Evidence map›Paper›PMID 24457556›Full record

ArticleOncotarget2014

AID downregulation is a novel function of the DNMT inhibitor 5-aza-deoxycytidine.

Chiou-Tsun Tsai, Pei-Ming Yang, Ting-Rong Chern, Shu-Hui Chuang, Jung-Hsin Lin, Lars Klemm, Markus Müschen, Ching-Chow Chen

Open access · hybridAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Synthesis and Biological Evaluation of PEGylated MWOMolecules (Basel, Switzerland) · 2022
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Prognostic impact of expression and methylation status of DENN/MADD domain-containing protein 2D in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2015
    Article
  9. 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

8 authors at 2 institutions in 2 countries.

Chiou-Tsun TsaiDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Pei-Ming Yang
Ting-Rong Chern
Shu-Hui Chuang
Jung-Hsin Lin
Lars Klemm
Markus Müschen
Ching-Chow Chen
National Taiwan University · TWUniversity of California, San Francisco · US

Funding

Targeted activation of autoimmune checkpoints in B cell malignanciesR01CA157644 · NCI · YALE UNIVERSITY · PI Markus Müschen · 2011 to 2026
$5.7M
PRE-B CELL RECEPTOR SIGNALING IN ACUTE LYMPHOBLASTIC LEUKEMIAR01CA137060 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MÜSCHEN, MARKUS · 2009 to 2016
$2.7M
AID-mediated genetic instability in BCR-ABL1-transformed B cell lineage leukemiaR01CA139032 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MÜSCHEN, MARKUS · 2009 to 2013
$1.6M
Negative feedback signaling in tyrosine kinase-driven leukemiaR01CA172558 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MÜSCHEN, MARKUS · 2013 to 2015
$972k
Targeting BCL6 in tyrosine kinase-driven leukemiaR01CA169458 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MÜSCHEN, MARKUS · 2013 to 2015
$972k
Cancer Research UK 18131NCI NIH HHS R01 CA137060NCI NIH HHS R01CA137060NCI NIH HHS R01 CA139032NCI NIH HHS R01CA139032NCI NIH HHS R01 CA157644NCI NIH HHS R01CA157644NCI NIH HHS R01 CA169458NCI NIH HHS R01 CA172558Wellcome Trust 101880
6 · The paper itself

Abstract

Activation-induced cytidine deaminase (AID) was originally identified as an inducer of somatic hypermutation (SHM) and class switch recombination (CSR) in immunoglobulin genes. However, AID can also cause mutations in host genes and contribute to cancer progression and drug resistance. In this study, molecular docking showed the interaction of free 5-aza-CdR and Zebularine (Zeb) with AID. However, only 5-aza-CdR-incorporated ssDNA bound to the active site of AID and inhibited AID expression through proteasomal degradation. 5-aza-CdR demonstrated cytotoxicity against AID-positive and -negative hematopoietic cancer cells. In contrast, Zeb exhibited a cytotoxic effect only in AID-negative cells due to its inability to inhibit AID expression. This differential effect might be due to the DNMT1 stabilization induced by AID, thus restricting the ability of Zeb to deplete DNMT1 and induce tumor suppressor genes (TSGs), such as p21, in AID-positive cells. Moreover, the in vivo anticancer effect of 5-aza-CdR but not Zeb in AID-positive hematopoietic cancer cells was demonstrated. The study not only displays the association of AID and DNMT1 and identifies a novel biological function of AID, but also provides novel information regarding the use of DNMT inhibitors to treat AID-positive hematopoietic cancers.

Indexed as

AICDA (Activation-Induced Cytidine Deaminase)AnimalsAzacitidineCytidine DeaminaseDecitabineDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDown-RegulationEnzyme InhibitorsHeterograftsHumansMiceMice, Inbred NODMice, SCIDMolecular Docking SimulationAICDA (Activation-Induced Cytidine Deaminase)AzacitidineCytidine DeaminaseDecitabineDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNMT1 protein, humanDnmt1 protein, mouseEnzyme Inhibitors

Identifiers

PMID24457556
PMCPMC3960202
OpenAlexW1948390230

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.