Evidence map›Paper›PMID 26440614›Full record

ArticlePloS one2015

High Endogenous Expression of Chitinase 3-Like 1 and Excessive Epithelial Proliferation with Colonic Tumor Formation in MOLF/EiJ Mice.

Daren Low, Arianna K DeGruttola, Alexander Poltrak, Atsushi Mizoguchi, Mari Mino-Kenudson, Emiko Mizoguchi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. The expression levels of CHI3L1 and IL15Rα correlate with TGM2 in duodenum biopsies of patients with celiac disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Article
  5. 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

6 authors at 3 institutions in 3 countries.

Daren LowGastrointestinal Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States of America.
Arianna K DeGruttolaGastrointestinal Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States of America.
Alexander PoltrakDepartment of Molecular Biology, Petrozavodsk State University, 185910, Petrozavodsk, Republic of Karelia, Russia; Graduate Program in Genetics, Sackler School of Biomedical Sciences, Tufts University, Boston, MA, United States of America.
Atsushi MizoguchiDepartment of Immunology, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Mari Mino-KenudsonDepartment of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States of America.
Emiko MizoguchiGastrointestinal Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States of America; Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States of America.
Harvard University · USKurume University · JPPetrozavodsk State University · RU

Funding

Inducible Regulatory B cells IBREGR01AI081807 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI REINECKER, HANS-CHRISTIAN · 2011 to 2015
$1.9M
Role of Mammalian Chitinases in Inflammatory Bowel DiseaseR01DK080070 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MIZOGUCHI, EMIKO · 2009 to 2013
$1.6M
IL-22 pathway in IBDR01DK091247 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI REINECKER, HANS-CHRISTIAN · 2013 to 2016
$1.4M
NIAID NIH HHS AI81807NIAID NIH HHS R01 AI081807NIDDK NIH HHS DK91247NIDDK NIH HHS R01 DK080070NIDDK NIH HHS R01 DK091247NIDDK NIH HHS R01-DK80070
6 · The paper itself

Abstract

Colorectal cancer (CRC) development is mediated by uncontrolled survival and proliferation of tumor progenitor cells. Using animal models to identify and study host-derived factors that underlie this process can aid interventions in preventing tumor expansion and metastasis. In healthy steady states in humans and mice (e.g. C57BL/6 strain), colonic Chitinase 3-like 1 (CHI3L1) gene expression is undetectable. However, this expression can be induced during intestinal inflammation and tumorigenesis where CHI3L1 plays an important role in tissue restitution and cell proliferation. Here, we show that a wild-derived mouse strain MOLF/EiJ expresses high levels of colonic epithelial CHI3L1 at the steady state due to several nucleotide polymorphisms in the proximal promoter regions of the CHI3L1 gene. Interestingly, these mice spontaneously developed polypoid nodules in the colon with signs of immune cell infiltrations at steady state. The CHI3L1 positive colonic epithelial cells were highly proliferative and exhibited malignant transformation and expansion when exposed in vivo to azoxymethane, one of the well-known colonic carcinogens.

Indexed as

AnimalsCell Transformation, NeoplasticChitinase-3-Like Protein 1Colonic NeoplasmsEnzyme-Linked Immunosorbent AssayEpithelial CellsGlycoproteinsImmunohistochemistryMiceMice, Inbred C57BLMicroscopy, ConfocalChil1 protein, mouseChitinase-3-Like Protein 1Glycoproteins

Identifiers

PMID26440614
PMCPMC4594921
OpenAlexW2188725868

What OpenQuestion holds

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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.