<?xml version="1.0" encoding="UTF-8" standalone="yes"?><?xml-stylesheet type="text/xsl" href="/oai-pmh-repository/static/oai2.xsl"?>
<OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd">
    <responseDate>2026-10-15T23:39:00Z</responseDate>
    <request verb="GetRecord" identifier="oai:data.mendeley.com/vdkpfzjjvg.1" metadataPrefix="oai_dc">https://data.mendeley.com/oai</request>
    <GetRecord>
        <record>
            <header>
                <identifier>oai:data.mendeley.com/vdkpfzjjvg.1</identifier>
                <datestamp>2021-01-05T23:11:27Z</datestamp>
            </header>
            <metadata><oai_dc:dc xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
    <dc:creator>Wang, Ting-You</dc:creator>
    <dc:title>A pan-cancer transcriptome analysis of exitron splicing identifies novel cancer driver genes and neoepitopes </dc:title>
    <dc:publisher>Mendeley Data</dc:publisher>
    <dc:description>An exitron is a cryptic intron within a protein-coding exon that, when spliced, alters the protein-coding potential of the transcript. Exitrons are poorly characterized, but emerging evidence suggests a role for exitron splicing (EIS) in cancer. Through a systematic investigation of EIS across 33 cancers from 9,599 tumor transcriptomes, we discovered EIS affected over 60% of human coding genes and 95% of those events were tumor-specific. Notably, we observed a mutually exclusive pattern between EIS and somatic mutations in their affected genes. Functionally, we discovered known and novel cancer driver genes were affected through gain- or loss-of-function EIS alterations to dictate cancer progression. Importantly, we identified EIS-derived neoepitopes that bind to MHC class I and II. Analysis of clinical data from a clear cell renal cell carcinoma cohort revealed EIS-derived neoantigen burden to be significantly associated with checkpoint inhibitor response. Our findings establish the importance of considering EIS alterations when nominating cancer driver events and neoantigens.</dc:description>
    <dc:subject>Transcriptome</dc:subject>
    <dc:type>Dataset</dc:type>
    <dc:identifier>doi:10.17632/vdkpfzjjvg.1</dc:identifier>
    <dc:identifier>oai:data.mendeley.com/vdkpfzjjvg.1</dc:identifier>
    <dc:rights>Creative Commons Attribution 4.0 International</dc:rights>
    <dc:rights>http://creativecommons.org/licenses/by/4.0</dc:rights>
    <dc:relation>https://data.mendeley.com/datasets/vdkpfzjjvg</dc:relation>
    <dc:date>2021-01-05T23:11:27Z</dc:date>
</oai_dc:dc></metadata>
        </record>
    </GetRecord>
</OAI-PMH>
