Evidence map›Paper›PMID 34201502›Full record

ReviewCancers2021

Analyzing the Opportunities to Target DNA Double-Strand Breaks Repair and Replicative Stress Responses to Improve Therapeutic Index of Colorectal Cancer.

Paula Pellenz Tomasini, Temenouga Nikolova Guecheva, Natalia Motta Leguisamo, Sarah Péricart, Anne-Cécile Brunac, Jean Sébastien Hoffmann, Jenifer Saffi

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Targeting the DNA damage response for cancer therapy.Biochemical Society transactions · 2023
    Article
  10. Article
  11. Review
  12. Review
  13. Review
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

7 authors at 2 institutions in 2 countries.

Paula Pellenz TomasiniLaboratory of Genetic Toxicology, Federal University of Health Sciences of Porto Alegre, Avenida Sarmento Leite, 245, Porto Alegre 90050-170, Brazil.ORCID 0000-0002-9621-688X
Temenouga Nikolova GuechevaCardiology Institute of Rio Grande do Sul, University Foundation of Cardiology (IC-FUC), Porto Alegre 90620-000, Brazil.ORCID 0000-0001-8671-7317
Natalia Motta LeguisamoLaboratory of Genetic Toxicology, Federal University of Health Sciences of Porto Alegre, Avenida Sarmento Leite, 245, Porto Alegre 90050-170, Brazil.
Sarah PéricartLaboratoire D'Excellence Toulouse Cancer (TOUCAN), Laboratoire de Pathologie, Institut Universitaire du Cancer-Toulouse, Oncopole, 1 Avenue Irène-Joliot-Curie, 31059 Toulouse, France.
Anne-Cécile BrunacLaboratoire D'Excellence Toulouse Cancer (TOUCAN), Laboratoire de Pathologie, Institut Universitaire du Cancer-Toulouse, Oncopole, 1 Avenue Irène-Joliot-Curie, 31059 Toulouse, France.
Jean Sébastien HoffmannLaboratoire D'Excellence Toulouse Cancer (TOUCAN), Laboratoire de Pathologie, Institut Universitaire du Cancer-Toulouse, Oncopole, 1 Avenue Irène-Joliot-Curie, 31059 Toulouse, France.ORCID 0000-0003-2222-354X
Jenifer SaffiLaboratory of Genetic Toxicology, Federal University of Health Sciences of Porto Alegre, Avenida Sarmento Leite, 245, Porto Alegre 90050-170, Brazil.ORCID 0000-0002-5372-2934
Institut universitaire du cancer de Toulouse Oncopole · FRUniversidade Federal do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the ample improvements of CRC molecular landscape, the therapeutic options still rely on conventional chemotherapy-based regimens for early disease, and few targeted agents are recommended for clinical use in the metastatic setting. Moreover, the impact of cytotoxic, targeted agents, and immunotherapy combinations in the metastatic scenario is not fully satisfactory, especially the outcomes for patients who develop resistance to these treatments need to be improved. Here, we examine the opportunity to consider therapeutic agents targeting DNA repair and DNA replication stress response as strategies to exploit genetic or functional defects in the DNA damage response (DDR) pathways through synthetic lethal mechanisms, still not explored in CRC. These include the multiple actors involved in the repair of DNA double-strand breaks (DSBs) through homologous recombination (HR), classical non-homologous end joining (NHEJ), and microhomology-mediated end-joining (MMEJ), inhibitors of the base excision repair (BER) protein poly (ADP-ribose) polymerase (PARP), as well as inhibitors of the DNA damage kinases ataxia-telangiectasia and Rad3 related (ATR), CHK1, WEE1, and ataxia-telangiectasia mutated (ATM). We also review the biomarkers that guide the use of these agents, and current clinical trials with targeted DDR therapies.

Indexed as

colorectal cancerDNA double strand break repairreplication stresstarget therapy

Identifiers

PMID34201502
PMCPMC8268241
OpenAlexW3175332634

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.