Evidence map›Paper›PMID 28535182›Full record

ArticleCarcinogenesis2017

Characterization of liver injury, oval cell proliferation and cholangiocarcinogenesis in glutathione S-transferase A3 knockout mice.

Dana R Crawford, Zoran Ilic, Ian Guest, Ginger L Milne, John D Hayes, Stewart Sell

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Nrf2 in liver toxicology.Archives of pharmacal research · 2020
    Review
  13. GSTA3 regulates TGF-The Journal of international medical research · 2019
    Article
  14. Article
  15. 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 5 institutions in 2 countries.

Dana R CrawfordAlbany Medical Center, Department of Immunology and Microbial Disease, 43 New Scotland Avenue, Albany, NY 12208, USA.
Zoran IlicWadsworth Center, New York State Department of Health, Albany, NY 12201, USA.
Ian GuestWadsworth Center, New York State Department of Health, Albany, NY 12201, USA.
Ginger L MilneVanderbilt University School of Medicine, Department of Medicine and Pharmacology, Nashville, TN 37323, USA.
John D HayesDivision of Cancer Research, Medical Research Institute, University of Dundee, Ninewells Hospital and Medical School, Dundee, DD1 9SY, UK.
Stewart SellWadsworth Center, New York State Department of Health, Albany, NY 12201, USA.
New York State Department of Health · USAlbany Medical Center Hospital · USNinewells Hospital · GBVanderbilt University · USWadsworth Center · US

Funding

Aflatoxin B1 hepatocarcinogenesis in the mGSTA3-/- mouseR01CA161694 · NCI · WADSWORTH CENTER · PI SELL, STEWART · 2012 to 2016
$1.4M
NCI NIH HHS R01 CA161694
6 · The paper itself

Abstract

We recently generated glutathione S-transferase (GST) A3 knockout (KO) mice as a novel model to study the risk factors for liver cancer. GSTA3 KO mice are sensitive to the acute cytotoxic and genotoxic effects of aflatoxin B1 (AFB1), confirming the crucial role of GSTA3 in resistance to AFB1. We now report histopathological changes, tumor formation, biochemical changes and gender response following AFB1 treatment as well as the contribution of oxidative stress. Using a protocol of weekly 0.5 mg AFB1/kg administration, we observed extensive oval (liver stem) cell (OC) proliferation within 1-3 weeks followed by microvesicular lipidosis, megahepatocytes, nuclear inclusions, cholangiomas and small nodules. Male and female GSTA3 KO mice treated with 12 and 24 weekly AFB1 injections followed by a rest period of 12 and 6 months, respectively, all had grossly distorted livers with macro- and microscopic cysts, hepatocellular nodules, cholangiomas and cholangiocarcinomas and OC proliferation. We postulate that the prolonged AFB1 treatment leads to inhibition of hepatocyte proliferation, which is compensated by OC proliferation and eventually formation of cholangiocarcinoma (CCA). At low-dose AFB1, male KO mice showed less extensive acute liver injury, OC proliferation and AFB1-DNA adducts than female KO mice. There were no significant compensatory changes in KO mice GST subunits, GST enzymatic activity, epoxide hydrolase, or CYP1A2 and CYP3A11 levels. Finally, there was a modest increase in F2-isoprostane and isofuran in KO mice that confirmed putative GSTA3 hydroperoxidase activity in vivo for the first time.

Indexed as

Aflatoxin B1AnimalsCarcinogenesisCell ProliferationCholangiocarcinomaCytochrome P-450 CYP1A2Cytochrome P-450 CYP3ADNA AdductsF2-IsoprostanesFemaleGlutathione TransferaseHumansMaleMembrane ProteinsMiceMice, KnockoutAflatoxin B1Cyp3a11 protein, mouseCytochrome P-450 CYP1A2Cytochrome P-450 CYP3ADNA AdductsF2-IsoprostanesGlutathione TransferaseGSTA3 protein, mouseMembrane Proteins

Identifiers

PMID28535182
PMCPMC5862260
OpenAlexW2619502510

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.