Evidence map›Paper›PMID 10682682›Full record

ArticleBritish journal of cancer2000

The role of p16-cyclin d/CDK-pRb pathway in the tumorigenesis of endometrioid-type endometrial carcinoma.

H Tsuda, K Yamamoto, T Inoue, I Uchiyama, N Umesaki

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Aberrant promoter hypermethylation of p16 gene in endometrial carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Pooled it
  2. A Phase II Study of Fulvestrant plus Abemaciclib in Hormone Receptor-Positive Advanced or Recurrent Endometrial Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Trial
  3. Article
  4. Article
  5. Article
  6. The promise of combining CDK4/6 inhibition with hormonal therapy in the first-line treatment setting for metastatic or recurrent endometrial adenocarcinoma.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2023
    Review
  7. Evolving treatment paradigms in metastatic or recurrent low-grade endometrial cancer: When is hormonal-based therapy the preferred option?International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2023
    Review
  8. Papillary mucinous metaplasia: a distinct precursor of mucinous adenocarcinoma of the endometrium.International journal of clinical and experimental pathology · 2022
    Article
  9. Article
  10. Article
  11. Role of Cyclin-Dependent Kinase Inhibitors in Endometrial Cancer.International journal of molecular sciences · 2019
    Review
  12. Article
  13. Article
  14. Review
  15. New therapies for advanced, recurrent, and metastatic endometrial cancers.Gynecologic oncology research and practice · 2017
    Review
  16. Article
  17. Signalling pathways in endometrial cancer.Contemporary oncology (Poznan, Poland) · 2014
    Review
  18. An epigenetic marker panel for detection of lung cancer using cell-free serum DNA.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011
    Article
  19. Emerging therapeutic targets in endometrial cancer.Nature reviews. Clinical oncology · 2011
    Review
  20. 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 3 institutions in 1 country.

H TsudaDepartment of Obstetrics & Gynaecology, Osaka City General Hospital, Osaka, Japan.
K Yamamoto
T Inoue
I Uchiyama
N Umesaki
Osaka City General Hospital · JPKajima Corporation (Japan) · JPOsaka City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We analysed p16 gene alteration and p16, cyclin-dependent kinase 4 (CDK4), CDK6, cyclin D1, cyclin D2, cyclin D3 and retinoblastoma protein (pRb) expression in ten normal endometriums (PE), 18 endometrial hyperplasias (EH) and 35 endometrial cancers (EC). Two of ten PE (20%), nine of 18 EH (50.0%) and 29 of 35 EC (82.9%) exhibited p16 nuclear staining. p16 expression was significantly higher in EC than EH (P = 0.0119). In the six p16 (-) EC, one was considered to have reduced gene dosage consistent with possible homozygous deletion of the CDKN2 gene and three had methylation in 5'CpG island in the promoter region of the p16 gene, whereas none showed such reduced gene dosage and four had methylation in the nine p16 (-) EH. Strong CDK4 staining was observed in 12 of 35 EC (34.3%) and one of 18 EH (5.6%). The strong expression of CDK4 was higher in EC than in EH (P = 0.0399). The expression of CDK4 was higher in EH than PE (P = 0.0054). The abnormalities of p16-cyclin D/CDK-pRb pathway were detected in 18 of 35 EC (51.4%). In conclusion, the expression of p16 and CDK4 may be an early event in the neoplastic transformation of endometrial cancer.

Indexed as

Base SequenceCpG IslandsCyclin DCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent KinasesCyclinsDNA MethylationDNA PrimersEndometrial NeoplasmsEndometriumFemaleGene DeletionHomozygoteHumansImmunohistochemistryPolymerase Chain ReactionCyclin DCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent KinasesCyclinsDNA PrimersRetinoblastoma Protein

Identifiers

PMID10682682
PMCPMC2363310
OpenAlexW1576770999

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.