Evidence map›Paper›PMID 35320711›Full record

ArticleCell reports2022

Prospectively defined patterns of APOBEC3A mutagenesis are prevalent in human cancers.

Rachel A DeWeerd, Eszter Németh, Ádám Póti, Nataliya Petryk, Chun-Long Chen, Olivier Hyrien, Dávid Szüts, Abby M Green

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Distinct repair processes produce APOBEC-induced deletions, tandem substitutions, and complex mutations in yeast and human cells.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

8 authors at 3 institutions in 3 countries.

Rachel A DeWeerdDepartment of Pediatrics, Washington University School of Medicine, St. Louis, MO, USA.
Eszter NémethInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.
Ádám PótiInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.
Nataliya PetrykEpigenetics & Cell Fate UMR7216, CNRS, University of Paris, 35 rue Hélène Brion, 75013 Paris, France.
Chun-Long ChenInstitut Curie, Université PSL, Sorbonne Université, CNRS UMR3244, Dynamics of Genetic Information, Paris, France.
Olivier HyrienInstitut de Biologie de l'Ecole Normale Supérieure (IBENS), Ecole Normale Supérieure, CNRS, INSERM, Université PSL, 46 rue d'Ulm, 75005 Paris, France.
Dávid SzütsInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary. Electronic address: szuts.david@ttk.hu.
Abby M GreenDepartment of Pediatrics, Washington University School of Medicine, St. Louis, MO, USA; Center for Genome Integrity, Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO, USA. Electronic address: abby.green@wustl.edu.
Centre National de la Recherche Scientifique · FRInstitute of Molecular Life Sciences · HUWashington University in St. Louis · US

Funding

Dignity Therapy RCT led by Nurses or Chaplains for Elderly Cancer OutpatientsR01CA200867 · NCI · UNIVERSITY OF FLORIDA · PI EMANUEL, LINDA LEAH, FITCHETT, GEORGE · 2016 to 2020
$3.2M
Molecular Interactions of APOBEC3 Enzymes with the Cancer GenomeK08CA212299 · NCI · WASHINGTON UNIVERSITY · PI GREEN, ABBY MARGARET · 2016 to 2020
$744k
NCI NIH HHS K08 CA212299NCI NIH HHS R01 CA200867
6 · The paper itself

Abstract

Mutational signatures defined by single base substitution (SBS) patterns in cancer have elucidated potential mutagenic processes that contribute to malignancy. Two prevalent mutational patterns in human cancers are attributed to the APOBEC3 cytidine deaminase enzymes. Among the seven human APOBEC3 proteins, APOBEC3A is a potent deaminase and proposed driver of cancer mutagenesis. In this study, we prospectively examine genome-wide aberrations by expressing human APOBEC3A in avian DT40 cells. From whole-genome sequencing, we detect hundreds to thousands of base substitutions per genome. The APOBEC3A signature includes widespread cytidine mutations and a unique insertion-deletion (indel) signature consisting largely of cytidine deletions. This multi-dimensional APOBEC3A signature is prevalent in human cancer genomes. Our data further reveal replication-associated mutations, the rate of stem-loop and clustered mutations, and deamination of methylated cytidines. This comprehensive signature of APOBEC3A mutagenesis is a tool for future studies and a potential biomarker for APOBEC3 activity in cancer.

Indexed as

NeoplasmsCytidineCytidine DeaminaseGenome, HumanHumansMutagenesisProteinsAPOBEC3A protein, humanCytidineCytidine DeaminaseProteinsAPOBEC3cancer genomeCP:Cancercytidine deaminaseindelmethylcytidinemutagenesismutational signature

Identifiers

PMID35320711
PMCPMC9283007
OpenAlexW4220708137

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.