Evidence map›Paper›PMID 31188020›Full record

ReviewDNA and cell biology2019

Progressing from Recurring Tissue Injury to Genomic Instability: A New Mechanism of Neutrophil Pathogenesis.

Triet M Bui, Ronen Sumagin

Open access · greenAbstract readReview
In one paragraph

Review in DNA and cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Exosomes in Intestinal Inflammation.Frontiers in pharmacology · 2021
    Review
  5. Review
  6. Article
  7. 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 at 1 institution in 1 country.

Triet M BuiDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Ronen SumaginDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Northwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant neutrophil (PMN) infiltration of the intestinal mucosa is a hallmark of inflammatory bowel diseases, including Crohn's disease and ulcerative colitis. While the genotoxic function of PMNs and its implications in carcinogenesis have been primarily associated with oxidative stress, recent work by Butin-Israeli and colleagues has defined a novel mechanism where PMN-derived microparticles through the delivery and activity of specific miRNAs promoted formation of double-strand breaks (DSBs), and in parallel, suppressed DSB repair through the downregulation of lamin B1 and Rad51. Respective downregulation of these two proteins compromised the nuclear envelope and high-fidelity repair by homologous recombination, increasing DSB accumulation and aneuploidy. This discovery defined a novel mode of action where PMN-mediated suppression of DSB repair leading to genomic instability in the injured mucosa may facilitate progression toward colorectal cancer.

Indexed as

Genomic InstabilityColorectal NeoplasmsDNA Breaks, Double-StrandedHumansInflammatory Bowel DiseasesLamin Type BMicroRNAsNeutrophilsOxidative StressReactive Oxygen SpeciesLamin Type BMicroRNAsMIRN155 microRNA, humanMIRN23a microRNA, humanReactive Oxygen SpeciescarcinogenesisIBDinflammationmicroRNAsneutrophilswound healing

Identifiers

PMID31188020
PMCPMC7643757
OpenAlexW2951721642

What OpenQuestion holds

Textmetadata
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.