| First Author | Robert F | Year | 2012 |
| Journal | Cancer Res | Volume | 72 |
| Issue | 3 | Pages | 747-56 |
| PubMed ID | 22158946 | Mgi Jnum | J:181113 |
| Mgi Id | MGI:5308836 | Doi | 10.1158/0008-5472.CAN-11-2739 |
| Citation | Robert F, et al. (2012) Targeting protein synthesis in a Myc/mTOR-driven model of anorexia-cachexia syndrome delays its onset and prolongs survival. Cancer Res 72(3):747-56 |
| abstractText | Anorexia-cachexia syndrome (ACS) is a major determinant of cancer-related death that causes progressive body weight loss due to depletion of skeletal muscle mass and body fat. Here, we report the development of a novel preclinical murine model of ACS in which lymphomas harbor elevated Myc and activated mTOR signaling. The ACS phenotype in this model correlated with deregulated expression of a number of cytokines, including elevated levels of interleukin-10 which was under the direct translational control of mTOR. Notably, pharmacologic intervention to impair protein synthesis restored cytokine production to near-normal levels, delayed ACS progression, and extended host survival. Together, our findings suggest a new paradigm to treat ACS by strategies which target protein synthesis to block the production of procachexic factors. |
