Evidence map›Paper›PMID 23175119›Full record

ReviewNature reviews. Cancer2012

DNA repair dysregulation from cancer driver to therapeutic target.

Nicola J Curtin

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 556 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
556citing papers in PubMed, 2 pooled it
27.3field-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

556 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,056 citations in OpenAlex.

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496 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

1 author at 1 institution in 1 country.

Nicola J CurtinNewcastle University, Northern Institute for Cancer Research, Newcastle upon Tyne NE2 4HH, UK. nicola.curtin@ncl.ac.uk
Newcastle University · GB

Funding

Medical Research Council
6 · The paper itself

Abstract

Dysregulation of DNA damage repair and signalling to cell cycle checkpoints, known as the DNA damage response (DDR), is associated with a predisposition to cancer and affects responses to DNA-damaging anticancer therapy. Dysfunction of one DNA repair pathway may be compensated for by the function of another compensatory DDR pathway, which may be increased and contribute to resistance to DNA-damaging chemotherapy and radiotherapy. Therefore, DDR pathways make an ideal target for therapeutic intervention; first, to prevent or reverse therapy resistance; and second, using a synthetic lethal approach to specifically kill cancer cells that are dependent on a compensatory DNA repair pathway for survival in the context of cancer-associated oxidative and replicative stress. These hypotheses are currently being tested in the laboratory and are being translated into clinical studies.

Indexed as

DNA RepairAnimalsAntineoplastic AgentsBiomarkersCell Cycle CheckpointsDNA DamageHomologous RecombinationHumansNeoplasmsSignal TransductionAntineoplastic AgentsBiomarkers

Identifiers

PMID23175119
OpenAlexW2083960841

What OpenQuestion holds

Textmetadata
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.