Doyle, jr lieffers, n.

This abstract will be presented at ASCO in 2011 annual meeting, but was published in connection with the meeting. CMM Prado, VE Baracos, TS Bekaii-Saab, L. Doyle, JR Lieffers, N. Esfandiari, S. Ghosh, S. Antoun, MB Sawyer, Department of Oncology, University of Alberta, Edmonton, Canada, The Ohio State University Medical Center, Columbus, Ohio, National Institutes of Health / National Cancer Institute, Rockville, Maryland, Department of Human Nutrition, University of Alberta, Edmonton, Canada, Gustavo Russo Institute, Villejuif, France

Background: potential for skeletal m 'anabolic muscles in patients with advanced cancer is not proven. Methods for quantitative analysis of computed tomography (CT) images for the loss / gain muscle in the population cohort (lung, colon, pancreas, cholangiocarcinoma) and cholangiocarcinoma patients selumetinib, an inhibitor of mitogen-activated protein / extracellular signal regulated kinase and interleukin- 6 secretion, the alleged middleman muscle atrophy. Results: Advanced cancer patients (n = 388, median survival 196 d) were a total of 1279 CT during their illness. While the loss of muscle mass was common, the overall rate of muscle mass was 154% and muscle was stable at 456% of intervals between any two scans. Polynomial logistic regression showed that being over 90 days (versus 90 g) of death was a major risk factor for loss of muscle mass (OR = 2. 68, P0. 002) and muscle mass was accordingly less likely (OR = 0. 49, P0. 009) at present. Gender, age, body mass index and tumor groups were not significant predictors of loss or muscle gain. Muscle mass occurs in 39% of patients cholangiocarcinoma after the selumetinib against 15% in patients receiving standard therapy (p00001). Loss of muscle mass was less likely (OR = 0. 14, P0. 0001) and the muscles are more likely (OR = 7. 33, P0. 0001) in patients with cholangiocarcinoma selumetinib. Conclusions: In cancer patients within 90 days of death are characterized by intense muscle loss and low risk for muscle mass. At the beginning of the disease trajectory, windows anabolic potential and there may be an appropriate time to treat cachexia. Results selumetinib offer potential interleukin-6 as a target for therapy of cachexia. Proceedings of CMM Prado:

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