Evidence map›Paper›PMID 25692284›Full record

ArticleThe Journal of pathology2015

Multifocal endometriotic lesions associated with cancer are clonal and carry a high mutation burden.

Michael S Anglesio, Ali Bashashati, Yi Kan Wang, Janine Senz, Gavin Ha, Winnie Yang, Mohamed R Aniba, Leah M Prentice, Hossein Farahani, Hector Li Chang and 7 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 2 pooled it
20.7field-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

88 citing papers in PubMed, 2 syntheses or guidelines pooled it, 180 citations in OpenAlex.

  1. A Systematic Review of Atypical Endometriosis-Associated Biomarkers.International journal of molecular sciences · 2022
    Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026
    Review
  10. Expanding the spectrum ofPathologica · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

28 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

17 authors at 3 institutions in 1 country.

Michael S AnglesioDepartment of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Ali BashashatiDepartment of Molecular Oncology, British Columbia Cancer Agency Research Center, Vancouver, Canada.
Yi Kan WangDepartment of Molecular Oncology, British Columbia Cancer Agency Research Center, Vancouver, Canada.
Janine SenzDepartment of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Gavin HaDepartment of Molecular Oncology, British Columbia Cancer Agency Research Center, Vancouver, Canada.
Winnie YangDepartment of Molecular Oncology, British Columbia Cancer Agency Research Center, Vancouver, Canada.
Mohamed R AnibaDepartment of Molecular Oncology, British Columbia Cancer Agency Research Center, Vancouver, Canada.
Leah M PrenticeDepartment of Molecular Oncology, British Columbia Cancer Agency Research Center, Vancouver, Canada.
Hossein FarahaniDepartment of Molecular Oncology, British Columbia Cancer Agency Research Center, Vancouver, Canada.
Hector Li ChangDepartment of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Anthony N KarnezisDepartment of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Marco A MarraMichael Smith Genome Science Centre, British Columbia Cancer Agency Research Center, Vancouver, Canada.
Paul J YongDepartment of Obstetrics and Gynaecology, University of British Columbia, Vancouver, Canada.
Martin HirstMichael Smith Genome Science Centre, British Columbia Cancer Agency Research Center, Vancouver, Canada.
Blake GilksDepartment of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Sohrab P ShahDepartment of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
David G HuntsmanDepartment of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
BC Cancer Agency · CAUniversity of British Columbia · CACanada's Michael Smith Genome Sciences Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis is a significant risk factor for clear cell and endometrioid ovarian cancers and is often found contiguous with these cancers. Using whole-genome shotgun sequencing of seven clear cell ovarian carcinomas (CCC) and targeted sequencing in synchronous endometriosis, we have investigated how this carcinoma may evolve from endometriosis. In every case we observed multiple tumour-associated somatic mutations in at least one concurrent endometriotic lesion. ARID1A and PIK3CA mutations appeared consistently in concurrent endometriosis when present in the primary CCC. In several cases, one or more endometriotic lesions carried the near-complete complement of somatic mutations present in the index CCC tumour. Ancestral mutations were detected in both tumour-adjacent and -distant endometriotic lesions, regardless of any cytological atypia. These findings provide objective evidence that multifocal benign endometriotic lesions are clonally related and that CCCs arising in these patients progress from endometriotic lesions that may already carry sufficient cancer-associated mutations to be considered neoplasms themselves, albeit with low malignant potential. We speculate that genomically distinct classes of endometriosis exist and that ovarian endometriosis with high mutational burden represents one class at high risk for malignant transformation.

Indexed as

Adenocarcinoma, Clear CellClass I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsDNA, NeoplasmEndometriosisFemaleGenome-Wide Association StudyHumansMutationNuclear ProteinsOvarian NeoplasmsPhosphatidylinositol 3-KinasesPrecancerous ConditionsSequence Analysis, DNATranscription FactorsARID1A protein, humanClass I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsDNA, NeoplasmNuclear ProteinsPhosphatidylinositol 3-KinasesPIK3CA protein, humanTranscription Factorscancer precursorclear cell carcinomaendometriosisovarian cancersequencing

Identifiers

PMID25692284
PMCPMC6680210
OpenAlexW1594350035

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.