Evidence map›Paper›PMID 33504942›Full record

ArticleLeukemia2021

Musashi 2 influences chronic lymphocytic leukemia cell survival and growth making it a potential therapeutic target.

Florencia Palacios, Xiao-Jie Yan, Gerardo Ferrer, Shih-Shih Chen, Stefano Vergani, Xuejing Yang, Jeffrey Gardner, Jaqueline C Barrientos, Philip Rock, Richard Burack and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Ro 08-2750 increases radiation-induced cytotoxicity in DLBCL by dysregulating the DNA damage response.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Regulation of VEGFR2 and AKT signaling by Musashi-2 in lung cancer.bioRxiv : the preprint server for biology · 2023
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 1 country.

Florencia PalaciosKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Xiao-Jie YanKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.ORCID http://orcid.org/0000-0002-3717-5803
Gerardo FerrerKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.ORCID http://orcid.org/0000-0002-4084-6815
Shih-Shih ChenKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Stefano VerganiKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Xuejing YangMolecular Pharmacology Program, Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Jeffrey GardnerHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Jaqueline C BarrientosKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Philip RockDepartment of Pathology, University of Rochester, Rochester, NY, USA.
Richard BurackDepartment of Pathology, University of Rochester, Rochester, NY, USA.ORCID http://orcid.org/0000-0002-5584-584X
Jonathan E KolitzKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Steven L AllenKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.ORCID http://orcid.org/0000-0002-3482-3182
Michael G KharasMolecular Pharmacology Program, Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0002-1165-6991
Omar Abdel-WahabHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Kanti R RaiKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Nicholas ChiorazziKarches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA. NChizzi@Northwell.edu.ORCID http://orcid.org/0000-0003-1023-6650
Northwell Health · USMemorial Sloan Kettering Cancer Center · USUniversity of Rochester · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
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
NCI NIH HHS P30 CA008748NIDDK NIH HHS R01 DK101989
6 · The paper itself

Abstract

Progression of chronic lymphocytic leukemia (CLL) results from the expansion of a small fraction of proliferating leukemic B cells. When comparing the global gene expression of recently divided CLL cells with that of previously divided cells, we found higher levels of genes involved in regulating gene expression. One of these was the oncogene Musashi 2 (MSI2), an RNA-binding protein that induces or represses translation. While there is an established role for MSI2 in normal and malignant stem cells, much less is known about its expression and role in CLL. Here we report for the first time ex vivo and in vitro experiments that MSI2 protein levels are higher in dividing and recently divided leukemic cells and that downregulating MSI2 expression or blocking its function eliminates primary human and murine CLL and mature myeloid cells. Notably, mature T cells and hematopoietic stem and progenitor cells are not affected. We also confirm that higher MSI2 levels correlate with poor outcome markers, shorter time-to-first-treatment, and overall survival. Thus, our data highlight an important role for MSI2 in CLL-cell survival and proliferation and associate MSI2 with poor prognosis in CLL patients. Collectively, these findings pinpoint MSI2 as a potentially valuable therapeutic target in CLL.

Indexed as

Biomarkers, TumorAnimalsAntineoplastic AgentsApoptosisCaspase 3Cell Cycle CheckpointsCell Line, TumorCell SurvivalCyclin-Dependent Kinase Inhibitor p27Disease Models, AnimalGene ExpressionGene Expression ProfilingGene Expression Regulation, LeukemicGene Knockdown TechniquesHumansImmunophenotypingAntineoplastic AgentsBiomarkers, TumorCaspase 3CDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p27MSI2 protein, humanRNA-Binding ProteinsRNA, Small InterferingTumor Suppressor Protein p53

Identifiers

PMID33504942
PMCPMC8024198
OpenAlexW3122367718

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.