Evidence map›Paper›PMID 17018593›Full record

ArticleCancer research2006

Critical roles for non-pRb targets of human papillomavirus type 16 E7 in cervical carcinogenesis.

Scott Balsitis, Fred Dick, Nicholas Dyson, Paul F Lambert

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

47 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. HPV18 E7 inhibits LATS1 kinase and activates YAP1 by degrading PTPN14.bioRxiv : the preprint server for biology · 2024
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Activating Mutations inClinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  18. Review
  19. Article
  20. Review
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

4 authors at 3 institutions in 2 countries.

Scott BalsitisMcArdle Laboratory for Cancer Research, University of Wisconsin Medical School, Madison, WI 53706, USA.
Fred Dick
Nicholas Dyson
Paul F Lambert
University of Wisconsin–Madison · USMassachusetts General Hospital · USWestern University · CA

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Visualizing EBV and HCMV DNA Dynamics During InfectionP01CA022443 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI WILLIAM M. SUGDEN · 1985 to 2026
$53.1M
MUTAGENESIS OF THE PRB POCKET DOMAINR01CA064402 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 1994 to 2015
$4.1M
Functional Analysis of the HPV-16 E6 and E7 OncogenesR01CA098428 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI LAMBERT, PAUL F. · 2003 to 2012
$3.7M
NCI NIH HHS CA098428NCI NIH HHS CA22443NCI NIH HHS CA64402NCI NIH HHS P01 CA022443NCI NIH HHS P30 CA014520NCI NIH HHS R01 CA064402NCI NIH HHS R01 CA098428NIGMS NIH HHS T32 GM00721
6 · The paper itself

Abstract

High-risk human papillomaviruses (HPV) encode two oncogenes, E6 and E7, expressed in nearly all cervical cancers. In vivo, HPV-16 E7 has been shown to induce multiple phenotypes in the context of transgenic mice, including cervical cancer. E7 is a multifunctional protein known best for its ability to inactivate the tumor suppressor pRb. To determine the importance of pRb inactivation by E7 in cervical cancer, we pursued studies with genetically engineered mice. E7 expression in estrogen-treated murine cervix induced dysplasia and invasive cancers as reported previously, but targeted Rb inactivation in cervical epithelium was not sufficient to induce any cervical dysplasia or neoplasia. Furthermore, E7 induced cervical cancer formation even when the E7-pRb interaction was disrupted by the use of a knock-in mouse carrying an E7-resistant mutant Rb allele. pRb inactivation was necessary but not sufficient for E7 to overcome differentiation-induced or DNA damage-induced cell cycle arrest, and expression patterns of the E2F-responsive genes Mcm7 and cyclin E indicate that other E2F regulators besides pRb are important targets of E7. Together, these data indicate that non-pRb targets of E7 play critical roles in cervical carcinogenesis.

Indexed as

AllelesAnimalsCarcinoma, Squamous CellCell CycleCell Cycle ProteinsCell DifferentiationCell Transformation, ViralCyclin EDNA-Binding ProteinsDNA DamageEstrogensFemaleGenes, RetinoblastomaGene TargetingHuman papillomavirus 16MiceCell Cycle ProteinsCyclin EDNA-Binding ProteinsEstrogensMcm7 protein, mouseMinichromosome Maintenance Complex Component 7Nuclear Proteinsoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 Proteins

Identifiers

PMID17018593
PMCPMC2858286
OpenAlexW2067697669

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.