Evidence map›Paper›PMID 10471054›Full record

ReviewBritish journal of cancer1999

The molecular genetics of cervical carcinoma.

P A Lazo

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of cancer, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
8.9field-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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 204 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Review
  4. Article
  5. Immunotherapy for Cervical Cancer: Are We Ready for Prime Time?International journal of molecular sciences · 2022
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Methylation ofOncology letters · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. HPV typing and its relation with apoptosis in cervical carcinoma from Indian population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
    Article
  17. Article
  18. Characterization of NOL7 gene point mutations, promoter methylation, and protein expression in cervical cancer.International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · 2012
    Article
  19. Article
  20. Zinc induces cell cycle arrest and apoptosis by upregulation of WIG-1 in esophageal squamous cancer cell line EC109.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011
    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

1 author at 1 institution in 1 country.

P A LazoCentro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Universidad de Salamanca, Spain.
Universidad de Salamanca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the pathogenesis of cervical carcinoma there are three major components, two of them related to the role of human papillomaviruses (HPV). First, the effect of viral E6 and E7 proteins. Second, the integration of viral DNA in chromosomal regions associated with well known tumour phenotypes. Some of these viral integrations occur recurrently at specific chromosomal locations, such as 8q24 and 12q15, both harbouring HPV18 and HPV16. And third, there are other recurrent genetic alterations not linked to HPV. Recurrent losses of heterozygosity (LOH) have been detected in chromosome regions 3p14-22, 4p16, 5p15, 6p21-22, 11q23, 17p13.3 without effect on p53, 18q12-22 and 19q13, all of them suggesting the alteration of putative tumour suppressor genes not yet identified. Recurrent amplification has been mapped to 3q+ arm, with the common region in 3q24-28 in 90% of invasive carcinomas. The mutator phenotype, microsatellite instability, plays a minor role and is detected in only 7% of cervical carcinomas. The development of cervical carcinoma requires the sequential occurrence and selection of several genetic alterations. The identification of the specific genes involved, and their correlation with specific tumour properties and stages could improve the understanding and perhaps the management of cervical carcinoma.

Indexed as

Chromosome MappingChromosomes, HumanFemaleHumansLoss of HeterozygosityPapillomaviridaeUterine Cervical NeoplasmsVirus Integration

Identifiers

PMID10471054
PMCPMC2374277
OpenAlexW2034598992

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.