Evidence map›Paper›PMID 22430211›Full record

ReviewOncogene2013

Endometrial carcinoma: molecular alterations involved in tumor development and progression.

A Yeramian, G Moreno-Bueno, X Dolcet, L Catasus, M Abal, E Colas, J Reventos, J Palacios, J Prat, X Matias-Guiu

Registry-linked trialOpen access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02558348 (A Phase 1/2a Evaluation of the Safety, Pharmacokinetics and Efficacy of AL3818, a Dual Receptor Tyrosine Kinase Inhibitor, in Subjects With Recurrent or Metastatic Endometrial, Ovarian or Cervical Cancer), which is not on this map. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 pooled it
17.0field-weighted citation impact, top 1% 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.

NCT02558348 phase1 / phase2terminatednot on this mapstarted 2015, after this paper: background citation

A Phase 1/2a Evaluation of the Safety, Pharmacokinetics and Efficacy of AL3818, a Dual Receptor Tyrosine Kinase Inhibitor, in Subjects With Recurrent or Metastatic Endometrial, Ovarian or Cervical Cancer (AL3818-US-001)

TypeinterventionalSponsorAdvenchen Laboratories, LLCRan2015 to 2017Enrolled12ConditionsEndometrial Cancer, Ovarian Cancer, Cervical CancerArmsAL3818
3 · Its place in the literature

Who cites it

89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 174 citations in OpenAlex.

  1. Pooled it
  2. 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
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

29 more citing papers are in PubMed but not listed here.

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

10 authors at 8 institutions in 1 country.

A YeramianDepartment of Pathology and Molecular Genetics and Research Laboratory, Hospital Universitari Arnau de Vilanova, University of Lleida, IRBLLEIDA, Lleida, Spain.
G Moreno-Bueno
X Dolcet
L Catasus
M Abal
E Colas
J Reventos
J Palacios
J Prat
X Matias-Guiu
Biomedical Research Institute of Lleida · ESVall d'Hebron Institut de Recerca · ESComplejo Hospitalario Universitario de Santiago · ESConsejo Superior de Investigaciones Científicas · ESHospital de Sant Pau · ESInstituto de Biomedicina de Sevilla · ESUniversitat Autònoma de Barcelona · ESUniversitat de Lleida · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the western world, endometrial carcinoma (EC) is the most common cancer of the female genital tract. The annual incidence has been estimated at 10-20 per 100,000 women. Two clinicopathological variants are recognized: the estrogen related (type I, endometrioid) and the non-estrogen related (type II, non-endometrioid).The clinicopathological differences are paralleled by specific genetic alterations, with type I showing microsatellite instability and mutations in phosphatase and tensin homologue deleted on chromosome 10, PIK3CA, K-RAS and CTNNB1 (β-catenin), and type II exhibiting TP53 mutations and chromosomal instability. Some non-endometrioid carcinomas probably arise from pre-existing endometrioid carcinomas as a result of tumor progression and, not surprisingly, some tumors exhibit combined or mixed features at the clinical, pathological and molecular levels. In EC, apoptosis resistance may have a role in tumor progression. Understanding pathogenesis at the molecular level is essential in identifying biomarkers for successful targeted therapies. In this review, the genetic changes of endometrial carcinogenesis are discussed in the light of the morphological features of the tumors and their precursors.

Indexed as

AnimalsCell Transformation, NeoplasticDisease ProgressionEndometrial NeoplasmsFemaleHumans

Identifiers

PMID22430211
OpenAlexW2021605685

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.