Abstract

Major contributions of the 2nd annual meeting of the International Society of Cancer Metabolism, held in Venice, September 16–19, 2015, are here described and discussed. Among these, the impact of cancer metabolism on local and systemic aggressiveness was analyzed in the context of interactions between cancer and stroma, microenvironmental changes, epigenetic, and stemness modulation.

Highlights

  • Major contributions of the 2nd annual meeting of the International Society of Cancer Metabolism, held in Venice, September 16–19, 2015, are here described and discussed

  • Regarding the use of new preclinical models to study cancer metabolism and microenvironment that were proposed during the conference, one must mention the use of large-scale in silico metabolic models or computational and mathematical approaches to predict the interaction between human cells in defined microenvironments, or to find suitable therapy protocols, like immunotherapy in cancer, and the use of engineered organotypic tumor microenvironment models that include both fibroblasts and cancer cells on a collagen matrix to recapitulate the microenvironmental architecture. This conference illustrated the high level of complexity of the interplay between cancer metabolism and microenvironment and the challenges ahead in our attempt to identify anticancer agents that can be translated to the clinics

  • A good example of cancer metabolism research that extends from the laboratory to the clinics was summarized by Michael Pollak (McGill University, Montreal, Canada) in the closing lecture that described the use of the antidiabetic biguanide drug metformin in cancer

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Summary

Introduction

Major contributions of the 2nd annual meeting of the International Society of Cancer Metabolism, held in Venice, September 16–19, 2015, are here described and discussed. Microenvironmental and metabolic control of epigenetic and stemness Data presented by Tokuhiro Chano (Shiga University of Medical Science, Otsu, Shiga, Japan) demonstrated that acidification of the tumor microenvironment by glycolytic osteosarcoma cells induces a negative feedback on glycolytic metabolism, associated with an increase in amino acid catabolism and urea cycle enhancement.

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