Evidence map›Paper›PMID 24918094›Full record

ReviewJournal of diabetes and metabolic disorders2014

Insight into the impact of diabetes mellitus on the increased risk of hepatocellular carcinoma: mini-review.

Maisa Mahmoud Ali Kamkar, Rasheed Ahmad, Osama Alsmadi, Kazem Behbehani

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of diabetes and metabolic disorders, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
1.1field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Narra J · 2025
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  13. Diabetes and cancer: A comprehensive review.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Diabetes Mellitus and Risk of Hepatocellular Carcinoma.BioMed research international · 2017
    Review
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  19. 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 1 institution in 1 country.

Maisa Mahmoud Ali KamkarDasman Genome Center, Biomedical Research Department, Dasman Diabetes Institute, Dasman, Kuwait ; Department of Biomedical Research, Genetics and Genomics Unit/Dasman Genome Center, Dasman Diabetes Institute, P.O.Box 1180, Dasman 15462, Kuwait.
Rasheed AhmadImmunology and Innovative Cell Therapy Unit, Biomedical Research Department, Dasman Diabetes Institute, Dasman, Kuwait.
Osama AlsmadiDasman Genome Center, Biomedical Research Department, Dasman Diabetes Institute, Dasman, Kuwait.
Kazem BehbehaniDasman Diabetes Institute, Dasman, Kuwait.
Dasman Diabetes Institute · KW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma is a multifactorial disease which is associated with a background of many causal risk factors. Diabetes mellitus however is one of the most common co-morbid illnesses found in hepatocellular carcinoma patients that are significantly associated with worsening of hepatocellular carcinoma development, patient prognosis and survival. Therefore, efforts have been focused on understanding the mechanisms underlying progression of hepatocellular carcinoma onset and development especially in diabetic patients. To our knowledge, there are no reports which address the impact of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) along with epigenetic regulations associated with increased risk of hepatocellular carcinoma confounded by diabetes mellitus. Therefore, this mini-review focuses on the possible intermediary mechanisms involved in worsening the onset and progression of hepatocellular carcinoma development confounded by diabetes mellitus. The first approach is to look at the role of inflammatory mediators (TNF-α and IL-6) in apoptosis and inflammation during hepatocarcinogenesis through monitoring levels of apoptotic regulators, B-cell lymphoma 2 protein which is encoded by BCL2 gene and apoptosis regulator BAX known as bcl-2-like protein 4 which is encoded by the BAX gene. The second approach is to focus on the possible epigenomic reprogramming that drives hepatocellular transformation since epigenetic modification of DNA is a key feature in the pathogenesis of hepatocarcinogenesis. Both approaches may suggest role of using Bcl2 and Bax as apoptotic and inflammatory markers for hepatocellular carcinoma detection as well as the importance impact of DNA methylation, hypomethylation or histone modifications as attractive candidates for early-detection biomarkers of hepatocellular carcinoma.

Indexed as

Apoptosis and inflammationDiabetes mellitusDNA methylation or histone modificationsEpigenomic reprogrammingHepatocarcinogenesisHepatocellular carcinoma

Identifiers

PMID24918094
PMCPMC4050993
OpenAlexW2169589100

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.