Evidence map›Paper›PMID 36381660›Full record

ArticleCancer research communications2022

Replication stress defines distinct molecular subtypes across cancers.

Nobuyuki Takahashi, Sehyun Kim, Christopher W Schultz, Vinodh N Rajapakse, Yang Zhang, Christophe E Redon, Haiqing Fu, Lorinc Pongor, Suresh Kumar, Yves Pommier and 2 more

Abstract read
In one paragraph

Article in Cancer research communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–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

44 citing papers in PubMed.

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  11. Targeting extrachromosomal DNA in human cancers.Nature reviews. Drug discovery · 2026
    Review
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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

12 authors.

Nobuyuki TakahashiDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Sehyun KimDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Christopher W SchultzDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Vinodh N RajapakseDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Yang ZhangDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Christophe E RedonDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Haiqing FuDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Lorinc PongorDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Suresh KumarDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Yves PommierDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Mirit I AladjemDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Anish ThomasDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.

Funding

Exploiting DNA Replicative Stress for Novel Small Cell Lung Cancer TherapiesZIABC011793 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI THOMAS, ANISH · 2018 to 2025
$16.4M
Intramural NIH HHS ZIA BC011793
6 · The paper itself

Abstract

Endogenous replication stress is a major driver of genomic instability. Current assessments of replication stress are low throughput precluding its comprehensive assessment across tumors. Here we develop and validate a transcriptional profile of replication stress by leveraging established cellular characteristics that portend replication stress. The repstress gene signature defines a subset of tumors across lineages characterized by activated oncogenes, aneuploidy, extrachromosomal DNA amplification, immune evasion, high genomic instability, and poor survival, and importantly predicts response to agents targeting replication stress more robustly than previously reported transcriptomic measures of replication stress. Repstress score profiles the dual roles of replication stress during tumorigenesis and in established cancers and defines distinct molecular subtypes within cancers that may be more vulnerable to drugs targeting this dependency. Altogether, our study provides a molecular profile of replication stress, providing novel biological insights of the replication stress phenotype, with clinical implications.

Indexed as

DNA ReplicationNeoplasmsCell Transformation, NeoplasticGenomic InstabilityHumansOncogenes

Identifiers

PMID36381660
PMCPMC9648410

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.