Evidence map›Paper›PMID 34751409›Full record

ArticleOncology reports2022

KLF4, DAPK1 and SPG20 promoter methylation is not affected by DNMT1 silencing and hypomethylating drugs in lymphoma cells.

Raffaele Frazzi, Vincenza Ylenia Cusenza, Mariaelena Pistoni, Laura Canovi, Luciano Cascione, Francesco Bertoni, Francesco Merli

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. KLF4 is an epigenetically modulated, context-dependent tumor suppressor.Frontiers in cell and developmental biology · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Do or Die: HPV E5, E6 and E7 in Cell Death Evasion.Pathogens (Basel, Switzerland) · 2022
    Review
  10. 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

7 authors at 2 institutions in 2 countries.

Raffaele FrazziLaboratory of Translational Research, Azienda Unità Sanitaria Locale ‑ IRCCS di Reggio Emilia, I‑42123 Reggio Emilia, Emilia‑Romagna, Italy.
Vincenza Ylenia CusenzaLaboratory of Translational Research, Azienda Unità Sanitaria Locale ‑ IRCCS di Reggio Emilia, I‑42123 Reggio Emilia, Emilia‑Romagna, Italy.
Mariaelena PistoniLaboratory of Translational Research, Azienda Unità Sanitaria Locale ‑ IRCCS di Reggio Emilia, I‑42123 Reggio Emilia, Emilia‑Romagna, Italy.
Laura CanoviImmunohematology and Transfusional Medicine Division, Azienda Unità Sanitaria Locale ‑ IRCCS di Reggio Emilia, I‑42123 Reggio Emilia, Emilia‑Romagna, Italy.
Luciano CascioneInstitute of Oncology Research, Faculty of Biomedical Sciences, University of Italian Switzerland, 6501 Bellinzona, Ticino, Switzerland.
Francesco BertoniInstitute of Oncology Research, Faculty of Biomedical Sciences, University of Italian Switzerland, 6501 Bellinzona, Ticino, Switzerland.
Francesco MerliHematology Division, Azienda Unità Sanitaria Locale ‑ IRCCS di Reggio Emilia, I‑42123 Reggio Emilia, Emilia‑Romagna, Italy.
Azienda Sanitaria Unità Locale di Reggio Emilia · ITInstitute of Oncology Research · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Promoter methylation represents one of the major epigenetic mechanisms responsible for the regulation of gene expression. Hypomethylating drugs are currently approved for the treatment of myelodysplastic syndromes and acute myeloid leukemia, and some studies have recently been carried out on diffuse large B cell lymphoma (DLBCL). DLBCL is a type of Non‑Hodgkin lymphoma. The aim of the present study was to assess the role of DNA methyltransferase (DNMT)1 in mediating the epigenetic regulation of some key targets previously emerged as hypermethylated in Non‑Hodgkin lymphoma. Reverse transcription‑quantitative PCR, genome‑wide arrays and methylation‑specific PCR were used to determine the level of methylation of specific targets. Gene silencing, gene expression and immunoblotting were used to investigate the role of DNMT1 and DNMT3a in lymphoma cells. The present study showed that lymphoma cell lines displayed a completely different methylation profile on selected targets compared with primary B lymphocytes and peripheral blood mononuclear cells. 5'‑aza‑cytidine (5AZA) and 5'‑aza‑2‑deoxycitidine (decitabine) exerted their activity through, at least in part, mechanisms independent of DNMT1 downregulation. Despite a global hypomethylating effect of 5AZA and decitabine, DNMT1 was not found to be necessary to maintain the hypermethylation of Krüppel‑like factor 4 (KLF4), death associated protein 1 (DAPK1) and spastic paraplegia 20 (

Indexed as

Antimetabolites, AntineoplasticCell Cycle ProteinsCell Line, TumorDeath-Associated Protein KinasesDecitabineDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticGene SilencingHumansKruppel-Like Factor 4Lymphoma, Non-HodgkinAntimetabolites, AntineoplasticCell Cycle ProteinsDAPK1 protein, humanDeath-Associated Protein KinasesDecitabineDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanKLF4 protein, humanKruppel-Like Factor 4SPART protein, humandiffuse large B cell lymphomaDNA methyltransferase 1open‑sea regionspromoter methylationspastic paraplegia 20

Identifiers

PMID34751409
PMCPMC8600396
OpenAlexW3212549422

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.