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      Fundamentals of cancer metabolism

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          Abstract

          Researchers provide a conceptual framework to understand current knowledge of the fundamentals of cancer metabolism.

          Abstract

          Tumors reprogram pathways of nutrient acquisition and metabolism to meet the bioenergetic, biosynthetic, and redox demands of malignant cells. These reprogrammed activities are now recognized as hallmarks of cancer, and recent work has uncovered remarkable flexibility in the specific pathways activated by tumor cells to support these key functions. In this perspective, we provide a conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis. Understanding these concepts will progressively support the development of new strategies to treat human cancer.

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          Most cited references 195

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          Hallmarks of Cancer: The Next Generation

          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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            On the origin of cancer cells.

             O WARBURG (1956)
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              mTOR signaling in growth control and disease.

              The mechanistic target of rapamycin (mTOR) signaling pathway senses and integrates a variety of environmental cues to regulate organismal growth and homeostasis. The pathway regulates many major cellular processes and is implicated in an increasing number of pathological conditions, including cancer, obesity, type 2 diabetes, and neurodegeneration. Here, we review recent advances in our understanding of the mTOR pathway and its role in health, disease, and aging. We further discuss pharmacological approaches to treat human pathologies linked to mTOR deregulation. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Sci Adv
                Sci Adv
                SciAdv
                advances
                Science Advances
                American Association for the Advancement of Science
                2375-2548
                May 2016
                27 May 2016
                : 2
                : 5
                Affiliations
                [1 ]Children’s Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
                [2 ]Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
                Author notes
                [* ]Corresponding author. Email: Ralph.Deberardinis@ 123456UTSouthwestern.edu (R.J.D.); nav@ 123456northwestern.edu (N.S.C.)
                Article
                1600200
                10.1126/sciadv.1600200
                4928883
                27386546
                Copyright © 2016, The Authors

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial license, which permits use, distribution, and reproduction in any medium, so long as the resultant use is not for commercial advantage and provided the original work is properly cited.

                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: ID0E1EAG7327
                Award ID: R01 CA123067
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000054, National Cancer Institute;
                Award ID: ID0EAMAG7328
                Award ID: 5R01CA157996
                Award Recipient :
                Categories
                Review
                Review
                SciAdv review
                Oncology
                Custom metadata
                Mikee Bernabe

                cancer, oncogenes, ros, glycolysis, mitochondria, metabolism

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