Evidence map›Paper›PMID 27709011›Full record

ReviewActa pharmaceutica Sinica. B2016

Exposure to inorganic arsenic can lead to gut microbe perturbations and hepatocellular carcinoma.

Jonathan Choiniere, Li Wang

Open access · diamondAbstract readReview
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 3 pooled it
3.0field-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

25 citing papers in PubMed, 3 syntheses or guidelines pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Hepatocellular Carcinoma (HCC) in Egypt: A comprehensive overview.Journal of the Egyptian National Cancer Institute · 2020
    Pooled it
  4. Article
  5. Review
  6. Article
  7. Article
  8. miR-184 in hepatocellular carcinoma: a promising therapeutic target.Journal of physiology and biochemistry · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Synthetic bacteria for the detection and bioremediation of heavy metals.Frontiers in bioengineering and biotechnology · 2023
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. 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

2 authors at 2 institutions in 2 countries.

Jonathan ChoiniereDepartment of Physiology and Neurobiology, The Institute for Systems Genomics, University of Connecticut, Storrs, CT 06269, USA.
Li WangDepartment of Physiology and Neurobiology, The Institute for Systems Genomics, University of Connecticut, Storrs, CT 06269, USA; School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China; Veterans Affairs Connecticut Healthcare System, West Haven, CT 06516, USA; Department of Internal Medicine, Section of Digestive Diseases, Yale University, New Haven, CT 06520, USA.
University of Connecticut · USYale University · US

Funding

Yale Liver CenterP30DK034989 · NIDDK · YALE UNIVERSITY · PI WAJAHAT Zafar MEHAL · 1986 to 2026
$31.1M
SHP-regulation of Lipid and Lipoprotein MetabolismR01DK080440 · NIDDK · UNIVERSITY OF UTAH · PI WANG, LI · 2008 to 2015
$2.3M
LncRNA as a New Mediator of Bile Acid HomeostasisR01DK104656 · NIDDK · UNIVERSITY OF CONNECTICUT STORRS · PI WANG, LI · 2015 to 2018
$1.7M
Molecular Basis of Cancer Cell Metabolic ReprogrammingR01ES025909 · NIEHS · UNIVERSITY OF CONNECTICUT STORRS · PI WANG, LI · 2015 to 2017
$1.0M
Alcohol, nuclear receptor signaling, and circadian clocksR21AA022482 · NIAAA · UNIVERSITY OF CONNECTICUT STORRS · PI WANG, LI · 2015 to 2016
$415k
Circadian Clock Regulation of Alcoholic Liver DiseaseI01BX002634 · VA · VA CONNECTICUT HEALTHCARE SYSTEM · PI WANG, LI · 2016 to 2019
–
BLRD VA I01 BX002634NIAAA NIH HHS R21 AA022482NIDDK NIH HHS P30 DK034989NIDDK NIH HHS R01 DK080440NIDDK NIH HHS R01 DK104656NIEHS NIH HHS R01 ES025909
6 · The paper itself

Abstract

Arsenic is a carcinogenic environmental factor found in food and drinking water around the world. The mechanisms in which arsenic alters homeostasis are not fully understood. Over the past few decades, light has been shed on varying mechanisms in which arsenic induces cancer. Such mechanisms include gut microbe perturbations, genotoxic effects, and epigenetic modification. Gut microbe perturbations have been shown to increase the level of pathogen-associated molecular patterns such as lipopolysaccharide (LPS) leading to uncontained inflammation. Increase in inflammation is the major factor in cirrhosis leading to hepatocellular carcinoma. Alterations in gut permeability and metabolites have also been observed as a fallout of arsenic induced gut microbe modification. The guts proximity and interaction through portal flow make the liver susceptible to gut perturbations and ensuing inflammatory responses. Genotoxic and epigenetic dysregulation induced by arsenic and its toxic metabolites present a more direct mechanism that works synergistically with gut microbe perturbations to induce the incidence of cancers. These pathways combined could be some of the main causes of arsenic-induced carcinogenesis.

Indexed as

ArsenicEpigeneticsGut microbiotaHepatocellular carcinomaLipopolysaccharideLiver cancerMicrobiome

Identifiers

PMID27709011
PMCPMC5045549
OpenAlexW2476848306

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.