Question:
Cancer associated cachexia is primarily mediated by which of the following cytokines?
Cancer associated cachexia is primarily mediated by which of the following cytokines?
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In board exams, whenever the historical mechanism of systemic wasting or cachexia in chronic disease (TB, cancer) is asked, TNF-$\alpha$ (cachectin) is almost always the answer. IL-6 is also heavily implicated, especially in stimulating CRP production.
Updated On: Sep 3, 2026
- IFN
- TNF-alpha
- Tumor related products
- Hormones
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The Correct Option is B
Solution and Explanation
Concept:
Cancer cachexia is a complex metabolic syndrome characterized by profound loss of muscle mass (with or without loss of fat mass) that cannot be fully reversed by conventional nutritional support.
It is driven by a systemic inflammatory state mediated by specific cytokines produced by both the tumor and the host immune system.
Explanation:
• Tumor Necrosis Factor-alpha (TNF-alpha) is a potent pro-inflammatory cytokine. Historically, before its role in tumor necrosis was fully understood, it was actually discovered and named cachectin because of its profound ability to induce severe wasting and cachexia in chronic diseases and cancer.
• TNF-alpha acts directly on skeletal muscle to increase protein degradation (via the ubiquitin-proteasome pathway) and decrease protein synthesis. It also acts on adipose tissue to promote lipolysis and acts on the hypothalamus to induce anorexia.
• Other major pro-inflammatory cytokines deeply involved in cancer cachexia include Interleukin-6 (IL-6) and Interleukin-1 beta (IL-1$\beta$).
• Option (A), Interferons, play a role in immune regulation and anti-viral states but are not the primary drivers of the massive metabolic shift seen in cachexia.
• Option (C), Tumor related products (like Proteolysis Inducing Factor - PIF), do play a role, but the question asks for the primary cytokine mediator, which classically points to host-derived cytokines like TNF-alpha.
Final answer:
TNF-alpha (cachectin) is the classical cytokine recognized as a central mediator of muscle wasting and metabolic derangement in cancer cachexia.
Cancer cachexia is a complex metabolic syndrome characterized by profound loss of muscle mass (with or without loss of fat mass) that cannot be fully reversed by conventional nutritional support.
It is driven by a systemic inflammatory state mediated by specific cytokines produced by both the tumor and the host immune system.
Explanation:
• Tumor Necrosis Factor-alpha (TNF-alpha) is a potent pro-inflammatory cytokine. Historically, before its role in tumor necrosis was fully understood, it was actually discovered and named cachectin because of its profound ability to induce severe wasting and cachexia in chronic diseases and cancer.
• TNF-alpha acts directly on skeletal muscle to increase protein degradation (via the ubiquitin-proteasome pathway) and decrease protein synthesis. It also acts on adipose tissue to promote lipolysis and acts on the hypothalamus to induce anorexia.
• Other major pro-inflammatory cytokines deeply involved in cancer cachexia include Interleukin-6 (IL-6) and Interleukin-1 beta (IL-1$\beta$).
• Option (A), Interferons, play a role in immune regulation and anti-viral states but are not the primary drivers of the massive metabolic shift seen in cachexia.
• Option (C), Tumor related products (like Proteolysis Inducing Factor - PIF), do play a role, but the question asks for the primary cytokine mediator, which classically points to host-derived cytokines like TNF-alpha.
Final answer:
TNF-alpha (cachectin) is the classical cytokine recognized as a central mediator of muscle wasting and metabolic derangement in cancer cachexia.
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