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      Erratum to: HDAC6 activity is a non-oncogene addiction hub for inflammatory breast cancers

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          Abstract

          Erratum After the publication of this article [1] the authors noticed two small mistakes in the affiliations listings Dr. Ruth Rodriguez should be marked as an equal contributor alongside Dr. Putcha and Dr. Yu. Dr. Ruth Rodriguez’s correct affiliation is ‘Department of Pathology, Icahn School of Medicine at Mount Sinai , New York, NY 10029-6574, USA’ and not ‘Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA’ as the original article states.

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          HDAC6 activity is a non-oncogene addiction hub for inflammatory breast cancers

          Introduction Inflammatory breast cancer (IBC) is the most lethal form of breast cancers with a 5-year survival rate of only 40 %. Despite its lethality, IBC remains poorly understood which has greatly limited its therapeutic management. We thus decided to utilize an integrative functional genomic strategy to identify the Achilles’ heel of IBC cells. Methods We have pioneered the development of genetic tools as well as experimental and analytical strategies to perform RNAi-based loss-of-function studies at a genome-wide level. Importantly, we and others have demonstrated that these functional screens are able to identify essential functions linked to certain cancer phenotypes. Thus, we decided to use this approach to identify IBC specific sensitivities. Results We identified and validated HDAC6 as a functionally necessary gene to maintain IBC cell viability, while being non-essential for other breast cancer subtypes. Importantly, small molecule inhibitors for HDAC6 already exist and are in clinical trials for other tumor types. We thus demonstrated that Ricolinostat (ACY1215), a leading HDAC6 inhibitor, efficiently controls IBC cell proliferation both in vitro and in vivo. Critically, functional HDAC6 dependency is not associated with genomic alterations at its locus and thus represents a non-oncogene addiction. Despite HDAC6 not being overexpressed, we found that its activity is significantly higher in IBC compared to non-IBC cells, suggesting a possible rationale supporting the observed dependency. Conclusion Our finding that IBC cells are sensitive to HDAC6 inhibition provides a foundation to rapidly develop novel, efficient, and well-tolerated targeted therapy strategies for IBC patients. Electronic supplementary material The online version of this article (doi:10.1186/s13058-015-0658-0) contains supplementary material, which is available to authorized users.
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            Author and article information

            Contributors
            alpaughm@mskcc.org
            califano@c2b2.columbia.edu
            jose.silva@mssm.edu
            Journal
            Breast Cancer Res
            Breast Cancer Res
            Breast Cancer Research : BCR
            BioMed Central (London )
            1465-5411
            1465-542X
            19 April 2017
            19 April 2017
            2017
            : 19
            : 49
            Affiliations
            [1 ]ISNI 0000 0001 0670 2351, GRID grid.59734.3c, Department of Pathology, , Icahn School of Medicine at Mount Sinai, ; New York, NY 10029-6574 USA
            [2 ]ISNI 0000000419368729, GRID grid.21729.3f, Department of Biomedical Informatics, Department of Systems Biology, Center for Computational Biology and Bioinformatics, Herbert Irving Comprehensive Cancer Center, , Columbia University, ; New York, NY 10032 USA
            [3 ]ISNI 0000000419368729, GRID grid.21729.3f, Department of Biochemistry and Molecular Biophysics, Institute for Cancer Genetics, , Columbia University, ; New York, NY 10032 USA
            [4 ]ISNI 0000000419368729, GRID grid.21729.3f, Herbert Irving Comprehensive Cancer Center, , Columbia University, ; 1130 St. Nicholas Avenue, New York, NY 10032 USA
            [5 ]ISNI 0000 0001 2285 2675, GRID grid.239585.0, Department of Pathology, , Columbia University Medical Center, ; 630 West168th Street, New York, NY 10032 USA
            [6 ]GRID grid.427616.0, , Acetylon Pharmaceuticals, Inc., ; 70 Fargo St, Suite 205, Boston, MA 02210 USA
            [7 ]ISNI 0000 0001 2171 9952, GRID grid.51462.34, Department of Surgery, , Memorial Sloan Kettering Cancer Center, ; New York, NY 10065 USA
            [8 ]ISNI 0000 0001 2291 4776, GRID grid.240145.6, Department of Radiation Oncology, , The University of Texas MD Anderson Cancer Center, ; Houston, TX USA
            [9 ]Centre de Recherche en Cancérologie de Marseille, Institut Paoli-Calmettes, Aix-Marseille Université, Marseille, France
            Article
            841
            10.1186/s13058-017-0841-6
            5397760
            28424080
            940bc2d7-cc1c-4723-ad49-1d164e2af50c
            © The Author(s). 2017

            Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

            History
            : 5 April 2017
            : 7 April 2017
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            © The Author(s) 2017

            Oncology & Radiotherapy
            Oncology & Radiotherapy

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