The well-characterized Drosophila RAS-SCRIB cancer model (FBhh0000585) has been used to investigate the phenomenon of cachexia, the dramatic loss of muscle mass associated with many advanced cancers. A larval system has been developed in which RAS-SCRIB neoplastic tumors are induced in the eye disc followed by quantification of the body wall muscle mass some days later.
Results using this system indicate that cachectic tissue wasting is dependent on the genetic characteristics of the tumor; neither host malnutrition nor significant tumor burden is sufficient to drive muscle wasting. JAK/STAT and TNF-α/Egr signaling were found to be elevated in cachectic muscle and to promote tissue wasting.
[updated Aug. 2021 by FlyBase; FBrf0222196]
Cachexia is characterized by a dramatic loss of skeletal muscle mass and adipose tissue, resulting in substantial weight loss. It is also known as "wasting syndrome", causing disproportionate muscle wasting, weakness, fatigue, and loss of appetite in affected individuals. Cachexia occurs in many cancers, usually at the advanced stages of disease. [http://www.news-medical.net/health/Cachexia-Wasting-Syndrome-.aspx and https://www.cancer.gov/about-cancer/treatment/research/cachexia]
Ortholog of human SCRIB and LRRC1 (1 Drosophila to 2 human); Dmel\scrib shares 33% identity and 45% similarity with the human SCRIB gene. The human LRRC1 gene encodes a much smaller protein, corresponding to the amino end of SCRIB and Dmel\scrib; it shares 57% identity and 73% similarity with Dmel\scrib within that extent.
