Evidence map›Paper›PMID 33467038›Full record

ReviewCancers2021

Diabetes and Pancreatic Cancer-A Dangerous Liaison Relying on Carbonyl Stress.

Stefano Menini, Carla Iacobini, Martina Vitale, Carlo Pesce, Giuseppe Pugliese

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
11.4field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. ZNF821 as a potential biomarker associated with immune infiltration in pancreatic adenocarcinoma.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026
    Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025
    Review
  12. Review
  13. Article
  14. Article
  15. Associations between Diabetes Mellitus and Selected Cancers.International journal of molecular sciences · 2024
    Review
  16. Review
  17. Article
  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

5 authors at 2 institutions in 1 country.

Stefano MeniniDepartment of Clinical and Molecular Medicine, "La Sapienza" University, 00189 Rome, Italy.ORCID 0000-0001-7328-2385
Carla IacobiniDepartment of Clinical and Molecular Medicine, "La Sapienza" University, 00189 Rome, Italy.
Martina VitaleDepartment of Clinical and Molecular Medicine, "La Sapienza" University, 00189 Rome, Italy.
Carlo PesceDepartment of Neurosciences, Rehabilitation, Ophtalmology, Genetic and Maternal Infantile Sciences (DINOGMI), Department of Excellence of MIUR, University of Genoa Medical School, 16132 Genoa, Italy.
Giuseppe PuglieseDepartment of Clinical and Molecular Medicine, "La Sapienza" University, 00189 Rome, Italy.ORCID 0000-0003-1574-0397
Sapienza University of Rome · ITUniversity of Genoa · IT

Funding

Associazione Italiana per la Ricerca sul Cancro IG - 17640Sapienza Università di Roma N/A
6 · The paper itself

Abstract

Both type 2 (T2DM) and type 1 (T1DM) diabetes mellitus confer an increased risk of pancreatic cancer in humans. The magnitude and temporal trajectory of the risk conferred by the two forms of diabetes are similar, suggesting a common mechanism. Carbonyl stress is a hallmark of hyperglycemia and dyslipidemia, which accompanies T2DM, prediabetes, and obesity. Accumulating evidence demonstrates that diabetes promotes pancreatic ductal adenocarcinoma (PDAC) in experimental models of T2DM, a finding recently confirmed in a T1DM model. The carbonyl stress markers advanced glycation end-products (AGEs), the levels of which are increased in diabetes, were shown to markedly accelerate tumor development in a mouse model of Kras-driven PDAC. Consistently, inhibition of AGE formation by trapping their carbonyl precursors (i.e., reactive carbonyl species, RCS) prevented the PDAC-promoting effect of diabetes. Considering the growing attention on carbonyl stress in the onset and progression of several cancers, including breast, lung and colorectal cancer, this review discusses the mechanisms by which glucose and lipid imbalances induce a status of carbonyl stress, the oncogenic pathways activated by AGEs and their precursors RCS, and the potential use of carbonyl-scavenging agents and AGE inhibitors in PDAC prevention and treatment, particularly in high-risk diabetic individuals.

Indexed as

carnosine derivativesepithelial growth factor receptorhyperglycemiamethylglyoxalobesitypancreatic ductal adenocarcinomareactive carbonyl speciesreceptor for advanced glycation end-productsyes-associated protein

Identifiers

PMID33467038
PMCPMC7830544
OpenAlexW3120685134

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.