Evidence map›Paper›PMID 23123447›Full record

ArticleLife sciences2013

Roles of alcohol and tobacco exposure in the development of hepatocellular carcinoma.

Vishnudutt Purohit, Rao Rapaka, Oh Sang Kwon, B J Song

Open access · hybridAbstract read
In one paragraph

Article in Life sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. A meta-analysis ofThe Journal of international medical research · 2019
    Pooled it
  2. Hepatocellular Carcinoma Survival in People With and Without HIV in the United States, 2001-2019.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Observational
  15. Article
  16. Disparities in Hepatocellular Carcinoma Incidence in California: An Update.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020
    Article
  17. Review
  18. Friend or foe, the role of EGR-1 in cancer.Medical oncology (Northwood, London, England) · 2019
    Review
  19. Article
  20. Growing burden of alcoholic liver disease in China: A review.World journal of gastroenterology · 2019
    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

4 authors at 3 institutions in 2 countries.

Vishnudutt PurohitChemistry and Physiological Systems Research Branch, Division of Basic Neuroscience & Behavioral Research, National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD 20892, USA. vpurohit@nida.nih.gov
Rao Rapaka
Oh Sang Kwon
B J Song
National Institutes of Health · USGachon University Gil Medical Center · KRNational Institute on Drug Abuse · US

Funding

Alcohol Metabolism, Functional Consequences, Apoptosis Signaling Pathways, and Organ DamageZIAAA000036 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI SONG, BYOUNG-JOON · 2009 to 2025
$14.8M
Intramural NIH HHS Z99 AA999999Intramural NIH HHS ZIA AA000036
6 · The paper itself

Abstract

The purpose of this report is to summarize the roles of alcohol and tobacco exposure in the development of hepatocellular carcinoma (HCC). Chronic heavy alcohol exposure is a major risk factor for HCC, which is the most frequent type of liver cancer. Alcohol ingestion may initiate and or promote the development of HCC by: 1) acetaldehyde-DNA adduct formation; 2) cytochrome P4502E1-associated reactive oxygen species (ROS) generation , lipid peroxidation, p53 mutation, and conversion of pro-carcinogens to carcinogens; 3) iron accumulation that leads to ROS generation, lipid peroxidation, p53 mutation, and initiation of inflammatory cascade via nuclear factor-KappaB (NF-kB) activation; 4) glutathione depletion leading to oxidative stress; 5) s-adenosylmethionine (SAM) depletion and associated DNA hypomethylation of oncogenes ; 6) retinoic acid depletion and resultant hepatocyte proliferation via up-regulation of activator protein-1 (AP-1); 7) initiating an inflammatory cascade through increased transfer of endotoxin from intestine to liver, Kupffer cell activation via CD14/toll-like receptor-4 (TLR-4), oxidative stress, NF-kB or early growth response-1(Egr-1) activation, and generation of inflammatory cytokines and chemokines; 8) induction of liver fibrosis; and 9) decreasing the number and/or function of natural killer cells. Tobacco exposure is also a risk factor for HCC. It may contribute to the initiation and promotion of HCC due the presence of mutagenic and carcinogenic compounds as well as by causing oxidative stress due to generation of ROS and depletion of endogenous antioxidants. Simultaneous exposure to alcohol and tobacco is expected to promote the development of HCC in an additive and/or synergistic manner.

Indexed as

Alcohol DrinkingAnimalsAntioxidantsCarcinoma, HepatocellularEthanolHumansInflammation MediatorsLiver NeoplasmsOxidative StressReactive Oxygen SpeciesRisk FactorsSmokingAntioxidantsEthanolInflammation MediatorsReactive Oxygen Species

Identifiers

PMID23123447
PMCPMC3822918
OpenAlexW2046374458

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.