Evidence map›Paper›PMID 24867690›Full record

ArticleBritish journal of cancer2014

Assessing the function of homologous recombination DNA repair in malignant pleural effusion (MPE) samples.

M J Patterson, R E Sutton, I Forrest, R Sharrock, M Lane, A Kaufmann, R O'Donnell, R J Edmondson, B T Wilson, N J Curtin

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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  13. BRCAness revisited.Nature reviews. Cancer · 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

10 authors at 3 institutions in 1 country.

M J PattersonNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
R E SuttonInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne NE1 3BZ, UK.
I ForrestRoyal Victoria Infirmary, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne NE1 4LP, UK.
R SharrockRoyal Victoria Infirmary, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne NE1 4LP, UK.
M LaneRoyal Victoria Infirmary, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne NE1 4LP, UK.
A Kaufmann1] Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne NE2 4HH, UK [2] The Northern Gynaecological Oncology Centre, Queen Elizabeth Hospital, Gateshead Foundation Trust, Gateshead NE9 6SX, UK.
R O'Donnell1] Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne NE2 4HH, UK [2] The Northern Gynaecological Oncology Centre, Queen Elizabeth Hospital, Gateshead Foundation Trust, Gateshead NE9 6SX, UK.
R J EdmondsonNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
B T WilsonInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne NE1 3BZ, UK.
N J CurtinNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
Newcastle University · GBRoyal Victoria Infirmary · GBGateshead Health NHS Foundation Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPatients with malignant pleural effusions (MPEs) generally have advanced disease with poor survival and few therapeutic options. Cells within MPEs may be used to stratify patients for targeted therapy. Targeted therapy with poly(ADP ribose) polymerase inhibitors (PARPi) depends on identifying homologous recombination DNA repair (HRR)-defective cancer cells. We aimed to determine the feasibility of assaying HRR status in MPE cells.

methodsA total of 15 MPE samples were collected from consenting patients with non-small-cell lung cancer (NSCLC), mesothelioma and ovarian and breast cancer. Primary cultures were confirmed as epithelial by pancytokeratin, and HRR status was determined by the detection of γH2AX and RAD51 foci following a 24-h exposure to rucaparib, by immunofluorescence microscopy. Massively parallel next-generation sequencing of DNA repair genes was performed on cultured MPE cells.

resultsFrom 15 MPE samples, 13 cultures were successfully established, with HRR function successfully determined in 12 cultures. Four samples - three NSCLC and one mesothelioma - were HRR defective and eight samples - one NSCLC, one mesothelioma, one sarcomatoid, one breast and four ovarian cancers - were HRR functional. No mutations in DNA repair genes were associated with HRR status, but there was probable loss of heterozygosity of FANCG, RPA1 and PARP1.

conclusionsHRR function can be successfully detected in MPE cells demonstrating the potential to stratify patients for targeted therapy with PARPi.

Indexed as

Recombinational DNA RepairAgedAged, 80 and overCarcinoma, Non-Small-Cell LungFeasibility StudiesFemaleHumansLung NeoplasmsMaleMiddle AgedPleural Effusion, Malignant

Identifiers

PMID24867690
PMCPMC4090730
OpenAlexW2026341466

What OpenQuestion holds

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LicenceCC BY-NC-SA
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Registered trials

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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.