Evidence map›Paper›PMID 18413729›Full record

ArticleCancer research2008

p53 Loss synergizes with estrogen and papillomaviral oncogenes to induce cervical and breast cancers.

Anny Shai, Henry C Pitot, Paul F Lambert

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

  1. Estrogen and viral infection.Frontiers in immunology · 2025
    Review
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  16. The p53-estrogen receptor loop in cancer.Current molecular medicine · 2013
    Review
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  18. Article
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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

3 authors at 1 institution in 1 country.

Anny ShaiMcArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53706, USA.
Henry C Pitot
Paul F Lambert
University of Wisconsin–Madison · US

Funding

Visualizing EBV and HCMV DNA Dynamics During InfectionP01CA022443 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI WILLIAM M. SUGDEN · 1985 to 2026
$53.1M
Training in Cancer Biology Training GrantT32CA009135 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SUGDEN, WILLIAM M. · 1985 to 2024
$10.4M
Functional Analysis of the HPV-16 E6 and E7 OncogenesR01CA098428 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI LAMBERT, PAUL F. · 2003 to 2012
$3.7M
Role of Estrogen in Cervical CancerR01CA120847 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI LAMBERT, PAUL F. · 2007 to 2011
$1.4M
NCI NIH HHS CA009135NCI NIH HHS CA022443NCI NIH HHS CA098428NCI NIH HHS P01 CA022443NCI NIH HHS R01 CA098428NCI NIH HHS R01 CA120847NCI NIH HHS T32 CA009135
6 · The paper itself

Abstract

Whereas the tumor suppressor p53 gene is frequently mutated in most human cancers, this is not the case in human papillomavirus (HPV)-associated cancers, presumably because the viral E6 oncoprotein inactivates the p53 protein. The ability of E6 to transform cells in tissue culture and induce cancers in mice correlates in part with its ability to inactivate p53. In this study, we compared the expression of the HPV16 E6 oncogene to the conditional genetic disruption of p53 in the context of a mouse model for cervical cancer in which estrogen is a critical cofactor. Nearly all of the K14Crep53(f/f) mice treated with estrogen developed cervical cancer, a stark contrast to its complete absence in like-treated K14E6(WT)p53(f/f) mice, indicating that HPV16 E6 must only partially inactivate p53. p53-independent activities of E6 also contributed to carcinogenesis, but in the female reproductive tract, these activities were manifested only in the presence of the HPV16 E7 oncogene. Interestingly, treatment of K14Crep53(f/f) mice with estrogen also resulted in mammary tumors after only a short latency, many of which were positive for estrogen receptor alpha. The majority of these mammary tumors were of mixed cell types, suggestive of their originating from a multipotent progenitor. Furthermore, a subset of mammary tumors arising in the estrogen-treated, p53-deficient mammary glands exhibited evidence of an epithelial to mesenchymal transition. These data show the importance of the synergy between estrogen and p53 insufficiency in determining basic properties of carcinogenesis in hormone-responsive tissues, such as the breast and the reproductive tract.

Indexed as

Gene DeletionGenes, p53OncogenesAnimalsBreast NeoplasmsCrosses, GeneticDisease Models, AnimalDNA DamageDNA ReplicationEstradiolEstrusFemaleHumansMaleMammary Neoplasms, AnimalMiceEstradiol

Identifiers

PMID18413729
PMCPMC2862766
OpenAlexW2167816562

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.