Evidence map›Paper›PMID 14562053›Full record

ArticleOncogene2003

Preferential integration of human papillomavirus type 18 near the c-myc locus in cervical carcinoma.

Matthew J Ferber, Erik C Thorland, Antoinette A T P Brink, Anton K Rapp, Leslie A Phillips, Renee McGovern, Bobbie S Gostout, Tak Hong Cheung, Tong Kwok Hung Chung, Wong Yick Fu and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
6.2field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

69 citing papers in PubMed, 181 citations in OpenAlex.

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9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 6 institutions in 3 countries.

Matthew J FerberDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA.
Erik C Thorland
Antoinette A T P Brink
Anton K Rapp
Leslie A Phillips
Renee McGovern
Bobbie S Gostout
Tak Hong Cheung
Tong Kwok Hung Chung
Wong Yick Fu
David I Smith
WinnMed · USChinese University of Hong Kong · CNLeiden University Medical Center · NLMayo Clinic · USMayo Clinic in Arizona · USPrince of Wales Hospital · CN

Funding

CHROMOSOME BREAKPOINTS, RENAL &SMALL CELL LUNG CANCERR01CA048031 · NCI · WAYNE STATE UNIVERSITY · PI SMITH, DAVID I · 1988 to 2000
$283k
NCI NIH HHS CA 48031
6 · The paper itself

Abstract

The development of cervical cancer is highly associated with human papillomavirus (HPV) infection. Greater than 99% of all cervical tumors contain HPV DNA. Integration of high-risk HPV has been temporally associated with the acquisition of a malignant phenotype. Recent work from our lab has shown that HPV16, the most common high-risk HPV associated with cervical carcinoma, preferentially integrates at loci containing human common fragile sites (CFSs). CFSs are regions of genomic instability that have also been associated with deletions, translocations, and gene amplification during cancer development. The current work shows that HPV18, the second most prevalent high-risk HPV type found in cervical tumors, preferentially targets the CFSs. We identified 27 unique HPV18 integrations in cervical tumors, of which 63% (P<0.001) occur in CFSs. However, the distribution of HPV18 integrations found were profoundly different from those found for HPV16. Specifically, 30% of all HPV18 integrations occurred within the chromosomal band 8q24 near the c-myc proto-oncogene. None of the HPV16 integrations occurred in this region. Previous low-resolution mapping suggested that c-myc may be a target of HPV integration. Our data at nucleotide resolution confirm that in HPV18-positive cervical tumors, the region surrounding c-myc is indeed a hot spot of viral integration. These results demonstrate that CFSs are preferred sites of integration for HPV18 in cervical tumors. In addition, we have identified multiple cellular genes that have been disrupted by HPV18 integration in cervical tumors. Our results suggest that the sites of HPV18 integration are nonrandom and may play an important role in the development of cervical tumors.

Indexed as

Chromosomes, Human, Pair 8Genes, mycChromosome MappingCrossing Over, GeneticFemaleHumansPapillomaviridaeProto-Oncogene MasUterine Cervical NeoplasmsVirus IntegrationProto-Oncogene Mas

Identifiers

PMID14562053
OpenAlexW2056956377

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.