Evidence map›Paper›PMID 24981601›Full record

ReviewNature reviews. Genetics2014

Mechanisms underlying mutational signatures in human cancers.

Thomas Helleday, Saeed Eshtad, Serena Nik-Zainal

Abstract readReview
In one paragraph

Review in Nature reviews. Genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 508 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
508citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

508 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Clinical Efficacy of Olaparib inJCO precision oncology · 2021
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448 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Thomas HelledayScience for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-171 21 Stockholm, Sweden.
Saeed EshtadScience for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-171 21 Stockholm, Sweden.
Serena Nik-Zainal1] Wellcome Trust Sanger Institute, Hinxton Genome Campus, Cambridge CB10 1SA, UK. [2] East Anglian Medical Genetics Service, Cambridge University Hospitals NHS Trust, Cambridge CB2 2QQ, UK.

Funding

Wellcome TrustWellcome Trust WT100183MA
6 · The paper itself

Abstract

The collective somatic mutations observed in a cancer are the outcome of multiple mutagenic processes that have been operative over the lifetime of a patient. Each process leaves a characteristic imprint--a mutational signature--on the cancer genome, which is defined by the type of DNA damage and DNA repair processes that result in base substitutions, insertions and deletions or structural variations. With the advent of whole-genome sequencing, researchers are identifying an increasing array of these signatures. Mutational signatures can be used as a physiological readout of the biological history of a cancer and also have potential use for discerning ongoing mutational processes from historical ones, thus possibly revealing new targets for anticancer therapies.

Indexed as

DNA DamageDNA RepairDNA Mutational AnalysisDNA, NeoplasmGenome, HumanHumansMutationNeoplasmsSequence Analysis, DNADNA, Neoplasm

Identifiers

PMID24981601
PMCPMC6044419

What OpenQuestion holds

Textmetadata
LicenceTDM
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.