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      Insertional mutagenesis identifies drivers of a novel oncogenic pathway in invasive lobular breast carcinoma

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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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            Non-muscle myosin II takes centre stage in cell adhesion and migration.

            Miguel Vicente-Manzanares, Xuefei Ma, Robert S Adelstein … (2009)
            Non-muscle myosin II (NM II) is an actin-binding protein that has actin cross-linking and contractile properties and is regulated by the phosphorylation of its light and heavy chains. The three mammalian NM II isoforms have both overlapping and unique properties. Owing to its position downstream of convergent signalling pathways, NM II is central in the control of cell adhesion, cell migration and tissue architecture. Recent insight into the role of NM II in these processes has been gained from loss-of-function and mutant approaches, methods that quantitatively measure actin and adhesion dynamics and the discovery of NM II mutations that cause monogenic diseases.
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              Collective epithelial migration and cell rearrangements drive mammary branching morphogenesis.

              Andrew Ewald, Audrey Brenot, Myhanh Duong … (2008)
              Epithelial organs are built through the movement of groups of interconnected cells. We observed cells in elongating mammary ducts reorganize into a multilayered epithelium, migrate collectively, and rearrange dynamically, all without forming leading cellular extensions. Duct initiation required proliferation, Rac, and myosin light-chain kinase, whereas repolarization to a bilayer depended on Rho kinase. We observed that branching morphogenesis results from the active motility of both luminal and myoepithelial cells. Luminal epithelial cells advanced collectively, whereas myoepithelial cells appeared to restrain elongating ducts. Significantly, we observed that normal epithelium and neoplastic hyperplasias are organized similarly, suggesting common mechanisms of epithelial growth.
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                Author and article information

                Journal
                Title: Nature Genetics
                Abbreviated Title: Nat Genet
                Publisher: Springer Nature
                ISSN (Print): 1061-4036
                ISSN (Electronic): 1546-1718
                Publication date Created: June 26 2017
                Publication date (Print): June 26 2017
                Volume:
                Issue:
                Article
                DOI: 10.1038/ng.3905
                PubMed ID: 28650484
                SO-VID: 6d068c25-8518-43ce-96c1-f96cbb1ea6cb
                Copyright © © 2017
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