Evidence map›Paper›PMID 26262998›Full record

ArticleRedox biology2015

Influence of myeloperoxidase on colon tumor occurrence in inflamed versus non-inflamed colons of Apc(Min/+) mice.

Mazin Al-Salihi, Ethan Reichert, F A Fitzpatrick

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Role of the Vanins-Myeloperoxidase Axis in Colorectal Carcinogenesis.International journal of molecular sciences · 2017
    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

3 authors at 3 institutions in 2 countries.

Mazin Al-SalihiSchool of Medicine, University of Jordan, Amman 11942, Jordan. Electronic address: mazin@fulbrightmail.org.
Ethan ReichertHuntsman Cancer Institute, University of Utah, 2000 Circle of Hope, Salt Lake City, UT 84112, USA.
F A FitzpatrickKansas City University of Medicine & Biosciences, Department of Pharmacology, 1750 Independence Avenue, Kansas City, MO 64106, USA. Electronic address: ffitzpatrick@kcumb.edu.
Kansas City University · USUniversity of Jordan · JOUniversity of Utah · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
NCI NIH HHS P30 CA042014NCI NIH HHS P30CA42014
6 · The paper itself

Abstract

Control of colorectal cancer needs to be tailored to its etiology. Tumor promotion mechanisms in colitis-associated colon cancer differ somewhat from the mechanisms involved in hereditary and sporadic colorectal cancer. Unlike sporadic or inherited tumors, some experimental models show that colitis-associated colon tumors do not require cyclooxygenase (COX) expression for progression, and non-steroidal anti-inflammatory drugs (NSAIDs) which prevent sporadic or inherited colon cancer do not prevent colitis-associated colon cancer. We report that myeloperoxidase (MPO), an ancestor of the COX isoenzymes, is a determinant of colitis-associated colon tumors in Apc(Min/+) mice. During experimentally induced colitis, inhibition of MPO by resorcinol dampened colon tumor development. Conversely, in the bowels of Apc(Min/+) mice without colitis, resorcinol administration or 'knockout' of MPO gene coincided with a slight, but discernible increase in colon tumor incidence. Acrolein, a by-product of MPO catalysis, formed a covalent adduct with the phosphatase tensin homolog (PTEN) tumor suppressor and enhanced the activity of the Akt kinase proto-oncogene in vitro and in vivo. Thus, MPO may be an important determinant of diet and inflammation on colon cancer risk via its effect on endogenous exposure to oxidants and acrolein. We propose a hypothetical model to explain an apparent dichotomy between colon tumor occurrence and MPO inhibition in inflamed versus non-inflamed colons.

Indexed as

AcroleinAnimalsColitisColonic NeoplasmsFemaleGene ExpressionInflammationMaleMiceMice, TransgenicOxidation-ReductionPeroxidaseProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseResorcinolsRNA, Small InterferingAcroleinPeroxidaseProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseresorcinolResorcinolsRNA, Small InterferingSodium Dodecyl SulfateColitisColon cancerInflammationMyeloperoxidase

Identifiers

PMID26262998
PMCPMC4536298
OpenAlexW1026060964

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.