Evidence map›Paper›PMID 27898521›Full record

ReviewCurrent opinion in obstetrics & gynecology2017

Pathogenesis and heterogeneity of ovarian cancer.

Paul T Kroeger, Ronny Drapkin

Open access · hybridAbstract readReview
In one paragraph

Review in Current opinion in obstetrics & gynecology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed
23.8field-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.

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

194 citing papers in PubMed, 311 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. BRCA Testing in Asian Patients with Ovarian Cancer: Standard Clinical Practice or Mutation Prediction Model?Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Ovarian cancer.Nature reviews. Disease primers · 2026
    Review
  13. Article
  14. Article
  15. Review
  16. Hereditary ovarian cancer.Discover oncology · 2026
    Review
  17. Article
  18. Frontiers in pharmacology · 2026
    Article
  19. LncRNANon-coding RNA research · 2025
    Article
  20. Article

134 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

2 authors at 2 institutions in 1 country.

Paul T KroegerDepartment of Obstetrics and Gynecology, Ovarian Cancer Research Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Ronny Drapkin
Cancer Research Center · USUniversity of Pennsylvania · US

Funding

Vaccinating against IGFBP-2 to prevent ovarian cancer relapseP50CA083636 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI DRESCHER, CHARLES, URBAN, NICOLE DENISE · 1999 to 2015
$35.1M
Proteomic, Genomic, and Longitudinal Pathways to Ovarian Cancer Biomarker DiscoveryU01CA152990 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI BIRRER, MICHAEL, SKATES, STEVEN J · 2010 to 2021
$8.9M
NCI NIH HHS P50 CA083636
6 · The paper itself

Abstract

purpose of reviewThe most common type of ovarian cancer, high-grade serous ovarian carcinoma (HGSOC), was originally thought to develop from the ovarian surface epithelium. However, recent data suggest that the cells that undergo neoplastic transformation and give rise to the majority of HGSOC are from the fallopian tube. This development has impacted both translational research and clinical practice, revealing new opportunities for early detection, prevention, and treatment of ovarian cancer. RECENT

findingsGenomic studies indicate that approximately 50% of HGSOC are characterized by mutations in genes involved in the homologous recombination pathway of DNA repair, especially BRCA1 and BRCA2. Clinical trials have demonstrated successful treatment of homologous recombination-defective cancers with poly-ribose polymerase inhibitors through synthetic lethality. Recently, amplification of CCNE1 was found to be another major factor in HGSOC tumorigenesis, accounting for approximately 20% of all cases. Interestingly, amplification of CCNE1 and mutation of homologous recombination repair genes are mutually exclusive in HGSOC. SUMMARY: The fallopian tube secretory cell is the cell of origin for the majority of ovarian cancers. Although it remains unclear what triggers neoplastic transformation of these cells, certain tumors exhibit loss of BRCA function or amplification of CCNE1. These alterations represent unique therapeutic opportunities in ovarian cancer.

Indexed as

Cyclin ECystadenocarcinoma, SerousFallopian TubesFemaleGenes, Tumor SuppressorHumansOncogene ProteinsOvarian NeoplasmsPoly(ADP-ribose) Polymerase InhibitorsCCNE1 protein, humanCyclin EOncogene ProteinsPoly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID27898521
PMCPMC5201412
OpenAlexW2557243447

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.