Evidence map›Paper›PMID 17602722›Full record

ArticleVirology2007

Human papillomavirus causes an angiogenic switch in keratinocytes which is sufficient to alter endothelial cell behavior.

W Chen, F Li, L Mead, H White, J Walker, D A Ingram, A Roman

Open access · greenAbstract read
In one paragraph

Article in Virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
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  7. Article
  8. Review
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  10. Article
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  12. Review
  13. The Interaction Between Human Papillomaviruses and the Stromal Microenvironment.Progress in molecular biology and translational science · 2016
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Human papillomaviruses as therapeutic targets in human cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2011
    Article
  20. Article
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

7 authors at 2 institutions in 1 country.

W ChenDepartment of Microbiology and Immunology and the Walther Oncology Center, Indiana University School of Medicine and the Walther Cancer Institute, Indianapolis, 635 Barnhill Drive, Indianapolis, IN 46202-5120, USA.
F Li
L Mead
H White
J Walker
D A Ingram
A Roman
Indiana University School of MedicineWalther Cancer Foundation · US

Funding

Tumor Microenvironment and Metastasis ProgramP30CA082709 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI AMBER L. MOSLEY · 1999 to 2026
$59.3M
VIRAL DETERMINANTS OF HSV DISEASE IN MICEU19AI031494 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SPINOLA, STANLEY M. · 1995 to 2009
$13.6M
Transgenic CoreP50NS052606 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI INGRAM, DAVID A · 2005 to 2014
$12.6M
Cancer Biology Training ProgramT32CA111198 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI NAKSHATRI, HARIKRISHNA · 2005 to 2009
$1.8M
Ras-PI3K Pathway in Nf1-/-Hematopoiesis and LeukemiaK08CA096579 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI INGRAM, DAVID A · 2002 to 2007
$639k
NCI NIH HHS K08 CA096579NCI NIH HHS K08 CA096579-01NCI NIH HHS P30 CA082709NCI NIH HHS P30 CA82709NCI NIH HHS T32 CA111198NCI NIH HHS T32 CA11 1198-02S1NIAID NIH HHS R01AI31494NIAID NIH HHS U19 AI031494NINDS NIH HHS P50 NS0 52606NINDS NIH HHS P50 NS052606PHS HHS NF043019
6 · The paper itself

Abstract

One of the requirements for tumor growth is the ability to recruit a blood supply, a process known as angiogenesis. Angiogenesis begins early in the progression of cervical disease from mild to severe dysplasia and on to invasive cancer. We have previously reported that expression of human papillomavirus type 16 E6 and E7 (HPV16 E6E7) proteins in primary foreskin keratinocytes (HFKs) decreases expression of two inhibitors and increases expression of two angiogenic inducers [Toussaint-Smith, E., Donner, D.B., Roman, A., 2004. Expression of human papillomavirus type 16 E6 and E7 oncoproteins in primary foreskin keratinocytes is sufficient to alter the expression of angiogenic factors. Oncogene 23, 2988-2995]. Here we report that HPV-induced early changes in the keratinocyte phenotype are sufficient to alter endothelial cell behavior both in vitro and in vivo. Conditioned media from HPV16 E6E7 expressing HFKs as well as from human cervical keratinocytes containing the intact HPV16 were able to stimulate proliferation and migration of human microvascular endothelial cells. In addition, introduction of the conditioned media into immunocompetent mice using a Matrigel plug model resulted in a clear angiogenic response. These novel data support the hypothesis that HPV proteins contribute not only to the uncontrolled keratinocyte growth seen following HPV infection but also to the angiogenic response needed for tumor formation.

Indexed as

KeratinocytesNeovascularization, PathologicAnimalsCells, CulturedCervix UteriCulture Media, ConditionedEndothelial CellsFemaleHuman papillomavirus 16HumansMiceMice, Inbred C57BLMicrocirculationOncogene Proteins, ViralPapillomavirus E7 ProteinsRepressor ProteinsCulture Media, ConditionedE6 protein, Human papillomavirus type 16oncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsRepressor Proteins

Identifiers

PMID17602722
PMCPMC2043482
OpenAlexW2088885245

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.