Evidence map›Paper›PMID 28623166›Full record

ReviewAdvances in biological regulation2017

Casein Kinase II (CK2), Glycogen Synthase Kinase-3 (GSK-3) and Ikaros mediated regulation of leukemia.

Chandrika Gowda, Mario Soliman, Malika Kapadia, Yali Ding, Kimberly Payne, Sinisa Dovat

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. IKAROS in Acute Leukemia: A Positive Influencer or a Mean Hater?International journal of molecular sciences · 2023
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
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

6 authors at 2 institutions in 1 country.

Chandrika GowdaDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. Electronic address: cgowda2@pennstatehealth.psu.edu.
Mario SolimanDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. Electronic address: msoliman@pennstatehealth.psu.edu.
Malika KapadiaDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. Electronic address: mkapadia@pennstatehealth.psu.edu.
Yali DingDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. Electronic address: yding@pennstatehealth.psu.edu.
Kimberly PayneDepartment of Anatomy, Loma Linda University, Loma Linda, CA, USA. Electronic address: kpayne@llu.edu.
Sinisa DovatDepartment of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. Electronic address: sdovat@hmc.psu.edu.
Pennsylvania State University · USLoma Linda 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

Signaling networks that regulate cellular proliferation often involve complex interactions between several signaling pathways. In this manuscript we review the crosstalk between the Casein Kinase II (CK2) and Glycogen Synthase Kinase-3 (GSK-3) pathways that plays a critical role in the regulation of cellular proliferation in leukemia. Both CK2 and GSK-3 are potential targets for anti-leukemia treatment. Previously published data suggest that CK2 and GSK-3 act synergistically to promote the phosphatidylinositol-3 kinase (PI3K) pathway via phosphorylation of PTEN. More recent data demonstrate another mechanism through which CK2 promotes the PI3K pathway - via transcriptional regulation of PI3K pathway genes by the newly-discovered CK2-Ikaros axis. Together, these data suggest that the CK2 and GSK-3 pathways regulate AKT/PI3K signaling in leukemia via two complementary mechanisms: a) direct phosphorylation of PTEN and b) transcriptional regulation of PI3K-promoting genes. Functional interactions between CK2, Ikaros and GSK3 define a novel signaling network that regulates proliferation of leukemia cells. This regulatory network involves both direct posttranslational modifications (by CK and GSK-3) and transcriptional regulation (via CK2-mediated phosphorylation of Ikaros). This information provides a basis for the development of targeted therapy for leukemia.

Indexed as

Gene Expression Regulation, LeukemicAntineoplastic AgentsCasein Kinase IIGlycogen Synthase Kinase 3HumansIkaros Transcription FactorLeukemiaPhosphatidylinositol 3-KinasesPhosphorylationPrognosisPTEN PhosphohydrolaseSignal TransductionSurvival AnalysisAntineoplastic AgentsCasein Kinase IIGlycogen Synthase Kinase 3Ikaros Transcription FactorIKZF1 protein, humanPhosphatidylinositol 3-KinasesPTEN PhosphohydrolasePTEN protein, humanCasein kinase II (CK2)CX4945GSK-3IkarosLeukemiaPhosphorylationTargeted therapy

Identifiers

PMID28623166
PMCPMC6022406
OpenAlexW2625257385

What OpenQuestion holds

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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.