Summary
Sample
ID |
Sample ID |
Age |
Gender |
Origin |
Detail |
1 |
SiHa |
|
F |
Europe |
View |
2 |
CaSki |
|
F |
Europe |
View |
3 |
UM-SCC-104 |
|
M |
Europe |
View |
4 |
UD-SCC-2 |
|
M |
Europe |
View |
5 |
UM-SCC-47 |
|
M |
Africa |
View |
6 |
UPCI:SCC090 |
|
M |
Europe |
View |
7 |
HMS001 |
|
M |
Asia |
View |
8 |
Tumor A |
|
M |
|
View |
9 |
Tumor B |
|
M |
Europe |
View |
10 |
CAL 27 |
|
M |
|
View |
11 |
D562 |
|
F |
|
View |
12 |
SCC-25 |
|
M |
|
View |
Seq Data
Literature
Item |
Summary |
PMID
|
24201445 |
Title
|
Genome-wide Analysis of HPV Integration in Human Cancers Reveals Recurrent, Focal Genomic Instability |
Abstract
|
Genomic instability is a hallmark of human cancers, including the 5% caused by human papillomavirus (HPV). Here we report a striking association between HPV integration and adjacent host genomic structural variation in human cancer cell lines and primary tumors. Whole-genome sequencing revealed HPV integrants flanking and bridging extensive host genomic amplifications and rearrangements, including deletions, inversions, and chromosomal translocations. We present a model of "looping" by which HPV integrant-mediated DNA replication and recombination may result in viral-host DNA concatemers, frequently disrupting genes involved in oncogenesis and amplifying HPV oncogenes E6 and E7. Our high-resolution results shed new light on a catastrophic process, distinct from chromothripsis and other mutational processes, by which HPV directly promotes genomic instability. |
|