<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.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>2026-05-17T01:15:42Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/25879" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/25879</identifier><datestamp>2025-12-18T12:56:20Z</datestamp><setSpec>com_20.500.12105_2173</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_19597</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Ruiz-Bañobre, Juan</subfield>
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      <subfield code="a">Tubio, Jose M C</subfield>
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      <subfield code="a">Campbell, Peter J</subfield>
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      <subfield code="a">Nakagawa, Hidewaki</subfield>
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      <subfield code="a">Van Loo, Peter</subfield>
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      <subfield code="c">2021-11-25</subfield>
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      <subfield code="a">Most cancers are characterized by the somatic acquisition of genomic rearrangements during tumour evolution that eventually drive the oncogenesis. Here, using multiplatform sequencing technologies, we identify and characterize a remarkable mutational mechanism in human hepatocellular carcinoma caused by Hepatitis B virus, by which DNA molecules from the virus are inserted into the tumour genome causing dramatic changes in its configuration, including non-homologous chromosomal fusions, dicentric chromosomes and megabase-size telomeric deletions. This aberrant mutational mechanism, present in at least 8% of all HCC tumours, can provide the driver rearrangements that a cancer clone requires to survive and grow, including loss of relevant tumour suppressor genes. Most of these events are clonal and occur early during liver cancer evolution. Real-time timing estimation reveals some HBV-mediated rearrangements occur as early as two decades before cancer diagnosis. Overall, these data underscore the importance of characterising liver cancer genomes for patterns of HBV integration.</subfield>
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      <subfield code="a">Nat Commun  . 2021 Nov 25;12(1):6910.</subfield>
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      <subfield code="a">Nature Communications</subfield>
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      <subfield code="a">34824211</subfield>
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      <subfield code="a">https://hdl.handle.net/20.500.12105/25879</subfield>
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      <subfield code="a">READ ALIGNMENT</subfield>
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      <subfield code="a">LIVER</subfield>
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      <subfield code="a">MUTATIONS</subfield>
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      <subfield code="a">Aberrant integration of Hepatitis B virus DNA promotes major restructuring of human hepatocellular carcinoma genome architecture.</subfield>
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