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Preclinical and clinical studies on cancer-associated cachexia

Preclinical and clinical studies on cancer-associated cachexia

作     者:D. Brooke Widner D. Clark Files Kathryn E. Weaver Yusuke Shiozawa 

作者机构:Department of Cancer Biology and Comprehensive Cancer Center Wake Forest School of Medicine Winston-Salem NC 27157 USA Internal Medicine-Sections inPulmonaryand Critical Care Medicine and Geriatrics and the Critical Illness Injury and Recovery Research Center Wake Forest School of Medicine W~nston-Salem NC 27157 USA Department of Social Sciences and Health Policy and Comprehensive Cancer Center of Wake Forest University Wake Forest School of Medicine Wtnston-Salem NC 27157 USA 

出 版 物:《Frontiers in Biology》 (生物学前沿(英文版))

年 卷 期:2018年第13卷第1期

页      面:11-18页

核心收录:

学科分类:090603[农学-临床兽医学] 090706[农学-园林植物与观赏园艺] 0907[农学-林学] 09[农学] 0906[农学-兽医学] 

基  金:supported by National Cancer Institute Grants (Y. Shiozawa) Department of Defense (Y. Shiozawa) the Wake Forest Baptist Comprehensive Cancer Center Internal Pilot Funding (Y. Shiozawa) the Wake Forest School of Medicine Internal Pilot Funding (Y. Shiozawa) supported by the National Center for Advancing Translational Sciences (NCATS) National Institutes of Health, through Grant Award supported by the National Cancer Institute’s Cancer Center Support Grant award issued to the Wake Forest Baptist Comprehensive Cancer Center 

主  题:cancer cachexia muscle wasting bodyweight loss metabolic changes increased protein degradation decreased protein synthesis 

摘      要:BACKGROUND: Cancer cachexia is the wasting condition that is often seen in advanced stage cancer patients. This wasting is largely attributable to a systemic and progressive loss of skeletal muscle mass that greatly hinders performance of normal daily activities, resulting in reduced quality of life. Moreover, it negatively influences the prognosis of cancer patients. A general consensus in the field is that the loss of muscle mass is due both to an increase in protein degradation and a decrease in protein synthesis. Recent studies using preclinical models for studying cachexia have been useful in identifying the contribution of inflammatory cytokines (e.g. tumor necrosis factor-a and Interleukin-6), and myostatin receptors (e.g. the type IIB activin receptor) to cachexia development, and have led to several clinical trials. However, many questions remain about the molecular mechanisms thought to play a role in the development of cachexia. METHODS: We conducted a literature search using search engines, such as PubMed and Google Scholar to identify publications within the cancer cachexia field. RESULTS- We summarized our current knowledge of: 1) the driving mechanisms of cancer cachexia, 2) the preclinical models available for studying the condition, and 3) the findings of recent clinical trials. CONCLUSION: Cancer cachexia is a complex and variable condition that currently has no standard effective therapeutic treatment. Further studies are desperately needed to better understand this condition and develop effective combination treatments for patients.

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