Evidence map›Paper›PMID 32504382›Full record

ReviewCellular oncology (Dordrecht, Netherlands)2020

DNMT1 as a therapeutic target in pancreatic cancer: mechanisms and clinical implications.

Kah Keng Wong

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular oncology (Dordrecht, Netherlands), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.1field-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

67 citing papers in PubMed, 150 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. [Molecular characteristics for poor prognosis related renal cell carcinoma with lymph metastases].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. DNMT1-Induced Downregulation of CBX7 Inhibits ERK Phosphorylation and Promotes Pancreatic Ductal Adenocarcinoma Progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  20. Review

7 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Kah Keng WongDepartment of Immunology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia. kahkeng@usm.my.ORCID https://orcid.org/0000-0001-7359-6202
Universiti Sains Malaysia · MY

Funding

Universiti Sains Malaysia 304.PPSP.6316332
6 · The paper itself

Abstract

backgroundPancreatic cancer or pancreatic ductal adenocarcinoma (PDAC) is one of the most devastating cancer types with a 5-year survival rate of only 9%. PDAC is one of the leading causes of cancer-related deaths in both genders. Epigenetic alterations may lead to the suppression of tumor suppressor genes, and DNA methylation is a predominant epigenetic modification. DNA methyltransferase 1 (DNMT1) is required for maintaining patterns of DNA methylation during cellular replication. Accumulating evidence has implicated the oncogenic roles of DNMT1 in various malignancies including PDACs.

conclusionsHerein, the expression profiles, oncogenic roles, regulators and inhibitors of DNMT1 in PDACs are presented and discussed. DNMT1 is overexpressed in PDAC cases compared with non-cancerous pancreatic ducts, and its expression gradually increases from pre-neoplastic lesions to PDACs. DNMT1 plays oncogenic roles in suppressing PDAC cell differentiation and in promoting their proliferation, migration and invasion, as well as in induction of the self-renewal capacity of PDAC cancer stem cells. These effects are achieved via promoter hypermethylation of tumor suppressor genes, including cyclin-dependent kinase inhibitors (e.g., p14, p15, p16, p21 and p27), suppressors of epithelial-mesenchymal transition (e.g., E-cadherin) and tumor suppressor miRNAs (e.g., miR-148a, miR-152 and miR-17-92 cluster). Pre-clinical investigations have shown the potency of novel non-nucleoside DNMT1 inhibitors against PDAC cells. Finally, phase I/II clinical trials of DNMT1 inhibitors (azacitidine, decitabine and guadecitabine) in PDAC patients are currently underway, where these inhibitors have the potential to sensitize PDACs to chemotherapy and immune checkpoint blockade therapy.

Indexed as

Molecular Targeted TherapyAnimalsCarcinogenesisCell Self RenewalDNA (Cytosine-5-)-Methyltransferase 1Epithelial-Mesenchymal TransitionHumansPancreatic NeoplasmsDNA (Cytosine-5-)-Methyltransferase 1Cancer stem cellsCyclin-dependent kinase inhibitorsDNMT1DNMT1 inhibitorsEpithelial-mesenchymal transitionPancreatic adenocarcinoma

Identifiers

PMID32504382
PMCPMC12990712
OpenAlexW3033369742

What OpenQuestion holds

Textmetadata
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.