Abstract：
:Integration of the human papillomavirus (HPV) genome into the host genome is associated with the disruption of the HPV E2 gene and with amplification and rearrangement of the viral and flanking cellular sequences. Molecular characterization of the genomic structures of coamplified HPV sequences and oncogenes provides essential information concerning the mechanisms of amplification and their roles in carcinogenesis. Using fluorescent hybridization on stretched DNA molecules in two cervical cancer-derived cell lines, we have elucidated the genomic structures of amplified regions containing HPV/myc genes over several hundreds of kilobases. Direct visualization of hybridization signals on individual DNA molecules suggests that overreplication and breakage-fusion-bridge-type mechanisms are involved in the genomic instability associated with HPV cervical cancers. Further analysis from two other genital cancer-derived cell lines reveals a recurrent motif of amplification, probably generated by a common mechanism involving overreplication upon viral integration. Interestingly, different amplification patterns seem to be correlated with the disease outcome, thus providing new insights into HPV-related cancer development and tumor progression.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Herrick J,Conti C,Teissier S,Thierry F,Couturier J,Sastre-Garau X,Favre M,Orth G,Bensimon Adoi
10.1158/0008-5472.CAN-04-2802subject
Has Abstractpub_date
2005-02-15 00:00:00pages
1174-9issue
4eissn
0008-5472issn
1538-7445pii
65/4/1174journal_volume
65pub_type
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