Evidence map›Paper›PMID 37591859›Full record

ArticleNature communications2023

An ATR-PrimPol pathway confers tolerance to oncogenic KRAS-induced and heterochromatin-associated replication stress.

Taichi Igarashi, Marianne Mazevet, Takaaki Yasuhara, Kimiyoshi Yano, Akifumi Mochizuki, Makoto Nishino, Tatsuya Yoshida, Yukihiro Yoshida, Nobuhiko Takamatsu, Akihide Yoshimi and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 31 citations in OpenAlex.

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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

17 authors at 8 institutions in 3 countries.

Taichi IgarashiLaboratory of Genome Stress Signaling, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan.
Marianne MazevetLaboratory of Genome Stress Signaling, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan.
Takaaki YasuharaDepartment of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8501, Japan.ORCID http://orcid.org/0000-0002-6719-5709
Kimiyoshi YanoLaboratory of Genome Stress Signaling, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan.
Akifumi MochizukiDivision of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan.
Makoto NishinoDivision of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan.
Tatsuya YoshidaDepartment of Thoracic Oncology, National Cancer Center Hospital, Chuo-ku, Tokyo, 104-0045, Japan.
Yukihiro YoshidaDepartment of Thoracic Surgery, National Cancer Center Hospital, Chuo-ku, Tokyo, 104-0045, Japan.
Nobuhiko TakamatsuDepartment of Biosciences, School of Science, Kitasato University, Minami-ku, Sagamihara-city, Kanagawa, 252-0373, Japan.
Akihide YoshimiDepartment of Biosciences, School of Science, Kitasato University, Minami-ku, Sagamihara-city, Kanagawa, 252-0373, Japan.ORCID http://orcid.org/0000-0002-0664-7281
Kouya ShiraishiDivision of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan.ORCID http://orcid.org/0000-0002-5821-7400
Hidehito HorinouchiDepartment of Thoracic Oncology, National Cancer Center Hospital, Chuo-ku, Tokyo, 104-0045, Japan.ORCID http://orcid.org/0000-0001-9090-801X
Takashi KohnoDivision of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan.ORCID http://orcid.org/0000-0002-5371-706X
Ryuji HamamotoDivision of Medical AI Research and Development, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan.ORCID http://orcid.org/0000-0002-2632-1334
Jun AdachiLaboratory of Proteomics for Drug Discovery, Laboratory of Clinical and Analytical Chemistry, Center for Drug Design Research, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki-city, Osaka, 567-0085, Japan.ORCID http://orcid.org/0000-0003-1220-3246
Lee ZouMassachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA, 02129, USA.
Bunsyo ShiotaniLaboratory of Genome Stress Signaling, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan. bshiotan@ncc.go.jp.ORCID http://orcid.org/0000-0002-3583-4318
National Cancer Center Hospital East · JPNational Cancer Centre Japan · JPKitasato University · JPNational Cancer Research Institute · GBHarvard University · USKyoto University · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of the KRAS oncogene is a source of replication stress, but how this stress is generated and how it is tolerated by cancer cells remain poorly understood. Here we show that induction of KRAS

Indexed as

HeterochromatinProto-Oncogene Proteins p21(ras)Ataxia Telangiectasia Mutated ProteinsChromatinDNA-Directed DNA PolymeraseDNA PrimaseGenomic InstabilityHumansMultifunctional EnzymesAtaxia Telangiectasia Mutated ProteinsATR protein, humanChromatinDNA-Directed DNA PolymeraseDNA PrimaseHeterochromatinKRAS protein, humanMultifunctional EnzymesPrimPol protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID37591859
PMCPMC10435487
OpenAlexW4385954572

What OpenQuestion holds

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LicenceCC BY
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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.