Escape Excel: A tool for preventing gene symbol and accession conversion errors

<div><p>Background</p><p>Microsoft Excel automatically converts certain gene symbols, database accessions, and other alphanumeric text into dates, scientific notation, and other numerical representations. These conversions lead to subsequent, irreversible, corruption of the imported text. A recent survey of popular genomic literature estimates that one-fifth of all papers with supplementary gene lists suffer from this issue.</p><p>Results</p><p>Here, we present an open-source tool, Escape Excel, which prevents these erroneous conversions by generating an escaped text file that can be safely imported into Excel. Escape Excel is implemented in a variety of formats (<a href="http://www.github.com/pstew/escape_excel" target="_blank">http://www.github.com/pstew/escape_excel</a>), including a command line based Perl script, a Windows-only Excel Add-In, an OS X drag-and-drop application, a simple web-server, and as a Galaxy web environment interface. Test server implementations are accessible as a Galaxy interface (<a href="http://apostl.moffitt.org" target="_blank">http://apostl.moffitt.org</a>) and simple non-Galaxy web server (<a href="http://apostl.moffitt.org:8000/" target="_blank">http://apostl.moffitt.org:8000/</a>).</p><p>Conclusions</p><p>Escape Excel detects and escapes a wide variety of problematic text strings so that they are not erroneously converted into other representations upon importation into Excel. Examples of problematic strings include date-like strings, time-like strings, leading zeroes in front of numbers, and long numeric and alphanumeric identifiers that should not be automatically converted into scientific notation. It is hoped that greater awareness of these potential data corruption issues, together with diligent escaping of text files prior to importation into Excel, will help to reduce the amount of Excel-corrupted data in scientific analyses and publications.</p></div

Screen capture of escape excel Galaxy web server interface.

<p>The results from an example data processing workflow are shown, ready for download (right pane), after uploading a file with the Upload Data tool (left pane) and processing the selected file with the Escape Excel tool (tool selected in the left pane, options selected in the middle pane). A step-by-step tutorial is provided underneath the form in the middle pane.</p

Screen capture of escape excel OS X application.

<p>Files to be escaped can be drag-and-dropped onto the application, which will then automatically export escaped versions of the files.</p

Screen capture of escape excel command line tool help text.

<p>Unknown command line options, including—help, will abort the program with a brief usage statement, including command syntax and descriptions of supported option flags.</p

Chemoproteomics Reveals Novel Protein and Lipid Kinase Targets of Clinical CDK4/6 Inhibitors in Lung Cancer

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GSK3 Alpha and Beta Are New Functionally Relevant Targets of Tivantinib in Lung Cancer Cells

Tivantinib has been described as a potent and highly selective inhibitor of the receptor tyrosine kinase c-MET and is currently in advanced clinical development for several cancers including non-small cell lung cancer (NSCLC). However, recent studies suggest that tivantinib’s anticancer properties are unrelated to c-MET inhibition. Consistently, in determining tivantinib’s activity profile in a broad panel of NSCLC cell lines, we found that, in contrast to several more potent c-MET inhibitors, tivantinib reduces cell viability across most of these cell lines. Applying an unbiased, mass-spectrometry-based, chemical proteomics approach, we identified glycogen synthase kinase 3 (GSK3) alpha and beta as novel tivantinib targets. Subsequent validation showed that tivantinib displayed higher potency for GSK3α than for GSK3β and that pharmacological inhibition or simultaneous siRNA-mediated loss of GSK3α and GSK3β caused apoptosis. In summary, GSK3α and GSK3β are new kinase targets of tivantinib that play an important role in its cellular mechanism-of-action in NSCLC