Evidence map›Paper›PMID 29181334›Full record

ReviewFrontiers in oncology2017

Inflammatory Signaling Pathways in Preleukemic and Leukemic Stem Cells.

Shayda Hemmati, Tamanna Haque, Kira Gritsman

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Article
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  4. The Yin-Yang of Stress and Senescence: Integrated Stress Response and SASP Crosstalk in Stem Cell Fate, Regeneration, and Disease.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2026
    Article
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  6. Review
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  12. Leukemic Stem Cells and Hematological Malignancies.International journal of molecular sciences · 2024
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

10 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

3 authors at 2 institutions in 1 country.

Shayda HemmatiDepartment of Medicine, Albert Einstein College of Medicine, Bronx, NY, United States.
Tamanna HaqueDepartment of Medicine, Albert Einstein College of Medicine, Bronx, NY, United States.
Kira GritsmanDepartment of Medicine, Albert Einstein College of Medicine, Bronx, NY, United States.
Albert Einstein College of Medicine · USMontefiore Medical Center · US

Funding

PI3K Isoform Dependence in Adult Hematopoiesis and Myeloid LeukemiaR01CA196973 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI GRITSMAN, KIRA · 2016 to 2020
$2.0M
6 · The paper itself

Abstract

Hematopoietic stem cells (HSCs) are a rare subset of bone marrow cells that usually exist in a quiescent state, only entering the cell cycle to replenish the blood compartment, thereby limiting the potential for errors in replication. Inflammatory signals that are released in response to environmental stressors, such as infection, trigger active cycling of HSCs. These inflammatory signals can also directly induce HSCs to release cytokines into the bone marrow environment, promoting myeloid differentiation. After stress myelopoiesis is triggered, HSCs require intracellular signaling programs to deactivate this response and return to steady state. Prolonged or excessive exposure to inflammatory cytokines, such as in prolonged infection or in chronic rheumatologic conditions, can lead to continued HSC cycling and eventual HSC loss. This promotes bone marrow failure, and can precipitate preleukemic states or leukemia through the acquisition of genetic and epigenetic changes in HSCs. This can occur through the initiation of clonal hematopoiesis, followed by the emergence preleukemic stem cells (pre-LSCs). In this review, we describe the roles of multiple inflammatory signaling pathways in the generation of pre-LSCs and in progression to myelodysplastic syndrome (MDS), myeloproliferative neoplasms, and acute myeloid leukemia (AML). In AML, activation of some inflammatory signaling pathways can promote the cycling and differentiation of LSCs, and this can be exploited therapeutically. We also discuss the therapeutic potential of modulating inflammatory signaling for the treatment of myeloid malignancies.

Indexed as

inflammatoryinterferoninterleukinleukemic stem cellNF-κBpreleukemictoll-like receptortumor necrosis factor

Identifiers

PMID29181334
PMCPMC5693908
OpenAlexW2767595816

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.