Evidence map›Paper›PMID 34588613›Full record

ArticleLeukemia2022

Stress hematopoiesis induces a proliferative advantage in TET2 deficiency.

Vinothkumar Rajan, Keon Collett, Rachel Woodside, Sergey V Prykhozhij, Michelle Moksa, Annäick Carles, Marcus Wong, Mira Liebman, Martin Hirst, Jason N Berman

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Zebrafish: a convenient tool for myelopoiesis research.Cell regeneration (London, England) · 2023
    Review
  3. Zebrafish models of inflammation in hematopoietic development and disease.Frontiers in cell and developmental biology · 2022
    Review
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

10 authors at 3 institutions in 1 country.

Vinothkumar RajanDepartment of Microbiology and Immunology, Dalhousie University, Halifax, NS, Canada.ORCID http://orcid.org/0000-0003-3323-181X
Keon Collett *Department of Pathology, Dalhousie University, Halifax, NS, Canada.
Rachel Woodside *Department of Biology, Dalhousie University, Halifax, NS, Canada.
Sergey V PrykhozhijChildren's Hospital of Eastern Ontario (CHEO) Research Institute and University of Ottawa, Ottawa, ON, Canada.
Michelle MoksaDepartment of Microbiology and Immunology and Michael Smith Laboratories, University of British Columbia, Vancouver, BC, Canada.
Annäick CarlesDepartment of Microbiology and Immunology and Michael Smith Laboratories, University of British Columbia, Vancouver, BC, Canada.
Marcus WongDepartment of Microbiology and Immunology and Michael Smith Laboratories, University of British Columbia, Vancouver, BC, Canada.
Mira LiebmanChildren's Hospital of Eastern Ontario (CHEO) Research Institute and University of Ottawa, Ottawa, ON, Canada.
Martin HirstDepartment of Microbiology and Immunology and Michael Smith Laboratories, University of British Columbia, Vancouver, BC, Canada.ORCID http://orcid.org/0000-0001-9136-9054
Jason N BermanDepartment of Microbiology and Immunology, Dalhousie University, Halifax, NS, Canada. JBerman@cheo.on.ca.ORCID http://orcid.org/0000-0002-4053-6067
Dalhousie University · CAUniversity of British Columbia · CAUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TET2 loss-of-function mutations are recurrent events in a wide range of hematological malignancies and a physiologic occurrence in blood cells of healthy older adults. It is currently unknown what determines if a person harboring a somatic TET2 mutation will progress to myelodysplastic syndrome or acute myeloid leukemia. Here we develop a zebrafish tet2 mutant through which we show that tet2 loss leads to restricted hematopoietic differentiation combined with a modest upregulation of p53, which is also characteristic of many inherited bone marrow failure syndromes. Uniquely in the context of emergency hematopoiesis by external stimuli, such as infection or cytokine stimulation, lack of tet2 leads hematopoietic stem cells to undergo excessive proliferation, resulting in an accumulation of immature cells, which are poised to become leukemogenic following additional genetic/epigenetic perturbations. This same phenomenon observed in zebrafish extends to human hematopoietic stem cells, identifying TET2 as a critical relay switch in the context of stress hematopoiesis.

Indexed as

HematopoiesisAnimalsCell ProliferationDioxygenasesDisease Models, AnimalGene DeletionGene SilencingHematologic NeoplasmsHematopoietic Stem CellsHumansLeukemia, Myeloid, AcuteLoss of Function MutationMyelodysplastic SyndromesZebrafishZebrafish ProteinsDioxygenasesTET2 protein, zebrafishZebrafish Proteins

Identifiers

PMID34588613
OpenAlexW3203854025

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.