Evidence map›Paper›PMID 35535491›Full record

ArticleeLife2022

Inflammatory response in hematopoietic stem and progenitor cells triggered by activating SHP2 mutations evokes blood defects.

Maja Solman, Sasja Blokzijl-Franke, Florian Piques, Chuan Yan, Qiqi Yang, Marion Strullu, Sarah M Kamel, Pakize Ak, Jeroen Bakkers, David M Langenau and 2 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Complex Roles ofAnnual review of cancer biology · 2024
    Article
  10. Zebrafish Congenital Heart Disease Models: Opportunities and Challenges.International journal of molecular sciences · 2024
    Review
  11. Review
  12. Article
  13. Inflammation in Development and Aging: Insights from the Zebrafish Model.International journal of molecular sciences · 2024
    Review
  14. Review
  15. Zebrafish: a convenient tool for myelopoiesis research.Cell regeneration (London, England) · 2023
    Review
  16. Review
  17. 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

12 authors at 4 institutions in 3 countries.

Maja SolmanHubrecht Institute-KNAW and UMC Utrecht, Utrecht, Netherlands.
Sasja Blokzijl-Franke *Hubrecht Institute-KNAW and UMC Utrecht, Utrecht, Netherlands.
Florian Piques *INSERM UMR_S1131, Institut de Recherche Saint-Louis, Université de Paris, Paris, France.
Chuan YanMolecular Pathology Unit, Massachusetts General Hospital Research Institute, Charlestown, United States.
Qiqi YangMolecular Pathology Unit, Massachusetts General Hospital Research Institute, Charlestown, United States.
Marion StrulluINSERM UMR_S1131, Institut de Recherche Saint-Louis, Université de Paris, Paris, France.
Sarah M KamelHubrecht Institute-KNAW and UMC Utrecht, Utrecht, Netherlands.ORCID 0000-0003-4424-9732
Pakize AkHubrecht Institute-KNAW and UMC Utrecht, Utrecht, Netherlands.
Jeroen BakkersHubrecht Institute-KNAW and UMC Utrecht, Utrecht, Netherlands.ORCID 0000-0002-9418-0422
David M LangenauMolecular Pathology Unit, Massachusetts General Hospital Research Institute, Charlestown, United States.ORCID 0000-0001-6664-8318
Hélène CavéINSERM UMR_S1131, Institut de Recherche Saint-Louis, Université de Paris, Paris, France.ORCID 0000-0003-2840-1511
Jeroen den HertogHubrecht Institute-KNAW and UMC Utrecht, Utrecht, Netherlands.ORCID 0000-0002-8642-8088
University Medical Center Utrecht · NLInserm · FRMassachusetts General Hospital · USLeiden University · NL

Funding

Immune Compromises Zebrafish for Cell TransplantationR24OD016761 · OD · MASSACHUSETTS GENERAL HOSPITAL · PI LANGENAU, DAVID MICHAEL · 2013 to 2021
$5.2M
Oncogenic pathways and therapeutic targets in T cell acute lymphoblastic leukemiaR01CA211734 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LANGENAU, DAVID MICHAEL · 2017 to 2021
$1.9M
Development of computational models to diagnose mechanical lesions of the earF31DC016761 · NIDCD · HARVARD MEDICAL SCHOOL · PI MASUD, SALWA · 2017 to 2018
$69k
NCI NIH HHS R01 CA211734NIDCD NIH HHS F31 DC016761NIH HHS R24 OD016761
6 · The paper itself

Abstract

Gain-of-function mutations in the protein-tyrosine phosphatase SHP2 are the most frequently occurring mutations in sporadic juvenile myelomonocytic leukemia (JMML) and JMML-like myeloproliferative neoplasm (MPN) associated with Noonan syndrome (NS). Hematopoietic stem and progenitor cells (HSPCs) are the disease propagating cells of JMML. Here, we explored transcriptomes of HSPCs with SHP2 mutations derived from JMML patients and a novel NS zebrafish model. In addition to major NS traits, CRISPR/Cas9 knock-in Shp2

Indexed as

Leukemia, Myelomonocytic, JuvenileNoonan SyndromeAnimalsHematopoietic Stem CellsHumansMutationProtein Tyrosine Phosphatase, Non-Receptor Type 11ZebrafishProtein Tyrosine Phosphatase, Non-Receptor Type 11PTPN11 protein, humancancer biologydevelopmental biologyhematopoiesisleukemiaNoonan syndromeRASopathiesSHP2zebrafish

Identifiers

PMID35535491
PMCPMC9119675
OpenAlexW4229447867

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.