Evidence map›Paper›PMID 27837030›Full record

ArticleMolecular cancer therapeutics2017

Clinicopathological and Functional Significance of RECQL1 Helicase in Sporadic Breast Cancers.

Arvind Arora, Swetha Parvathaneni, Mohammed A Aleskandarany, Devika Agarwal, Reem Ali, Tarek Abdel-Fatah, Andrew R Green, Graham R Ball, Emad A Rakha, Ian O Ellis and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

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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

12 authors at 4 institutions in 2 countries.

Arvind AroraAcademic Unit of Oncology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Swetha ParvathaneniDepartment of Biochemistry and Molecular Biology, College of Medicine, Howard University, Washington, DC.
Mohammed A AleskandaranyDepartment of Pathology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Devika AgarwalSchool of Science and Technology, Nottingham Trent University, Clifton campus, Nottingham, United Kingdom.
Reem AliAcademic Unit of Oncology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Tarek Abdel-FatahDepartment of Oncology, Nottingham University Hospitals, Nottingham, United Kingdom.
Andrew R GreenDepartment of Pathology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Graham R BallSchool of Science and Technology, Nottingham Trent University, Clifton campus, Nottingham, United Kingdom.
Emad A RakhaDepartment of Pathology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Ian O EllisDepartment of Pathology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Sudha SharmaDepartment of Biochemistry and Molecular Biology, College of Medicine, Howard University, Washington, DC. srinivasan.madhusudan@nottingham.ac.uk sudha.sharma@Howard.edu.
Srinivasan MadhusudanAcademic Unit of Oncology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom. srinivasan.madhusudan@nottingham.ac.uk sudha.sharma@Howard.edu.
University of Nottingham · GBNottingham University Hospitals NHS Trust · GBHoward University · USNottingham Trent University · GB

Funding

PROTEOMICS CORE FACILITYG12MD007597 · NIMHD · HOWARD UNIVERSITY · PI SOUTHERLAND, WILLIAM M. · 2012 to 2018
$14.8M
Molecular Analysis of RECQ1 Functions in Genome MaintenanceSC1GM093999 · NIGMS · HOWARD UNIVERSITY · PI SHARMA, SUDHA · 2010 to 2019
$3.0M
NIGMS NIH HHS SC1 GM093999NIMHD NIH HHS G12 MD007597
6 · The paper itself

Abstract

RECQL1, a key member of the RecQ family of DNA helicases, is required for DNA replication and DNA repair. Two recent studies have shown that germline RECQL1 mutations are associated with increased breast cancer susceptibility. Whether altered RECQL1 expression has clinicopathologic significance in sporadic breast cancers is unknown. We evaluated RECQL1 at the transcriptomic level (METABRIC cohort, n = 1,977) and at the protein level [cohort 1, n = 897; cohort 2, n = 252; cohort 3 (BRCA germline deficient), n = 74]. In RECQL1-depleted breast cancer cells, we investigated anthracycline sensitivity. High RECQL1 mRNA was associated with intClust.3 (P = 0.026), which is characterized by low genomic instability. On the other hand, low RECQL1 mRNA was linked to intClust.8 [luminal A estrogen receptor-positive (ER

Indexed as

Biomarkers, TumorAntineoplastic AgentsBreast NeoplasmsCell CycleCell Line, TumorDNA RepairDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticGenetic Association StudiesHumansNeoplasm GradingNeoplasm StagingPrognosisReceptors, EstrogenRecQ HelicasesAntineoplastic AgentsBiomarkers, TumorReceptors, EstrogenRecQ HelicasesRNA, Messenger

Identifiers

PMID27837030
PMCPMC5222686
OpenAlexW2550439605

What OpenQuestion holds

Textmetadata
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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.