Evidence map›Paper›PMID 35708734›Full record

ReviewMolecular oncology2022

Exploring the genetic space of the DNA damage response for cancer therapy through CRISPR-based screens.

Jordan Wilson, Joanna I Loizou

Abstract readReview
In one paragraph

Review in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Polθ Inhibition: An Anticancer Therapy for HR-Deficient Tumours.International journal of molecular sciences · 2022
    Review
  3. Article
  4. Article
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

2 authors.

Jordan WilsonCenter for Cancer Research, Comprehensive Cancer Centre, Medical University of Vienna, Austria.ORCID 0000-0001-7765-8597
Joanna I LoizouCenter for Cancer Research, Comprehensive Cancer Centre, Medical University of Vienna, Austria.ORCID 0000-0003-1853-0424

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The concepts of synthetic lethality and viability have emerged as powerful approaches to identify vulnerabilities and resistances within the DNA damage response for the treatment of cancer. Historically, interactions between two genes have had a longstanding presence in genetics and have been identified through forward genetic screens that rely on the molecular basis of the characterized phenotypes, typically caused by mutations in single genes. While such complex genetic interactions between genes have been studied extensively in model organisms, they have only recently been prioritized as therapeutic strategies due to technological advancements in genetic screens. Here, we discuss synthetic lethal and viable interactions within the DNA damage response and present how CRISPR-based genetic screens and chemical compounds have allowed for the systematic identification and targeting of such interactions for the treatment of cancer.

Indexed as

CRISPR-Cas SystemsNeoplasmsDNA DamageGenetic TestingHumansMutationcancer therapyCRISPR-Cas9 screensDNA damage responsedrug discoverysynthetic lethalitysynthetic viability

Identifiers

PMID35708734
PMCPMC9627789

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.