Evidence map›Paper›PMID 22220169›Full record

ArticleJournal of oncology2012

Molecular Mechanism and Potential Targets for Blocking HPV-Induced Lesion Development.

E Guzmán-Olea, V H Bermúdez-Morales, O Peralta-Zaragoza, K Torres-Poveda, V Madrid-Marina

Open access · hybridAbstract read
In one paragraph

Article in Journal of oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Immunologic treatments for precancerous lesions and uterine cervical cancer.Journal of experimental & clinical cancer research : CR · 2014
    Review
  10. Article
  11. Article
  12. 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

5 authors at 2 institutions in 1 country.

E Guzmán-OleaDivision of Chronic Infections and Cancer, Research Center for Infectious Diseases, Instituto Nacional de Salud Pública, Avenida Universidad No. 655, Cuernavaca 62100, Morelos, Mexico.
V H Bermúdez-Morales
O Peralta-Zaragoza
K Torres-Poveda
V Madrid-Marina
Instituto Nacional de Salud Pública · MXUniversidad Politecnica del Estado de Morelos · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent infection with high-risk HPV is the etiologic agent associated with the development of cervical cancer (CC) development. However, environmental, social, epidemiological, genetic, and host factors may have a joint influence on the risk of disease progression. Cervical lesions caused by HPV infection can be removed naturally by the host immune response and only a small percentage may progress to cancer; thus, the immune response is essential for the control of precursor lesions and CC. We present a review of recent research on the molecular mechanisms that allow HPV-infected cells to evade immune surveillance and potential targets of molecular therapy to inhibit tumor immune escape.

Identifiers

PMID22220169
PMCPMC3246776
OpenAlexW2000676236

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.