Evidence map›Paper›PMID 25690937›Full record

ArticleBreast cancer research and treatment2015

DNA damage response markers are differentially expressed in BRCA-mutated breast cancers.

Mohammed Aleskandarany, Daniela Caracappa, Christopher C Nolan, R Douglas Macmillan, Ian O Ellis, Emad A Rakha, Andrew R Green

Open access · hybridAbstract read
In one paragraph

Article in Breast cancer research and treatment, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 3 pooled it
4.0field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 3 syntheses or guidelines pooled it, 58 citations in OpenAlex.

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  3. Association Between BRCA Status and P53 Status in Breast Cancer: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2016
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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

7 authors at 3 institutions in 3 countries.

Mohammed AleskandaranyDivision of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, UK, Mohammed.Aleskandarany@nottingham.ac.uk.
Daniela Caracappa
Christopher C Nolan
R Douglas Macmillan
Ian O Ellis
Emad A Rakha
Andrew R Green
University of Nottingham · GBMenoufia University · EGUniversity of Perugia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells have stringent DNA repair pathways that are specific for each different set of DNA lesions which is accomplished through the integration of complex array of proteins. However, BRCA-mutated breast cancer (BC) has defective DNA repair mechanisms. This study aims to investigate differential expression of a large panel of DNA repair markers to characterise DNA repair mechanisms in BRCA-associated tumours compared to sporadic tumours in an attempt to characterise these tumours in routine practice. Immunohistochemistry and tissue microarray technology were applied to a cohort of clinically annotated series of sporadic (n = 1849), BRCA1-mutated (n = 48), and BRCA2-mutated (n = 27) BC. The following DNA damage response (DDR) markers are used; BRCA1, BRCA2, RAD51, Ku70/Ku80, BARD, PARP1 (cleaved), PARP1 (non-cleaved), and P53 in addition to basal cytokeratins, ER, PR, and HER2. A significant proportion of BRCA1 tumours were positive for PARP1 (non-cleaved), and negative for BARD1 and RAD51 compared with sporadic BC. BRCA2 tumours were significantly positive for PARP1 (non-cleaved) compared with sporadic tumours. RAD51 was significantly higher in BRCA1 compared with BRCA2 tumours (p = 0.005). When BRCA1/2 BCs were compared to triple-negative (TN) sporadic tumours of the studied DDR proteins, BARD1 (p < 0.001), PARP1 (non-cleaved) (p < 0.001), and P53 (p = 0.002) remained significantly different in BRCA1/2 tumours compared with TN BC. DNA repair markers showed differential expression in BRCA-mutated tumours, with a substantial degree of disruption of DNA repair pathways in sporadic BC especially TN BC. DNA double-strand break (DSB) repair is assisted by PARP1 expression in BRCA-mutated tumours, whereas the loss of DSB repair via RAD51 is predominant in BRCA1 rather than BRCA2 BC.

Indexed as

DNA DamageDNA RepairGene Expression Regulation, NeoplasticMutationBiomarkers, TumorBRCA1 ProteinBRCA2 ProteinBreast NeoplasmsFemaleHumansNeoplasm GradingNeovascularization, PathologicPatient Outcome AssessmentPrognosisRetrospective StudiesTumor BurdenBiomarkers, TumorBRCA1 ProteinBRCA2 Protein

Identifiers

PMID25690937
PMCPMC4344553
OpenAlexW2083778750

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LicenceCC BY-NC
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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.