Evidence map›Paper›PMID 12214255›Full record

ReviewOncogene2002

Human papillomaviruses and centrosome duplication errors: modeling the origins of genomic instability.

Stefan Duensing, Karl Münger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 121 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. TheProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Contribution of Tumor Endothelial Cells in Cancer Progression.International journal of molecular sciences · 2018
    Review
  15. Article
  16. Expression of the HPV18/E6 oncoprotein induces DNA damage.European journal of histochemistry : EJH · 2017
    Article
  17. Molecular transitions from papillomavirus infection to cervical precancer and cancer: Role of stromal estrogen receptor signaling.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Stefan DuensingDepartment of Pathology, Harvard Medical School, Armenise Research Building, D2-537, 200 Longwood Avenue, Boston, Massachusetts, MA 02115, USA.
Karl Münger
Harvard University · US

Funding

BIOLOGICAL ACTIVITY OF HPV E7 IN HUMAN EPITHELIAL CELLSR01CA066980 · NCI · TUFTS UNIVERSITY BOSTON · PI MUNGER, KARL · 1996 to 2019
$7.4M
MODULATION OF HOST CELL APOPTOTIC RESPONSES BY HPVE7R01CA081135 · NCI · TUFTS UNIVERSITY BOSTON · PI MUNGER, KARL · 2000 to 2014
$4.2M
NCI NIH HHS R01 CA66980NCI NIH HHS R01 CA81135NIDCR NIH HHS P01 DE00275
6 · The paper itself

Abstract

The majority of human cancers are genomically unstable, often with gains or losses of whole chromosomes. In high-risk human papillomavirus (HPV)-associated cervical neoplasia, the two HPV-encoded oncoproteins E6 and E7 have been implicated in mitotic infidelity by their ability to induce centrosome-related mitotic disturbances. However, the mechanisms by which HPV E6 and E7 subvert centrosome homeostasis are strikingly different. Whereas the E7 oncoprotein rapidly drives centrosome duplication errors in cells that appear phenotypically normal, expression of the HPV E6 oncoprotein results in an accumulation of supernumerary centrosomes in multinucleated cells. The primary centrosome duplication defect in HPV E7 expressing cells may be linked to the ability of E7 to disrupt regulatory nodes that govern both the host cell division cycle machinery and the initiation of centrosome duplication. Most importantly, the E7 oncoprotein has been shown to dysregulate cdk2 activity, a major determinant for the initiation of centrosome duplication. HPV-induced centrosome abnormalities, multipolar mitoses, and aneuploidy often occur at early stages during cervical carcinogenesis and increase with malignant conversion. These findings suggest that HPV oncoprotein-induced chromosomal instability increases the risk for genetic changes that may ultimately facilitate carcinogenic progression.

Indexed as

CentrosomeGenomeCell Transformation, NeoplasticCell Transformation, ViralHumansPapillomaviridaeVirus Replication

Identifiers

PMID12214255
OpenAlexW2032011773

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.