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Cervical cancer (CC) is one of the main causes of gynaecological cancer-related deaths worldwide, and it is also the second most common malignant tumor in women.
although the clinical performance of CC patients is different, HPV (high-risk human papillomavirus) infection is still an important starting event in CC and one of the most important risk factors.
most HPV infections are removed spontaneously by the immune system, but in some cases they persist and lead to cancer.
infection, the virus can remain free or may be integrated into the host's genome, and the two patterns may exist together (transient/integrated).
study aims to analyze the link between different viral integration characteristics, clinical parameters, and results in pre-processed CCs.
HPV integration feature distribution researchers identified different virus integration characteristics by double-capture of HPV and high-flu vehicle sequencing technology (NGS) in 272 CC patients in the BioRAIDs study .NCT02428842.
and evaluate the correlation between HPV's integrated characteristics and clinical, biological, and molecular characteristics.
non-progression survival researchers in 272 HPV-positive cervical cancer patients found a much lower incidence of free HPV in CC than in cancer.
researchers identified 300 different forms of HPV chromosomal connections (between or within genes).
most common integration in CC patients was in the MACROD2 gene, followed by the MIPOL1/TTC6 and TP63 genes.
the integration characteristics of HPV were independent of histological subsypes, FIGO subsethics, patient therapy, or PFS periods.
free HPV is more common in tumors with PIC3CA mutations.
further studies have shown that the form of virus integration depends on the genotype of the HPV virus, and that HPV18 and HPV45 are always integrated.
high HPV copies were also associated with longer PFS in patients.
In summary, the study was the first to assess the prognostic value of HPV integration in a forward-looking CC queue, and found that the MACROD2 gene is an integration hotspot for HPV, which can affect impaired PARP1 activity and chromosomal instability.
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