Evidence map›Paper›PMID 21221135›Full record

ReviewNature reviews. Clinical oncology2011

Emerging therapeutic targets in endometrial cancer.

Konstantin J Dedes, Daniel Wetterskog, Alan Ashworth, Stan B Kaye, Jorge S Reis-Filho

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07435623 (Assessment of Late Gastrointestinal and Genitourinary Toxicities in Cervical and Endometrial Cancer Requiring Postoperative IMRT and/or Brachytherapy), which is not on this map. Cited by 128 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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.

NCT07435623 recruitingnot on this mapstarted 2025, after this paper: background citation

Assessment of Late Gastrointestinal and Genitourinary Toxicities in Cervical and Endometrial Cancer Requiring Postoperative IMRT and/or Brachytherapy

TypeobservationalSponsorTata Memorial HospitalRan2025 to 2026Enrolled300ConditionsEndometrial Cancer, Cervix Cancer
3 · Its place in the literature

Who cites it

128 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Review
  8. Article
  9. Article
  10. Uterine organoids reveal insights into epithelial specification and plasticity in development and disease.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. mCell biology and toxicology · 2023
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

68 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

5 authors.

Konstantin J DedesThe Breakthrough Breast Cancer Research Center, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK. konstantin.dedes@ usz.ch
Daniel Wetterskog
Alan Ashworth
Stan B Kaye
Jorge S Reis-Filho

Funding

Breast Cancer Now BREAST CANCER NOW RESEARCH CENTRE
6 · The paper itself

Abstract

Endometrial cancer comprises a heterogeneous group of tumors, with distinct risk factors, clinical presentation, histopathological features and molecular characteristics. Currently, treatment of metastatic or recurrent disease is based on conventional chemotherapy combination regimens. Advances in the understanding of the molecular pathology of the two types of endometrial carcinoma--type I (endometrioid) and type II (non-endometrioid)--have underpinned the first steps in the development and testing of targeted therapies. Of the potential therapeutic targets identified to date, clinical trials have only assessed the efficacy of inhibition of the EGFR, VEGFR and PI3K/PTEN/AKT/mTOR signaling pathways; responses to these targeted therapies were modest. Despite the striking molecular differences between type I and type II endometrial cancers, most clinical trials have not taken this diversity into account. The identification of activating mutations of kinases (for example PIK3CA and FGFR2) and loss of function of genes related to DNA repair (for example PTEN) may lead to more biology-driven clinical trials exploiting the concepts of oncogene addiction and synthetic lethality.

Indexed as

AnimalsAntineoplastic AgentsClinical Trials as TopicEndometrial NeoplasmsFemaleHumansNeoplasm ProteinsAntineoplastic AgentsNeoplasm Proteins

Identifiers

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.