Evidence map›Paper›PMID 10471040›Full record

ArticleBritish journal of cancer1999

CDKN2A gene inactivation in epithelial sporadic ovarian cancer.

D Niederacher, H Y Yan, H X An, H G Bender, M W Beckmann

Open access · hybridAbstract read
In one paragraph

Article 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 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.2field-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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Epigenetics in ovarian cancer.Seminars in cancer biology · 2018
    Review
  8. Quantitative assessment of aberrantCancer management and research · 2018
    Review
  9. Article
  10. Epigenetic alteration of p16 and retinoic acid receptor beta genes in the development of epithelial ovarian carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  11. Article
  12. A phase I study of a tropism-modified conditionally replicative adenovirus for recurrent malignant gynecologic diseases.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010
    Article
  13. Epigenomics and ovarian carcinoma.Biomarkers in medicine · 2010
    Review
  14. Role of p53 and Rb in ovarian cancer.Advances in experimental medicine and biology · 2008
    Review
  15. 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 2 countries.

D NiederacherDepartment of Obstetrics and Gynaecology, Heinrich-Heine-University, Düsseldorf, Germany.
H Y Yan
H X An
H G Bender
M W Beckmann
Heinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumour suppressor gene CDKN2A, located on chromosome 9p21, encodes the cell cycle regulatory protein p16. Inactivation of the CDKN2A gene could lead to uncontrolled cell growth. In order to determine the role of CDKN2A in the development of sporadic ovarian cancer, loss of heterozygosity at 9p21-22, homozygous deletion, mutation and methylation status of the CDKN2A gene as well as CDKN2A expression were examined in a panel of serous papillary ovarian cancer. The frequency of loss of heterozygosity (LOH) for one or more informative markers at 9p21-22 was 65% (15/23). The most common deleted region was located between interferon (IFN)-alpha and D9S171. Homozygous deletions and mutations of the CDKN2A gene were not found. There was no evidence of methylation in exon 1, but methylation in exon 2 of CDKN2A gene was found in 26% (6/23). Absence of CDKN2A gene expression was shown in 27% (6/22) at mRNA level and 21% (4/19) at protein level. These data suggest that the CDKN2A gene is involved in the tumorigenesis of ovarian cancer, but the mechanisms of CDKN2A gene inactivation in serous papillary ovarian cancer remains unclear.

Indexed as

Chromosomes, Human, Pair 9Gene DeletionGenes, p16Loss of HeterozygosityChromosome MappingCyclin-Dependent Kinase Inhibitor p16Cystadenoma, PapillaryDNA MethylationDNA PrimersFemaleGenetic MarkersHomozygoteHumansOvarian NeoplasmsPolymerase Chain ReactionProtein BiosynthesisCyclin-Dependent Kinase Inhibitor p16DNA PrimersGenetic MarkersRNA, Messenger

Identifiers

PMID10471040
PMCPMC2363140
OpenAlexW1986504147

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.