The Emerging Role of Interleukin 1β (IL-1β) in Cancer Cachexia

Laird, Barry; Skipworth, Richard J E; Fallon, Marie; Paval, D Robert; McNeish, Iain A.; Gallagher, Iain J.

doi:10.1007/s10753-021-01429-8

Cited by 34 publications

(20 citation statements)

References 54 publications

(69 reference statements)

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“…Furthermore, intensive preoperative rehabilitation and weight training have similarly failed to improve outcomes, although studies are limited 50 . Numerous other trials in patients with cachexia have or are underway including supplementation with ghrelin 51 and androgen receptor 52 agonists, supplementation with omega‐3 fatty acids 53 and essential amino acids, 10 cannabinoid agonists, 54 and anti‐inflammatory antibodies (anti‐IL‐1) 55 . Although some have demonstrated improvement in body weight and skeletal muscle mass, there is little evidence to suggest any benefit in major outcomes such as survival and/or postoperative results 1 .…”

Section: Discussionmentioning

confidence: 99%

“…50 Numerous other trials in patients with cachexia have or are underway including supplementation with ghrelin 51 and androgen receptor 52 agonists, supplementation with omega-3 fatty acids 53 and essential amino acids, 10 cannabinoid agonists, 54 and anti-inflammatory antibodies (anti-IL-1). 55 Although some have demonstrated improvement in body weight and skeletal muscle mass, there is little evidence to suggest any benefit in major outcomes such as survival and/or postoperative results. 1 With such limited improvement of patients with cachexia using current therapies, more targeted animal and clinical trials have emerged which hold promising future interventions to mitigate or reverse the cachectic process and improve patient outcomes.…”

Section: Discussionmentioning

confidence: 99%

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Postoperative consequences of cancer cachexia after head and neck free flap reconstruction

et al. 2022

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Background Cachexia is detrimental for patients with head and neck cancer (HNC). However, postoperative consequences of HNC cachexia remain unknown. Methods A 2014–2019 retrospective review was performed of adults undergoing aerodigestive HNC resection with free tissue reconstruction. Propensity score matching using inverse probability of treatment weighting (IPTW) of cachectic and control groups was employed to adjust for covariate imbalances followed by binary logistic regression on postoperative outcomes. Results Out of 252 total patients, 135 (53.6%) had cancer cachexia. The cohort was predominantly white (94.4%) males (65.1%) aged 61.5 ± 11.5 years with stage III–IV (84.1%) malignancy of the oral cavity (66.3%). After matching cohort pre‐ and intra‐operative covariates using IPTW, cancer cachexia remained a strong, significant predictor of serious National Surgical Quality Improvement Program (NSQIP) complications (OR [95%CI] = 3.84 [1.80–8.21]) and major Clavien‐Dindo complications (OR [95%CI] = 3.00 [1.18–7.60]). Conclusions Cancer cachexia is associated with worse HNC free flap reconstruction outcomes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Postoperative consequences of cancer cachexia after head and neck free flap reconstruction

et al. 2022

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“…Upd3 has been considered a homolog of mammalian interleukins (ILs), which canonically activate Jak/Stat signaling and are highly associated with cancer cachexia and muscle wasting ( Bonetto et al, 2012 ; Flint et al, 2016 ; Laird et al, 2021 ; Strass-mann et al, 1992 ). However, ILs are produced mostly in host organs, and the effects on muscle atrophy of different ILs, such as IL-1, IL-6, IL-8, and IL-12, remain controversial ( Aoyagi et al, 2015 ), probably because of functional compensation and context-dependent differences.…”

Section: Discussionmentioning

confidence: 99%

Coordination of tumor growth and host wasting by tumor-derived Upd3

Ding

Xiang

et al. 2021

Cell Reports

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SUMMARY yki -induced gut tumors in Drosophila are associated with host wasting, including muscle dysfunction, lipid loss, and hyperglycemia, a condition reminiscent of human cancer cachexia. We previously used this model to identify tumor-derived ligands that contribute to host wasting. To identify additional molecular networks involved in host-tumor interactions, we develop PathON, a web-based tool analyzing the major signaling pathways in Drosophila , and uncover the Upd3/Jak/Stat axis as an important modulator. We find that yki -gut tumors secrete Upd3 to promote self-overproliferation and enhance Jak/Stat signaling in host organs to cause wasting, including muscle dysfunction, lipid loss, and hyperglycemia. We further reveal that Upd3/Jak/Stat signaling in the host organs directly triggers the expression of ImpL2 , an antagonistic binding protein for insulin-like peptides, to impair insulin signaling and energy balance. Altogether, our results demonstrate that yki -gut tumors produce a Jak/Stat pathway ligand, Upd3, that regulates both self-growth and host wasting.

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“…IL-1β is shown to have a similar effect on cancer-associated cachexia (Laird et al, 2021). By use of IL1-receptor antagonists tumor cachexia, as well as growth of colon cancer in C57BL6 mice, are attenuated (Strassmann et al, 1993).…”

Section: The Role Of An Inflammatory Response Originated From the Heart Or Cancer And Its Implication In Metabolic Disordersmentioning

confidence: 99%

Cancer—A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism

et al. 2021

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Cardiovascular diseases have multifactorial causes. Classical cardiovascular risk factors, such as arterial hypertension, smoking, hyperlipidemia, and diabetes associate with the development of vascular stenoses and coronary heart disease. Further comorbidities and its impact on cardiovascular metabolism have gotten more attention recently. Thus, also cancer biology may affect the heart, apart from cardiotoxic side effects of chemotherapies. Cancer is a systemic disease which primarily leads to metabolic alterations within the tumor. An emerging number of preclinical and clinical studies focuses on the interaction between cancer and a maladaptive crosstalk to the heart. Cachexia and sarcopenia can have dramatic consequences for many organ functions, including cardiac wasting and heart failure. These complications significantly increase mortality and morbidity of heart failure and cancer patients. There are concurrent metabolic changes in fatty acid oxidation (FAO) and glucose utilization in heart failure as well as in cancer, involving central molecular regulators, such as PGC-1α. Further, specific inflammatory cytokines (IL-1β, IL-6, TNF-α, INF-β), non-inflammatory cytokines (myostatin, SerpinA3, Ataxin-10) and circulating metabolites (D2-HG) may mediate a direct and maladaptive crosstalk of both diseases. Additionally, cancer therapies, such as anthracyclines and angiogenesis inhibitors target common metabolic mechanisms in cardiomyocytes and malignant cells. This review focuses on cardiovascular, cancerous, and cancer therapy-associated alterations on the systemic and cardiac metabolic state.

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The Emerging Role of Interleukin 1β (IL-1β) in Cancer Cachexia

Cited by 34 publications

References 54 publications

Postoperative consequences of cancer cachexia after head and neck free flap reconstruction

Postoperative consequences of cancer cachexia after head and neck free flap reconstruction

Coordination of tumor growth and host wasting by tumor-derived Upd3

Cancer—A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism

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