Evidence map›Paper›PMID 29944714›Full record

ArticlePloS one2018

Susceptibility of epithelial cells cultured from different regions of human cervix to HPV16-induced immortalization.

Han Deng, Eric Hillpot, Philomina Yeboah, Sumona Mondal, Craig D Woodworth

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Is an oropharyngeal HPV infection more frequently detectable in women with a genital HPV infection?European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. An epithelial organoid model with Langerhans cells for assessing virus-host interactions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Article
  7. 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 1 institution in 1 country.

Han DengDepartment of Biology, Clarkson University, Potsdam, New York, United States of America.ORCID 0000-0003-3342-6780
Eric HillpotDepartment of Biology, Clarkson University, Potsdam, New York, United States of America.
Philomina YeboahDepartment of Biology, Clarkson University, Potsdam, New York, United States of America.
Sumona MondalDepartment of Mathematics, Clarkson University, Potsdam, New York, United States of America.
Craig D WoodworthDepartment of Biology, Clarkson University, Potsdam, New York, United States of America.ORCID 0000-0003-0467-8460
Clarkson University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent infection with high-risk human papillomavirus (HPV) is a major risk factor for cervical cancer. Greater than 90% of these cancers originate in the cervical transformation zone (TZ), a narrow region of metaplastic squamous epithelium that develops at the squamocolumnar junction between the ectocervix and endocervix. It is unclear why the TZ has high susceptibility to malignant transformation and few studies have specifically examined cells from this region. We hypothesized that cells cultured from TZ are more susceptible to cellular immortalization, an alteration that contributes to malignant development. We cultured primary epithelial cells from each region of human cervix (ectocervix, endocervix and TZ) and measured susceptibility to immortalization after transfection with the complete HPV-16 genome or infection of HPV16 E6/E7 retroviruses. Cells cultured from each cervical region expressed keratin markers (keratin 14 and 18) that confirmed their region of origin. In contrast to our prediction, cells from TZ were equally susceptible to immortalization as cells from ectocervix or endocervix. Thus, increased susceptibility of the TZ to cervical carcinogenesis is not due to increased frequency of immortalization by HPV-16. We developed a series of HPV16-immortalized cell lines from ectocervix, endocervix and TZ that will enable comparisons of how these cells respond to factors that promote cervical carcinogenesis.

Indexed as

Cell Transformation, ViralCervix UteriEpithelial CellsPapillomavirus InfectionsUterine Cervical NeoplasmsCells, CulturedFemaleHuman papillomavirus 16Humans

Identifiers

PMID29944714
PMCPMC6019754
OpenAlexW2810192430

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.