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<identifier identifierType='DOI'>10.1038/s41416-020-01153-4</identifier>
<creators>
<creator>
<creatorName>Kamal, M.</creatorName>
<affiliation>Institut Curie, Franţa</affiliation>
</creator>
<creator>
<creatorName>Lameiras, S.</creatorName>
<affiliation>Institut Curie, Franţa</affiliation>
</creator>
<creator>
<creatorName>Sameţ, N.</creatorName>
<affiliation>IMSP Institutul Oncologic, Moldova, Republica</affiliation>
</creator>
<creator>
<creatorName>Noi, A.</creatorName>
</creator>
</creators>
<titles>
<title xml:lang='en'>Human papilloma virus (HPV) integration signature in Cervical Cancer: identification of MACROD2 gene as HPV hot spot integration site</title>
</titles>
<publisher>Instrumentul Bibliometric National</publisher>
<publicationYear>2021</publicationYear>
<relatedIdentifier relatedIdentifierType='ISSN' relationType='IsPartOf'>0007-0920</relatedIdentifier>
<subjects>
<subject>Human papilloma virus 16</subject>
<subject>Oropharyngeal Neoplasms</subject>
<subject>Viral Genes</subject>
</subjects>
<dates>
<date dateType='Issued'>2021-02-16</date>
</dates>
<resourceType resourceTypeGeneral='Text'>Journal article</resourceType>
<descriptions>
<description xml:lang='en' descriptionType='Abstract'><p>Background: Cervical cancer (CC) remains a leading cause of gynaecological cancer-related mortality with infection by human papilloma virus (HPV) being the most important risk factor. We analysed the association between different viral integration signatures, clinical parameters and outcome in pre-treated CCs. Methods: Different integration signatures were identified using HPV double capture followed by next-generation sequencing (NGS) in 272 CC patients from the BioRAIDs study [NCT02428842]. Correlations between HPV integration signatures and clinical, biological and molecular features were assessed. Results: Episomal HPV was much less frequent in CC as compared to anal carcinoma (p &lt; 0.0001). We identified &gt;300 different HPV-chromosomal junctions (inter- or intra-genic). The most frequent integration site in CC was in MACROD2 gene followed by MIPOL1/TTC6 and TP63. HPV integration signatures were not associated with histological subtype, FIGO staging, treatment or PFS. HPVs were more frequently episomal in PIK3CA mutated tumours (p = 0.023). Viral integration type was dependent on HPV genotype (p &lt; 0.0001); HPV18 and HPV45 being always integrated. High HPV copy number was associated with longer PFS (p = 0.011). Conclusions: This is to our knowledge the first study assessing the prognostic value of HPV integration in a prospectively annotated CC cohort, which detects a hotspot of HPV integration at MACROD2; involved in impaired PARP1 activity and chromosome instability.&nbsp;</p></description>
</descriptions>
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<format>application/pdf</format>
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