Evidence map›Paper›PMID 26898884›Full record

ArticleNature communications2016

MSI2 is required for maintaining activated myelodysplastic syndrome stem cells.

James Taggart, Tzu-Chieh Ho, Elianna Amin, Haiming Xu, Trevor S Barlowe, Alexendar R Perez, Benjamin H Durham, Patrick Tivnan, Rachel Okabe, Arthur Chow and 14 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. The Role of RNA-Binding Proteins in Hematological Malignancies.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Review
  8. RNA Regulators in Leukemia and Lymphoma.Cold Spring Harbor perspectives in medicine · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Musashi RNA-Binding Proteins as Cancer Drivers and Novel Therapeutic Targets.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    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

24 authors at 5 institutions in 1 country.

James TaggartMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Tzu-Chieh HoMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Elianna AminMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Haiming XuMemorial Sloan Kettering Cancer Center, Cancer Biology Program, New York, New York 10065, USA.
Trevor S BarloweMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Alexendar R PerezComputational Biology Program Memorial Sloan Kettering Cancer Center, Memorial Sloan Kettering Institute, New York, New York 10065, USA.
Benjamin H DurhamMemorial Sloan Kettering Cancer Center, Human Oncology and Pathogenesis Program, New York, New York 10065, USA.
Patrick TivnanMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Rachel OkabeMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Arthur ChowMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Ly VuMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Sun Mi ParkMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Camila PrietoMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Christopher FamulareMemorial Sloan Kettering Cancer Center, Department of Medicine, Leukemia Service, New York, New York 10065, USA.
Minal PatelMemorial Sloan Kettering Cancer Center, Department of Medicine, Leukemia Service, New York, New York 10065, USA.
Christopher J LengnerDepartment of Animal Biology, Department of Cell and Developmental Biology and Institute for Regenerative Medicine, Schools of Veterinary Medicine and Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Amit VermaMontefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Gail RobozJoan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York, New York 10065, USA.
Monica GuzmanDivision of Hematology and Medical Oncology, Department of Medicine and Pharmacology, Weill Cornell Medical College, Cornell University, New York, New York 10065, USA.
Virginia M KlimekMemorial Sloan Kettering Cancer Center, Department of Medicine, Leukemia Service, New York, New York 10065, USA.
Omar Abdel-WahabMemorial Sloan Kettering Cancer Center, Human Oncology and Pathogenesis Program, New York, New York 10065, USA.
Christina LeslieComputational Biology Program Memorial Sloan Kettering Cancer Center, Memorial Sloan Kettering Institute, New York, New York 10065, USA.
Stephen D NimerSylvester Comprehensive Cancer Center, Department of Medicine, Miller School of Medicine, University of Miami, Miami, Florida 33136, USA.
Michael G KharasMolecular Pharmacology and Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.ORCID http://orcid.org/0000-0002-1165-6991
Memorial Sloan Kettering Cancer Center · USCornell University · USAlbert Einstein College of Medicine · USCalifornia Institute for Regenerative Medicine · USUniversity of Miami · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Uncovering the role for MSI2 network in hematopoietic stem cellsR01DK101989 · NIDDK · SLOAN-KETTERING INST CAN RESEARCH · PI Michael Kharas, Vijay Ganesh Sankaran · 2014 to 2026
$6.2M
Characterizing the MSI2 network in leukemiaR01CA193842 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI KHARAS, MICHAEL · 2015 to 2025
$4.1M
NCI NIH HHS 1R01CA193842-01NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA193842NIDDK NIH HHS R01 DK101989NIDDK NIH HHS R01DK101989-01A1NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

Myelodysplastic syndromes (MDS) are driven by complex genetic and epigenetic alterations. The MSI2 RNA-binding protein has been demonstrated to have a role in acute myeloid leukaemia and stem cell function, but its role in MDS is unknown. Here, we demonstrate that elevated MSI2 expression correlates with poor survival in MDS. Conditional deletion of Msi2 in a mouse model of MDS results in a rapid loss of MDS haematopoietic stem and progenitor cells (HSPCs) and reverses the clinical features of MDS. Inversely, inducible overexpression of MSI2 drives myeloid disease progression. The MDS HSPCs remain dependent on MSI2 expression after disease initiation. Furthermore, MSI2 expression expands and maintains a more activated (G1) MDS HSPC. Gene expression profiling of HSPCs from the MSI2 MDS mice identifies a signature that correlates with poor survival in MDS patients. Overall, we identify a role for MSI2 in MDS representing a therapeutic target in this disease.

Indexed as

AgedAnimalsCase-Control StudiesDisease Models, AnimalFemaleHematopoietic Stem CellsHumansLeukemia, Myeloid, AcuteMaleMice, Inbred C57BLMice, TransgenicMyelodysplastic SyndromesRNA-Binding ProteinsMsi2h protein, mouseMSI2 protein, humanRNA-Binding Proteins

Identifiers

PMID26898884
PMCPMC4764878
OpenAlexW2283016435

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.