Evidence map›Paper›PMID 34483003›Full record

ReviewTrends in genetics : TIG2022

Therapeutic and prognostic insights from the analysis of cancer mutational signatures.

Samuel W Brady, Alexander M Gout, Jinghui Zhang

Open access · bronzeAbstract readReview
In one paragraph

Review in Trends in genetics : TIG, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.5field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 80 citations in OpenAlex.

  1. The Landscape of Genomic and Socioeconomic Variables in Patients with Colorectal Cancer Based on Genetic Ancestry.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
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  11. Chemotherapy-associated mutational process signature and genomic alterations associated with outcome in metastatic pancreatic cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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  15. A Thiopurine-like Mutagenic Process Defines TGCT Subtypes.bioRxiv : the preprint server for biology · 2025
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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

3 authors at 1 institution in 1 country.

Samuel W BradyDepartment of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. Electronic address: samuelw.brady@stjude.org.
Alexander M GoutDepartment of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Jinghui ZhangDepartment of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. Electronic address: jinghui.zhang@stjude.org.
St. Jude Children's Research Hospital · US

Funding

Late Effects Prediction using Clinical Phenotypes and Whole Genome SequencingR01CA216354 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI YASUI, YUTAKA, ZHANG, JINGHUI · 2017 to 2021
$3.4M
Discovery of Somatic Noncoding Variants that Serve as Drivers in Pediatric CancersR01CA216391 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI ZHANG, JINGHUI · 2018 to 2022
$2.8M
NCI NIH HHS R01 CA216354NCI NIH HHS R01 CA216391
6 · The paper itself

Abstract

The somatic mutations in each cancer genome are caused by multiple mutational processes, each of which leaves a characteristic imprint (or 'signature'), potentially caused by specific etiologies or exposures. Deconvolution of these signatures offers a glimpse into the evolutionary history of individual tumors. Recent work has shown that mutational signatures may also yield therapeutic and prognostic insights, including the identification of cell-intrinsic signatures as biomarkers of drug response and prognosis. For example, mutational signatures indicating homologous recombination deficiency are associated with poly(ADP)-ribose polymerase (PARP) inhibitor sensitivity, whereas APOBEC-associated signatures are associated with ataxia telangiectasia and Rad3-related kinase (ATR) inhibitor sensitivity. Furthermore, therapy-induced mutational signatures implicated in cancer progression have also been uncovered, including the identification of thiopurine-induced TP53 mutations in leukemia. In this review, we explore the various ways mutational signatures can reveal new therapeutic and prognostic insights, thus extending their traditional role in identifying disease etiology.

Indexed as

NeoplasmsHumansMutationPoly(ADP-ribose) PolymerasesPrognosisPoly(ADP-ribose) Polymerases

Identifiers

PMID34483003
PMCPMC8752466
OpenAlexW3198053574

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.