The rationale for preventing cancer cachexia: targeting excessive fatty acid oxidation.

Chao-Nan Qian

doi:10.1186/s40880-016-0129-8

Abstract

Cachexia commonly occurs at the terminal stage of cancer and has largely unclear molecular mechanisms. A recent study published in Nature Medicine, entitled “Excessive fatty acid oxidation induces muscle atrophy in cancer cachexia,” reveals that cachectic cancer cells can secrete multiple cytokines that induce excessive fatty acid oxidation, which is responsible for muscle loss in cancer cachexia. Inhibition of fatty acid oxidation using etomoxir can increase muscle mass and body weight in cancer cachexia animal models. The usage of stable cachexia animal models is also discussed in this research highlight.

Highlights

Cachexia commonly occurs at the terminal stage of cancer and has largely unclear molecular mechanisms
In patients with nasopharyngeal carcinoma from endemic areas, whose tumors are naturally sensitive to radiotherapy [4, 5], cachexia can be induced by radical radiotherapy in patients with post-irradiation nasopharyngeal necrosis [6]
It is believed that early diagnosis of and intervention in cancer cachexia can control its fetal progression, improve a patient’s quality of life, and prolong survival [8]

Summary

Introduction

Cachexia commonly occurs at the terminal stage of cancer and has largely unclear molecular mechanisms. In the terminal stages of many chronic diseases, including cancer, loss of body mass may occur, which cannot be prevented or corrected by nutritional supplementation. This condition is termed cachexia, defined as >5% weight loss within 6 months.

Results

Conclusion