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July 21-25, 2012
Metro Toronto Convention Centre
Toronto, ON, Canada


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CANCER CACHEXIA'S METABOLIC FINGERPRINT IN A MURINE MODEL CONFIRMS A DISTINCT ENTITY

Presentation: P163
Topic: Basic Science
Type: Poster
Date: Sunday - Tuesday, July 22 - 24, 2012
Session: Designated Poster viewing times
Authors: Hirak Der-Torossian, MD MPH, Scott A Asher, MD, Ashley Wysong, MD, Xiaoying Yin, MD, Monte S Willis, MD PhD, Tom M O'Connell, MD, Marion E Couch, MD PhD FACS MBA
Institution(s): University of Vermont, University of North Carolina

Despite recent consensus definitions of cancer cachexia, lack of specific diagnostic biomarkers remains a major hurdle towards more accurate diagnosis of cancer cachexia, but also towards the understanding of cachexia as a separate entity from other wasting syndromes. In a previous pilot study, we have shown that cancer-cachectic mice have a unique metabolic fingerprint with distinct glucose and lipid alterations when compared to healthy controls. Further 1H NMR-based metabolomics studies were carried out to investigate the differences in metabolic profiles of cancer-cachectic mice when compared to tumor-bearing non-cachectic mice, calorie-restricted mice, and surgically-treated cancer-cachectic mice. Male CD2F1 mice were divided into 5 groups: 1) Cachexia Group received cachexia-inducing C26 undifferentiated colon carcinoma cells; 2) Tumor-Burden Group received, non-cachectic, P388 lymphoma cells; 3) Starvation Group remained cancer-free but were subjected to caloric-restriction; 4) Surgery Group was similar to Cachexia Group but tumors were resected mid-experiment; and 5) Control Group was left to age intact. Baseline, mid-experiment and final serum samples were collected for 1H-NMR spectroscopic analysis. After data reduction, unsupervised Principal Component Analysis (PCA) and Orthogonal Projections to Latent Structures (OPLS) demonstrate that the unique metabolic fingerprint is independent of tumor burden and distinct from profiles of starvation and aging. Furthermore, mice that underwent surgical tumor removal have a metabolic profile that differentiates itself from that of cachectic mice, seemingly reverting to a profile more congruent with healthy controls, indicating a return to a normal state with cure in murine models. Hyperlipidemia, hyperglycemia, and reduced branched-chain amino acids (BCAAs), distinguish the metabolomic profile of cachexia from other groups. The findings that metabolomic analysis of murine serum is able to completely differentiate cachexia from tumor burden and caloric-restriction warrant similar translational investigations in patients to better understand cancer cachexia’s unique disease progression and treatment response.

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