Evidence map›Paper›PMID 34290399›Full record

ReviewOncogene2021

Oxidative stress in obesity-associated hepatocellular carcinoma: sources, signaling and therapeutic challenges.

Manoja K Brahma, Eduardo H Gilglioni, Lang Zhou, Eric Trépo, Pengyu Chen, Esteban N Gurzov

Open access · hybridAbstract readReview
In one paragraph

Review in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Inflammation in MASLD progression and cancer.JHEP reports : innovation in hepatology · 2025
    Review
  15. Article
  16. Review
  17. Article
  18. GABAMedComm · 2025
    Review
  19. Article
  20. 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

6 authors at 2 institutions in 2 countries.

Manoja K Brahma *Signal Transduction and Metabolism Laboratory, Laboratoire de Gastroentérologie Expérimental et Endotools, Université libre de Bruxelles, Brussels, Belgium.
Eduardo H Gilglioni *Signal Transduction and Metabolism Laboratory, Laboratoire de Gastroentérologie Expérimental et Endotools, Université libre de Bruxelles, Brussels, Belgium.ORCID http://orcid.org/0000-0001-5137-4051
Lang ZhouMaterials Research and Education Center, Auburn University, Auburn, AL, 36849, United States.
Eric TrépoDepartment of Gastroenterology, Hepatopancreatology and Digestive Oncology, C.U.B. Hôpital Erasme, Université libre de Bruxelles, Brussels, Belgium.
Pengyu ChenMaterials Research and Education Center, Auburn University, Auburn, AL, 36849, United States.
Esteban N GurzovSignal Transduction and Metabolism Laboratory, Laboratoire de Gastroentérologie Expérimental et Endotools, Université libre de Bruxelles, Brussels, Belgium. esteban.gurzov@ulb.be.ORCID http://orcid.org/0000-0003-4642-0273
Université Libre de Bruxelles · BEAuburn University · US

Funding

Purchase of a modularized confocal microscopeR35GM133795 · NIGMS · AUBURN UNIVERSITY AT AUBURN · PI Pengyu Chen · 2019 to 2026
$3.3M
NIGMS NIH HHS R35 GM133795
6 · The paper itself

Abstract

Obesity affects more than 650 million individuals worldwide and is a well-established risk factor for the development of hepatocellular carcinoma (HCC). Oxidative stress can be considered as a bona fide tumor promoter, contributing to the initiation and progression of liver cancer. Indeed, one of the key events involved in HCC progression is excessive levels of reactive oxygen species (ROS) resulting from the fatty acid influx and chronic inflammation. This review provides insights into the different intracellular sources of obesity-induced ROS and molecular mechanisms responsible for hepatic tumorigenesis. In addition, we highlight recent findings pointing to the role of the dysregulated activity of BCL-2 proteins and protein tyrosine phosphatases (PTPs) in the generation of hepatic oxidative stress and ROS-mediated dysfunctional signaling, respectively. Finally, we discuss the potential and challenges of novel nanotechnology strategies to prevent ROS formation in obesity-associated HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsObesityOxidative StressReactive Oxygen SpeciesSignal TransductionAnimalsHumansReactive Oxygen Species

Identifiers

PMID34290399
PMCPMC9277657
OpenAlexW3183942466

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.