Evidence map›Paper›PMID 23371017›Full record

ArticleDigestive diseases and sciences2013

Chronic ingestion of ethanol induces hepatocellular carcinoma in mice without additional hepatic insult.

Mutsumi Tsuchishima, Joseph George, Hisakazu Shiroeda, Tomiyasu Arisawa, Tsutomu Takegami, Mikihiro Tsutsumi

Abstract readEvaluation Study
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Cytochrome P450s and Alcoholic Liver Disease.Current pharmaceutical design · 2018
    Review
  7. Review
  8. Effects of alcohol on c-Myc protein in the brain.Behavioural brain research · 2017
    Article
  9. Article
  10. Article
  11. Review
  12. Pharmacological blockage of CYP2E1 and alcohol-mediated liver cancer: is the time ready?Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2013
    Article
  13. 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 1 institution in 1 country.

Mutsumi TsuchishimaDepartment of Gastroenterology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Joseph George
Hisakazu Shiroeda
Tomiyasu Arisawa
Tsutomu Takegami
Mikihiro Tsutsumi
Kanazawa Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic intake of alcohol increases the risk of gastrointestinal and hepatic carcinogenesis. The present study was focused to investigate the incidence and mechanism of pathogenesis of hepatocellular carcinoma (HCC) during chronic ingestion of alcohol without any additional hepatic injury.

methodsEthanol was administered to Institute for Cancer Research male mice through drinking water for 70 weeks at concentrations of 5 % (first week), 10 % (next 8 weeks), and 15 % thereafter. The animals were killed at 60 and 70 weeks, the livers were examined for hepatic tumors, and evaluated for foci of cellular alteration (FCA). Immunohistochemical staining was performed in the liver sections for cytochrome P4502E1 (CYP2E1), 4-hydroxy-nonenal (4-HNE), and proto-oncogene, c-Myc.

resultsAt the 60th week, 40 % of the mice in the ethanol group had visible white nodules (5-10 mm) in the liver, but not in the control mice. At the 70th week, several larger nodules (5-22 mm) were present in the livers of 50 % mice in the ethanol group. In the control group, one mouse developed a single nodule. All nodules were histologically trabecular HCC composed of eosinophilic and vacuolated cells. In the livers of both control and ethanol group, several foci with cellular alteration were present, which were significantly higher in ethanol group. Staining for CYP2E1, 4-HNE and c-Myc depicted marked upregulation of all these molecules in the FCA.

conclusionsOur data demonstrated that upregulation of CYP2E1 and subsequent production of reactive oxygen species along with the persistent expression of c-Myc play a significant role in the pathogenesis of HCC during chronic ingestion of ethanol.

Indexed as

AnimalsBiomarkers, TumorCarcinoma, HepatocellularCentral Nervous System DepressantsEthanolLiverLiver NeoplasmsMaleMiceMice, Inbred ICRToxicity Tests, ChronicBiomarkers, TumorCentral Nervous System DepressantsEthanol

Identifiers

PMID23371017
OpenAlexW2082181068

What OpenQuestion holds

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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.