HPV VIS Detail Information

> This page shows VIS [5001282] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

Literature Information

PubMed PMID	25581428
Published year	2015
Journal	Nature genetics
Title	Genome-wide profiling of HPV integration in cervical cancer identifies clustered genomic hot spots and a potential microhomology-mediated integration mechanism.
Author	Hu Z,Zhu D,Wang W,Li W,Jia W,Zeng X,Ding W,Yu L,Wang X,Wang L,Shen H,Zhang C,Liu H,Liu X,Zhao Y,Fang X,Li S,Chen W,Tang T,Fu A,Wang Z,Chen G,Gao Q,Li S,Xi L,Wang C,Liao S,Ma X,Wu P,Li K,Wang S,Zhou J,Wang J,Xu X,Wang H,Ma D
Evidence	Human papillomavirus (HPV) integration is a key genetic event in cervical carcinogenesis. By conducting whole-genome sequencing and high-throughput viral integration detection, we identified 3,667 HPV integration breakpoints in 26 cervical intraepithelial neoplasias, 104 cervical carcinomas and five cell lines. Beyond recalculating frequencies for the previously reported frequent integration sites POU5F1B (9. Protein expression from FHIT and LRP1B was downregulated when HPV integrated in their introns. Protein expression from MYC and HMGA2 was elevated when HPV integrated into flanking regions. Moreover, microhomologous sequence between the human and HPV genomes was significantly enriched near integration breakpoints, indicating that fusion between viral and human DNA may have occurred by microhomology-mediated DNA repair pathways. Our data provide insights into HPV integration-driven cervical carcinogenesis.