Evidence map›Paper›PMID 23558894›Full record

ArticleBritish journal of cancer2013

DNA copy number profiling reveals extensive genomic loss in hereditary BRCA1 and BRCA2 ovarian carcinomas.

M M Kamieniak, I Muñoz-Repeto, D Rico, A Osorio, M Urioste, J García-Donas, S Hernando, L Robles-Díaz, T Ramón Y Cajal, A Cazorla and 9 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.4field-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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Ovarian Cancer-SpecificClinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Trial
  2. Tissue-Specific Prevalence and Clonal Architecture ofbioRxiv : the preprint server for biology · 2026
    Article
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  6. Deletions Rate-Limit Breast and Ovarian Cancer Initiation.bioRxiv : the preprint server for biology · 2024
    Article
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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

19 authors at 11 institutions in 2 countries.

M M KamieniakHuman Cancer Genetics, Spanish National Cancer Research Center (CNIO), C/Melchor Fernández Almagro 3, 28029 Madrid, Spain.
I Muñoz-Repeto
D Rico
A Osorio
M Urioste
J García-Donas
S Hernando
L Robles-Díaz
T Ramón Y Cajal
A Cazorla
R Sáez
J M García-Bueno
S Domingo
S Borrego
J Palacios
M A van de Wiel
B Ylstra
J Benítez
M J García
Spanish National Cancer Research Centre · ESInstituto de Salud Carlos III · ESAmsterdam UMC Location Vrije Universiteit Amsterdam · NLBiogipuzkoa Health Research Institute · ESHospital de Sant Pau · ESHospital General Universitario de Albacete · ESHospital Universitario 12 De Octubre · ESHospital Universitario Fundación Alcorcón · ESHospital Universitario Fundación Jiménez Díaz · ESHospital Universitario Ramón y Cajal · ESHospital Universitario Virgen del Rocío · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFew studies have attempted to characterise genomic changes occurring in hereditary epithelial ovarian carcinomas (EOCs) and inconsistent results have been obtained. Given the relevance of DNA copy number alterations in ovarian oncogenesis and growing clinical implications of the BRCA-gene status, we aimed to characterise the genomic profiles of hereditary and sporadic ovarian tumours.

methodsHigh-resolution array Comparative Genomic Hybridisation profiling of 53 familial (21 BRCA1, 6 BRCA2 and 26 non-BRCA1/2) and 15 sporadic tumours in combination with supervised and unsupervised analysis was used to define common and/or specific copy number features.

resultsUnsupervised hierarchical clustering did not stratify tumours according to their familial or sporadic condition or to their BRCA1/2 mutation status. Common recurrent changes, spanning genes potentially fundamental for ovarian carcinogenesis, regardless of BRCA mutations, and several candidate subtype-specific events were defined. Despite similarities, greater contribution of losses was revealed to be a hallmark of BRCA1 and BRCA2 tumours.

conclusionSomatic alterations occurring in the development of familial EOCs do not differ substantially from the ones occurring in sporadic carcinomas. However, some specific features like extensive genomic loss observed in BRCA1/2 tumours may be of clinical relevance helping to identify BRCA-related patients likely to respond to PARP inhibitors.

Indexed as

DNA Copy Number VariationsGenes, BRCA1Genes, BRCA2Germ-Line MutationCarcinoma, Ovarian EpithelialComparative Genomic HybridizationDNA, NeoplasmFemaleFormaldehydeGenomic InstabilityHumansImmunohistochemistryNeoplasms, Glandular and EpithelialOvarian NeoplasmsParaffin EmbeddingTissue FixationDNA, NeoplasmFormaldehyde

Identifiers

PMID23558894
PMCPMC3668473
OpenAlexW2066679474

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.