Evidence map›Paper›PMID 30714316›Full record

ReviewMolecular oncology2019

Exploiting DNA repair defects in colorectal cancer.

Nicole M Reilly, Luca Novara, Federica Di Nicolantonio, Alberto Bardelli

Open access · goldAbstract readReview
In one paragraph

Review in Molecular oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
11.8field-weighted citation impact, top 1% 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

84 citing papers in PubMed, 133 citations in OpenAlex.

  1. Inhibition of WEE1 Is Effective inJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2021
    Trial
  2. Review
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  12. Genomic characterization of patients with colorectal cancer.Hereditary cancer in clinical practice · 2025
    Article
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  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

24 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Nicole M ReillyFondazione Piemontese per la Ricerca sul Cancro ONLUS, Candiolo, Italy.
Luca NovaraCandiolo Cancer Institute, FPO-IRCCS, Candiolo, Italy.
Federica Di NicolantonioCandiolo Cancer Institute, FPO-IRCCS, Candiolo, Italy.ORCID 0000-0001-9618-2010
Alberto BardelliCandiolo Cancer Institute, FPO-IRCCS, Candiolo, Italy.
Candiolo Cancer Institute · ITFondazione Piemontese per la Ricerca sul Cancro Onlus · IT

Funding

Associazione Italiana per la Ricerca sul Cancro 16788Associazione Italiana per la Ricerca sul Cancro 17707Associazione Italiana per la Ricerca sul Cancro 21091Associazione Italiana per la Ricerca sul Cancro 9970European Community's Seventh Framework Programme 602901 MErCuRICFondazione Piemontese per la Ricerca sul Cancro-ONLUSFondo per la Ricerca LocaleH2020 635342-2 MoTriColor
6 · The paper itself

Abstract

Colorectal cancer (CRC) is the third leading cause of cancer-related deaths worldwide. Therapies that take advantage of defects in DNA repair pathways have been explored in the context of breast, ovarian, and other tumor types, but not yet systematically in CRC. At present, only immune checkpoint blockade therapies have been FDA approved for use in mismatch repair-deficient colorectal tumors. Here, we discuss how systematic identification of alterations in DNA repair genes could provide new therapeutic opportunities for CRCs. Analysis of The Cancer Genome Atlas Colon Adenocarcinoma (TCGA-COAD) and Rectal Adenocarcinoma (TCGA-READ) PanCancer Atlas datasets identified 141 (out of 528) cases with putative driver mutations in 29 genes associated with DNA damage response and repair, including the mismatch repair and homologous recombination pathways. Genetic defects in these pathways might confer repair-deficient characteristics, such as genomic instability in the absence of homologous recombination, which can be exploited. For example, inhibitors of poly(ADP)-ribose polymerase are effectively used to treat cancers that carry mutations in BRCA1 and/or BRCA2 and have shown promising results in CRC preclinical studies. HR deficiency can also occur in cells with no detectable BRCA1/BRCA2 mutations but exhibiting BRCA-like phenotypes. DNA repair-targeting therapies, such as ATR and CHK1 inhibitors (which are most effective against cancers carrying ATM mutations), can be used in combination with current genotoxic chemotherapies in CRCs to further improve therapy response. Finally, therapies that target alternative DNA repair mechanisms, such as thiopurines, also have the potential to confer increased sensitivity to current chemotherapy regimens, thus expanding the spectrum of therapy options and potentially improving clinical outcomes for CRC patients.

Indexed as

DNA RepairAnimalsClinical Trials as TopicColorectal NeoplasmsHumansMolecular Targeted TherapyPhenotypecolorectal cancergenome instabilityhomologous recombinationmicrosatellite instabilitymismatch repair

Identifiers

PMID30714316
PMCPMC6441925
OpenAlexW2912626193

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.