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      The Metabolic Landscape of RAS-Driven Cancers from biology to therapy

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Our understanding of how the RAS protein family, and in particular mutant KRAS promote metabolic dysregulation in cancer cells has advanced significantly over the last decade. In this Review, we discuss the metabolic reprogramming mediated by oncogenic RAS in cancer, and elucidating the underlying mechanisms could translate to novel therapeutic opportunities to target metabolic vulnerabilities in RAS-driven cancers.

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          Hallmarks of Cancer: The Next Generation

          Douglas Hanahan, Robert A. Weinberg (2011)
          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.
          Article 0 comments Cited 12043 times – based on 0 reviews     Review now
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            Integrative analysis of complex cancer genomics and clinical profiles using the cBioPortal.

            J. Gao, B. A. Aksoy, U Dogrusoz … (2015)
            The cBioPortal for Cancer Genomics (http://cbioportal.org) provides a Web resource for exploring, visualizing, and analyzing multidimensional cancer genomics data. The portal reduces molecular profiling data from cancer tissues and cell lines into readily understandable genetic, epigenetic, gene expression, and proteomic events. The query interface combined with customized data storage enables researchers to interactively explore genetic alterations across samples, genes, and pathways and, when available in the underlying data, to link these to clinical outcomes. The portal provides graphical summaries of gene-level data from multiple platforms, network visualization and analysis, survival analysis, patient-centric queries, and software programmatic access. The intuitive Web interface of the portal makes complex cancer genomics profiles accessible to researchers and clinicians without requiring bioinformatics expertise, thus facilitating biological discoveries. Here, we provide a practical guide to the analysis and visualization features of the cBioPortal for Cancer Genomics.
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              The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data.

              Ethan Cerami, Jianjiong Gao, Ugur Dogrusoz … (2012)
              The cBio Cancer Genomics Portal (http://cbioportal.org) is an open-access resource for interactive exploration of multidimensional cancer genomics data sets, currently providing access to data from more than 5,000 tumor samples from 20 cancer studies. The cBio Cancer Genomics Portal significantly lowers the barriers between complex genomic data and cancer researchers who want rapid, intuitive, and high-quality access to molecular profiles and clinical attributes from large-scale cancer genomics projects and empowers researchers to translate these rich data sets into biologic insights and clinical applications. © 2012 AACR.
              Article 0 comments Cited 4297 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 101761119
                Journal ID (pubmed-jr-id): 49159
                Journal ID (nlm-ta): Nat Cancer
                Journal ID (iso-abbrev): Nat Cancer
                Title: Nature cancer
                ISSN (Electronic): 2662-1347
                Publication date Nihms-submitted: 3 April 2021
                Publication date (Electronic): 24 March 2021
                Publication date (Print): March 2021
                Publication date PMC-release: 01 September 2021
                Volume: 2
                Issue: 3
                Pages: 271-283
                Affiliations
                [1 ]National Cancer Institute RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21701
                [2 ]Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139
                [3 ]Dana–Farber Cancer Institute, Boston, MA 02215
                [4 ]Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94158
                [5 ]present address: Perlmutter Cancer Center, New York University Langone Medical Center, New York, NY 10016
                Author notes

                Author contributions

                All authors conceived of the article, performed literature searches, integrated the information, and wrote, discussed and edited the manuscript.

                [* ] Corresponding Author: Frank McCormick, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94158 frank.mccormick@ 123456ucsf.edu
                Article
                Manuscript ID: NIHMS1684793
                DOI: 10.1038/s43018-021-00184-x
                PMC ID: 8045781
                PubMed ID: 33870211
                SO-VID: 1f5761b2-48b5-42f5-9c85-2d36530dcacd
                License:

                Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Categories
                Subject: Article

                Keywords: kras,metabolism,autophagy,glutaminolysis,glycolysis,macropinocytosis,chemoresistance,ferroptosis,cancer therapeutics
                Data availability:
                Keywords: kras, metabolism, autophagy, glutaminolysis, glycolysis, macropinocytosis, chemoresistance, ferroptosis, cancer therapeutics

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