Evidence map›Paper›PMID 25427908›Full record

ReviewAdvances in experimental medicine and biology2015

Alcohol consumption, Wnt/β-catenin signaling, and hepatocarcinogenesis.

K E Mercer, L Hennings, M J J Ronis

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
10.0field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 37 citations in OpenAlex.

  1. Polydatin: A natural compound with multifaceted anticancer properties.Journal of traditional and complementary medicine · 2025
    Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Wnt signaling in liver regeneration, disease, and cancer.Clinical and molecular hepatology · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Measuring signal transduction and transcription molecules for clinical use.Asian biomedicine : research, reviews and news · 2020
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Garlic-derived compoundActa pharmaceutica Sinica. B · 2018
    Article
  19. Polydatin inhibits cell proliferation, invasion and migration, and induces cell apoptosis in hepatocellular carcinoma.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
    Article
  20. 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

3 authors at 2 institutions in 1 country.

K E MercerArkansas Children's Nutrition Center, University of Arkansas for Medical Sciences, Little Rock, AR, USA, kmercer@uams.edu.
L Hennings
M J J Ronis
University of Arkansas for Medical Sciences · USArkansas Children's Nutrition Center · US

Funding

The role of oxidative stress in alcohol-induced osteopeniaR37AA018282 · NIAAA · LSU HEALTH SCIENCES CENTER · PI RONIS, MARTIN J J · 2016 to 2025
$4.7M
Prevention of EtOH-induced promotion of hepatocarcinogenesis by genistein/soyR21CA169389 · NCI · ARKANSAS CHILDREN'S HOSPITAL RES INST · PI RONIS, MARTIN J J · 2012 to 2013
$344k
NCI NIH HHS R21 CA169389NIAAA NIH HHS R37 AA018282
6 · The paper itself

Abstract

Alcohol is a well-established risk factor for hepatocellular carcinoma, and the mechanisms by which alcohol liver cancer is complex. It has been suggested that ethanol (EtOH) metabolism may enhance tumor progression by increasing hepatocyte proliferation. To test this hypothesis, ethanol (EtOH) feeding of male mice began 7 weeks post-injection of the chemical carcinogen diethylnitrosamine (DEN), and continued for 16 weeks, with a final EtOH concentration of 28% of total calories. As expected, EtOH increased the total number of cancerous foci and liver tumors identified in situ fixed livers from the EtOH+DEN group compared to corresponding pair-fed (PF)+DEN and chow+DEN control groups. In the EtOH+DEN group, tumor multiplicity corresponded to a 3- to 4-fold increase in proliferation and immunohistochemical staining of β-catenin in non-tumorigenic hepatocytes when compared to the PF+DEN and chow+DEN groups, p<0.05. Analysis of EtOH-treated livers from a previously published rat model of chronic liver disease revealed increases in hepatocyte proliferation accompanied by a hepatic depletion of retinol and retinoic acid stores (p<0.05), nuclear accumulation of β-catenin (p<0.05), increased cytosolic expression p-GSK3β (p<0.05), significant upregulation of soluble Wnts, Wnt2, and Wnt7a, and increased expression of several β-catenin targets involved in tumor promotion and progression, cyclin D1, c-myc, WISP1, and MMP7 (p<0.05). These data suggest that chronic EtOH consumption activates the Wnt/β-catenin signaling pathway, which increases hepatocyte proliferation thus promoting tumorigenesis following an initiating insult in the liver.

Indexed as

Alcohol DrinkingAnimalsbeta CateninDiethylnitrosamineLiver NeoplasmsMaleMiceMice, Inbred C57BLWnt Signaling Pathwaybeta CateninCTNNB1 protein, mouseDiethylnitrosamine

Identifiers

PMID25427908
PMCPMC5600155
OpenAlexW152466120

What OpenQuestion holds

Textmetadata
LicenceTDM
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.