Evidence map›Paper›PMID 27666503›Full record

ReviewAdvances in biological regulation2017

Regulation of cellular proliferation in acute lymphoblastic leukemia by Casein Kinase II (CK2) and Ikaros.

Chandrika Gowda, Chunhua Song, Malika Kapadia, Jonathon L Payne, Tommy Hu, Yali Ding, Sinisa Dovat

Abstract readReview
In one paragraph

Review in Advances in biological regulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.7field-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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Yeast Protein Asf1 Possesses Modulating Activity towards Protein Kinase CK2.International journal of molecular sciences · 2022
    Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Normal Hematopoiesis Is a Balancing Act of Self-Renewal and Regeneration.Cold Spring Harbor perspectives in medicine · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

7 authors at 1 institution in 1 country.

Chandrika GowdaDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA.
Chunhua SongDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA.
Malika KapadiaDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA.
Jonathon L PayneDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA; Loma Linda University, Loma Linda, CA, USA.
Tommy HuDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA.
Yali DingDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA.
Sinisa DovatDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA. Electronic address: sdovat@hmc.psu.edu.
Pennsylvania State University · US

Funding

Targeting CRLF2 and Ikaros Alterations to Reduce Health Disparities in Childhood LeukemiaR01CA209829 · NCI · LOMA LINDA UNIVERSITY · PI DOVAT, SINISA, DUERKSEN-HUGHES, PENELOPE J · 2016 to 2020
$2.0M
NCI NIH HHS R01 CA209829
6 · The paper itself

Abstract

The IKZF1 gene encodes the Ikaros protein, a zinc finger transcriptional factor that acts as a master regulator of hematopoiesis and a tumor suppressor in leukemia. Impaired activity of Ikaros is associated with the development of high-risk acute lymphoblastic leukemia (ALL) with a poor prognosis. The molecular mechanisms that regulate Ikaros' function as a tumor suppressor and regulator of cellular proliferation are not well understood. We demonstrated that Ikaros is a substrate for Casein Kinase II (CK2), an oncogenic kinase that is overexpressed in ALL. Phosphorylation of Ikaros by CK2 impairs Ikaros' DNA-binding ability, as well as Ikaros' ability to regulate gene expression and function as a tumor suppressor in leukemia. Targeting CK2 with specific inhibitors restores Ikaros' function as a transcriptional regulator and tumor suppressor resulting in a therapeutic, anti-leukemia effect in a preclinical model of ALL. Here, we review the genes and pathways that are regulated by Ikaros and the molecular mechanisms through which Ikaros and CK2 regulate cellular proliferation in leukemia.

Indexed as

AnimalsAntineoplastic AgentsCasein Kinase IICell CycleCell ProliferationChromatinChromatin Assembly and DisassemblyDNA NucleotidylexotransferaseGene Expression RegulationHumansIkaros Transcription FactorJumonji Domain-Containing Histone DemethylasesNaphthyridinesNuclear ProteinsPhenazinesPhosphorylationAntineoplastic AgentsCasein Kinase IIChromatinDNA NucleotidylexotransferaseIkaros Transcription FactorIKZF1 protein, humanJumonji Domain-Containing Histone DemethylasesKDM5B protein, humanNaphthyridinesNuclear ProteinsPhenazinesRepressor ProteinssilmitasertibCasein Kinase II (CK2)CX4945IkarosLeukemiaPhosphorylationPP1Protein phosphatase 1

Identifiers

PMID27666503
PMCPMC6053069
OpenAlexW2519174807

What OpenQuestion holds

Textmetadata
LicenceTDM
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.