Evidence map›Paper›PMID 30831321›Full record

ArticleCellular and molecular gastroenterology and hepatology2019

Mouse Model of Mutated in Colorectal Cancer Gene Deletion Reveals Novel Pathways in Inflammation and Cancer.

Nicola Currey, Zeenat Jahan, C Elizabeth Caldon, Phuong N Tran, Fahad Benthani, Penelope De Lacavalerie, Daniel L Roden, Brian S Gloss, Claudia Campos, Elaine G Bean and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Cancers · 2022
    Article
  6. Article
  7. PersistentMicroorganisms · 2021
    Article
  8. Article
  9. 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

17 authors at 4 institutions in 2 countries.

Nicola CurreyGarvan Institute of Medical Research, Sydney, New South Wales, Australia.
Zeenat JahanGarvan Institute of Medical Research, Sydney, New South Wales, Australia.
C Elizabeth CaldonGarvan Institute of Medical Research, Sydney, New South Wales, Australia; St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
Phuong N TranGarvan Institute of Medical Research, Sydney, New South Wales, Australia; St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
Fahad BenthaniGarvan Institute of Medical Research, Sydney, New South Wales, Australia; St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
Penelope De LacavalerieGarvan Institute of Medical Research, Sydney, New South Wales, Australia; St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
Daniel L RodenGarvan Institute of Medical Research, Sydney, New South Wales, Australia; St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
Brian S GlossGarvan Institute of Medical Research, Sydney, New South Wales, Australia; St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
Claudia CamposInstituto Gulbenkian de Ciência, Oeiras, Portugal.
Elaine G BeanACT Pathology, The Canberra Hospital, Australian National University Medical School, Canberra, Australian Capital Territory, Australia.
Amanda BullmanACT Pathology, The Canberra Hospital, Australian National University Medical School, Canberra, Australian Capital Territory, Australia.
Saskia Reibe-PalGarvan Institute of Medical Research, Sydney, New South Wales, Australia.
Marcel E DingerGarvan Institute of Medical Research, Sydney, New South Wales, Australia; St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
Mark A FebbraioGarvan Institute of Medical Research, Sydney, New South Wales, Australia; St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
Stephen J ClarkeRoyal North Shore Hospital, University of Sydney, Sydney, New South Wales, Australia.
Jane E DahlstromACT Pathology, The Canberra Hospital, Australian National University Medical School, Canberra, Australian Capital Territory, Australia.
Maija R J Kohonen-CorishGarvan Institute of Medical Research, Sydney, New South Wales, Australia; School of Medicine, Western Sydney University, Sydney, New South Wales, Australia; Microbiome Research Centre, St George and Sutherland Clinical School, University of New South Wales, Sydney, New South Wales, Australia. Electronic address: m.corish@garvan.org.au.
Garvan Institute of Medical Research · AUAustralian National University · AUInstituto Gulbenkian de Ciência · PTThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsThe early events by which inflammation promotes cancer are still not fully defined. The MCC gene is silenced by promoter methylation in colitis-associated and sporadic colon tumors, but its functional significance in precancerous lesions or polyps is not known. Here, we aimed to determine the impact of Mcc deletion on the cellular pathways and carcinogenesis associated with inflammation in the mouse proximal colon.

methodsWe generated knockout mice with deletion of Mcc in the colonic/intestinal epithelial cells (Mcc

resultsTranscriptome profiling of the lesions showed a strong response to colon barrier destruction, such as up-regulation of key inflammation and cancer-associated genes as well as 28 interferon γ-induced guanosine triphosphatase genes, including the homologs of Crohn's disease susceptibility gene IRGM. These features were shared by both Mcc-expressing and Mcc-deficient mice and many of the altered gene expression pathways were similar to the mesenchymal colorectal cancer subtype known as consensus molecular subtype 4 (CMS4). However, Mcc deletion was required for increased carcinogenesis in the lesions, with adenocarcinoma in 59% of Mcc

conclusionsLoss of Mcc may promote cancer through a failure to repair inflammation-induced DNA damage. We provide a comprehensive transcriptome data set of early colorectal lesions and evidence for the in vivo significance of MCC silencing in colorectal cancer.

Indexed as

Gene DeletionGenes, MCCAnimalsbeta CateninCadherinsColonColorectal NeoplasmsDisease Models, AnimalDNA RepairDown-RegulationFemaleGene Expression Regulation, NeoplasticGTP PhosphohydrolasesInflammationInterferon-gammaMalebeta CateninCadherinsGTP PhosphohydrolasesInterferon-gammaCMS4DNA RepairE2F TargetsIFNγ-Induced GTPases

Identifiers

PMID30831321
PMCPMC6476813
OpenAlexW2918604901

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.