Evidence map›Paper›PMID 12154409›Full record

ReviewOncogene2002

5-Azacytidine and 5-aza-2'-deoxycytidine as inhibitors of DNA methylation: mechanistic studies and their implications for cancer therapy.

Judith K Christman

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04722952 (an Single Center,Single Arm, Phase 3 Study to Evaluate Efficacy and Safety of PD-1 Inhibitor Combined With Azacytidine and HAG Regimen for Patients With Relapsed or Refractory Acute Myeloid Leukemia.), which is not on this map. Cited by 702 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
702citing papers in PubMed, 1 pooled it
9.5field-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.

NCT04722952 phase3unknown statusnot on this mapstarted 2021, after this paper: background citation

an Single Center,Single Arm, Phase 3 Study to Evaluate Efficacy and Safety of PD-1 Inhibitor Combined With Azacytidine and HAG Regimen for Patients With Relapsed or Refractory Acute Myeloid Leukemia.

TypeinterventionalSponsorThe First Affiliated Hospital of Soochow UniversityRan2021 to 2024Enrolled30ConditionsImmunotherapy, Refractory Leukemia, Relapsed Adult AML, Acute Myeloid LeukemiaArmsVisilizumab
3 · Its place in the literature

Who cites it

702 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,516 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. DNA Methylation Dynamics inBiomolecules · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Allele-specific methylation ofScience advances · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Nonsense-mediated mRNA decay: friend or foe in cancer biology?Cell communication and signaling : CCS · 2026
    Review
  17. Article
  18. Article
  19. Review
  20. Article

642 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.

Judith K ChristmanDepartment of Biochemistry and Molecular Biology and UNMC/Eppley Cancer Center, University of Nebraska Medical Center, 984525 University Medical Center, Omaha, Nebraska, NE 68198-4525, USA. jchristm@unmc.edu
University of Nebraska Medical Center · US

Funding

DeNovo DNA Methyltransferases as Anticancer Drug TargetsR21CA091315 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI CHRISTMAN, JUDITH K · 2001 to 2002
$283k
NCI NIH HHS R21 CA091315-01
6 · The paper itself

Abstract

5-Azacytidine was first synthesized almost 40 years ago. It was demonstrated to have a wide range of anti-metabolic activities when tested against cultured cancer cells and to be an effective chemotherapeutic agent for acute myelogenous leukemia. However, because of 5-azacytidine's general toxicity, other nucleoside analogs were favored as therapeutics. The finding that 5-azacytidine was incorporated into DNA and that, when present in DNA, it inhibited DNA methylation, led to widespread use of 5-azacytidine and 5-aza-2'-deoxycytidine (Decitabine) to demonstrate the correlation between loss of methylation in specific gene regions and activation of the associated genes. There is now a revived interest in the use of Decitabine as a therapeutic agent for cancers in which epigenetic silencing of critical regulatory genes has occurred. Here, the current status of our understanding of the mechanism(s) by which 5-azacytosine residues in DNA inhibit DNA methylation is reviewed with an emphasis on the interactions of these residues with bacterial and mammalian DNA (cytosine-C5) methyltransferases. The implications of these mechanistic studies for development of less toxic inhibitors of DNA methylation are discussed.

Indexed as

Antimetabolites, AntineoplasticAzacitidineDecitabineDNA MethylationDNA Modification MethylasesDNA, NeoplasmEnzyme InhibitorsHumansNeoplasmsAntimetabolites, AntineoplasticAzacitidineDecitabineDNA Modification MethylasesDNA, NeoplasmEnzyme Inhibitors

Identifiers

PMID12154409
OpenAlexW2086492419

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.