| Literature DB >> 29898649 |
Eun A Kang1, Young-Min Han1, Jeong Min An1, Yong Jin Park2, Predrag Sikiric3, Deok Hwan Kim4, Kwang An Kwon5, Yoon Jae Kim5, Donghwa Yang5, Hann Tchah5, Ki Baik Hahm1,4.
Abstract
Cancer cachexia, one of the metabolic syndromes caused by cancer, is a devastating and miserable condition encountered in more than 50% of terminal cancer patients presenting with significant weight loss associated with skeletal muscle atrophy and fat loss. Though cachexia may account for up to 20% of cancer deaths, no significant treatment is still lacking and is of urgent unmet medical need in cancer treatment. Therefore, understanding the underlying molecular mechanisms is essential for anticipating therapeutic approaches. Since the primary events driving cachexia are mediated via either the central nervous system relatedor inflammation related-anorexia, hypoanabolism, and hypercatabolism, therapy usually targets nutritional support to compensate reduced food intake along with some anti-inflammatory agents to cover specific inflammation-related metabolic derangement, and encourages exercise to supplement reduced physical activity, but all proven to be not so effective so far. Therefore, combination therapies such as a standard multi-modal package including an anorexic agent, megestrol acetate, and anti-inflammatory agent coupled with the development of potential novel therapeutics promise a new era in rescuing patients from cancer cachexia. In this review, we propose the potential application of BPC157, one of the active cytoprotective agents isolated from gastric juices for cancer cachexia. Before clinical trial, we introduced the evidence showing BPC157 rescued from cancer cachexia supported with explored mode of actions. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.Entities:
Keywords: BPC157; Cancer cachexia; cytoprotection; hypercatabolism; hypoanabolism; muscle atrophy.
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Year: 2018 PMID: 29898649 DOI: 10.2174/1381612824666180614082950
Source DB: PubMed Journal: Curr Pharm Des ISSN: 1381-6128 Impact factor: 3.116