O.36 Pentoxifylline prevents the muscle wasting of tumour-be-ring rats by suppressing the activation of 20S and 26S proteasomes

Combaret, Lydie; Rallière, Cécile; Taillandier, Daniel; Attaix, Didier

doi:10.1016/s0261-5614(98)80104-0

Cited by 3 publications

(1 citation statement)

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“…Pentoxifylline is known to inhibit production of proinflammatory cytokines, including TNF, and suppresses protein breakdown in a tumor-bearing rat model of cachexia [123]. However, a controlled trial of pentoxifylline in patients with cancer cachexia failed to demonstrate any benefit in terms of appetite or nutritional measures compared with placebo [124].…”

Section: Pharmacologic Approachesmentioning

confidence: 99%

Disordered Metabolic Response with Cancer and Its Management

2000

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The metabolic changes in cancer cachexia appear to be mediated by a complex network of proinflammatory cytokines, neuroendocrine hormones, neurotransmitters, eicosanoids, and tumor-derived factors produced by the body in response to the tumor and by the tumor itself. The relative importance of these various mediator pathways in relation to either the anorexia or hypermetabolism associated with weight loss in cancer remains to be fully elucidated. Our current understanding suggests that proinflammatory mediators may indeed be a valid target for therapeutic intervention. Trials attempting to modify the inflammatory response to cancer with the hope of improving appetite and reversing catabolism and perhaps thereby improving qualityof life and survival are currently underway.

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Section: Pharmacologic Approachesmentioning

confidence: 99%

Disordered Metabolic Response with Cancer and Its Management

2000

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Cancer cachexia

Fearon

Moses

2002

International Journal of Cardiology

123

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Cancer cachexia is a complex, multifactorial syndrome that results from a reduction in food intake, a variety of metabolic abnormalities (including hypermetabolism) or more often a combination of the two. Multiple mediator pathways including pro-inflammatory cytokines, neuroendocrine hormones and tumour-specific factors are involved. Therapy requires a multi-model approach that addresses both reduced food intake and metabolic change. Combination treatments such as nutritional support plus metabolic/inflammation modulation promise improved functional capacity and quality of life.

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