Evidence map›Paper›PMID 33869040›Full record

ReviewFrontiers in oncology2021

The Dual-Role of Methylglyoxal in Tumor Progression - Novel Therapeutic Approaches.

Alessia Leone, Cecilia Nigro, Antonella Nicolò, Immacolata Prevenzano, Pietro Formisano, Francesco Beguinot, Claudia Miele

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.6field-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

37 citing papers in PubMed, 55 citations in OpenAlex.

  1. Methylglyoxal AttenuatesInternational journal of molecular sciences · 2026
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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

7 authors at 2 institutions in 1 country.

Alessia LeoneURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Naples, Italy.
Cecilia NigroURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Naples, Italy.
Antonella NicolòURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Naples, Italy.
Immacolata PrevenzanoURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Naples, Italy.
Pietro FormisanoURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Naples, Italy.
Francesco BeguinotURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Naples, Italy.
Claudia MieleURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Naples, Italy.
University of Naples Federico II · ITInstitute for Experimental Endocrinology and Oncology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the hallmarks of cancer cells is their metabolic reprogramming, which includes the preference for the use of anaerobic glycolysis to produce energy, even in presence of normal oxygen levels. This phenomenon, known as "Warburg effect", leads to the increased production of reactive intermediates. Among these Methylglyoxal (MGO), a reactive dicarbonyl known as the major precursor of the advanced glycated end products (AGEs), is attracting great attention. It has been well established that endogenous MGO levels are increased in several types of cancer, however the MGO contribution in tumor progression is still debated. Although an anti-cancer role was initially attributed to MGO due to its cytotoxicity, emerging evidence has highlighted its pro-tumorigenic role in several types of cancer. These apparently conflicting results are explained by the hormetic potential of MGO, in which lower doses of MGO are able to establish an adaptive response in cancer cells while higher doses cause cellular apoptosis. Therefore, the extent of MGO accumulation and the tumor context are crucial to establish MGO contribution to cancer progression. Several therapeutic approaches have been proposed and are currently under investigation to inhibit the pro-tumorigenic action of MGO. In this review, we provide an overview of the early and latest evidence regarding the role of MGO in cancer, in order to define its contribution in tumor progression, and the therapeutic strategies aimed to counteract the tumor growth.

Indexed as

cancer therapyglycolysisglyoxalasemethylglyoxaloncometabolitestumor progression

Identifiers

PMID33869040
PMCPMC8044862
OpenAlexW3137943098

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.