Evidence map›Paper›PMID 33048426›Full record

ReviewCancer science2021

TET2: A cornerstone in normal and malignant hematopoiesis.

Hiroyoshi Kunimoto, Hideaki Nakajima

Abstract readReview
In one paragraph

Review in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
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  9. Article
  10. The role of TET2 in solid tumors and its therapeutic potential: a comprehensive review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review
  11. CHIP: a clonal odyssey of the bone marrow niche.The Journal of clinical investigation · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. Lower Levels of TET2 Gene Expression, with a Higher Level of TET2 Promoter Methylation in Patients with AML; Evidence for the Role of Aberrant Methylation in AML Pathogenesis.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2024
    Article
  16. Article
  17. Article
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  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

2 authors.

Hiroyoshi KunimotoDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Hideaki NakajimaDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, Yokohama, Japan.ORCID https://orcid.org/0000-0002-8967-4954

Funding

American Society of HematologyAstellas Foundation for Research on Metabolic DisordersIchiro Kanehara Foundation for the Promotion of Medical Sciences and Medical CareJapanese Society of HematologyJapan Society for the Promotion of ScienceKanae Foundation for the Promotion of Medical ScienceNaito FoundationNippon Shinyaku Public Research GrantPrincess Takamatsu Cancer Research FundProject Mirai Cancer Research GrantsSuzuken Memorial FoundationTakeda Medical Research FoundationUehara Memorial FoundationYokohama Foundation for Advanced Medical Science
6 · The paper itself

Abstract

Regulation of genome-wide DNA methylation is fundamental for a variety of biological processes such as mammalian development, stem cell function, cellular proliferation/differentiation, and oncogenesis. Among the regulators of DNA methylation, ten-eleven translocation 2 (TET2) is one of the most frequently mutated genes in clonal hematopoiesis of indeterminate potential and in various hematological malignancies, underscoring a pivotal role for TET2 in blood homeostasis and hematopoietic transformation. TET2 oxidizes methylated cytosines to further modify cytosines, which behave as intermediates in active/passive DNA demethylation processes. TET2 itself associates with histone modifiers, thereby regulating histone modifications and expression of target genes. A number of studies have reported pleiotropic effects of TET2 on hematopoietic stem cell self-renewal, hematopoietic differentiation, genome instability and inflammatory response. Recent single-cell genomics studies have identified gene promoters as well as transcription factor binding sites as TET2-targeted genetic loci in which disruption of DNA methylation can fundamentally modify hematopoietic differentiation and promote leukemogenesis. TET2 mutations show convergent cooperativity with other disease alleles in signaling molecules, epigenetic modifiers, and spliceosome factors in hematopoietic transformation. Future studies focusing on the molecular basis of stem cell and immune regulation by TET2 loss will further deepen our understanding of the entire landscape of pathophysiology and molecular vulnerabilities of TET2-mutated hematological malignancies.

Indexed as

AnimalsCell DifferentiationCell Transformation, NeoplasticDNA-Binding ProteinsDNA MethylationHematopoiesisHumansMutationSignal TransductionDNA-Binding Proteinscytosine demethylationhematological malignancyhematopoietic stem cellTET2

Identifiers

PMID33048426
PMCPMC7780023

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.