nutrients to prevent the progression of cancer cachexia. Supplements may benefit treatment outcomes in cancer cachexia without side effects while supporting nutritional and therapeutic needs.

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The Latest Treatments for Cancer Cachexia: An Overview

Cited by 16 publications

References 76 publications

Identification and characterization of human GDF15 knockouts

Identification and characterization of human GDF15 knockouts

Cancer cachexia: molecular mechanisms and treatment strategies

Relevance of Dietary Supplement Use in Gastrointestinal-Cancer-Associated Cachexia

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