Evidence map›Paper›PMID 28951560›Full record

ReviewLeukemia2018

Therapeutic targeting of CK2 in acute and chronic leukemias.

F Buontempo, J A McCubrey, E Orsini, M Ruzzene, A Cappellini, A Lonetti, C Evangelisti, F Chiarini, C Evangelisti, J T Barata and 1 more

Open access · hybridAbstract readReview
In one paragraph

Review in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
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  8. Review
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  11. Characterization ofInternational journal of molecular sciences · 2025
    Article
  12. Haematologica · 2024
    Article
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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

11 authors at 7 institutions in 3 countries.

F BuontempoDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
J A McCubreyDepartment of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
E OrsiniDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
M RuzzeneDepartment of Biomedical Sciences, University of Padova, Padova, Italy.
A CappelliniDepartment of Human, Social and Health Sciences, University of Cassino, Cassino, Italy.
A LonettiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
C EvangelistiInstitute of Molecular Genetics, National Research Council, Bologna, Italy.
F ChiariniInstitute of Molecular Genetics, National Research Council, Bologna, Italy.
C EvangelistiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
J T BarataInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal.
A M MartelliDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
University of Bologna · ITNational Research Council · ITEast Carolina University · USOrthopedic Institute · USUniversità degli studi di Cassino e del Lazio Meridionale · ITUniversity of Lisbon · PTUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CK2 is a ubiquitously expressed, constitutively active Ser/Thr protein kinase, which is considered the most pleiotropic protein kinase in the human kinome. Such a pleiotropy explains the involvement of CK2 in many cellular events. However, its predominant roles are stimulation of cell growth and prevention of apoptosis. High levels of CK2 messenger RNA and protein are associated with CK2 pathological functions in human cancers. Over the last decade, basic and translational studies have provided evidence of CK2 as a pivotal molecule driving the growth of different blood malignancies. CK2 overexpression has been demonstrated in nearly all the types of hematological cancers, including acute and chronic leukemias, where CK2 is a key regulator of signaling networks critical for cell proliferation, survival and drug resistance. The findings that emerged from these studies suggest that CK2 could be a valuable therapeutic target in leukemias and supported the initiation of clinical trials using CK2 antagonists. In this review, we summarize the recent advances on the understanding of the signaling pathways involved in CK2 inhibition-mediated effects with a particular emphasis on the combinatorial use of CK2 inhibitors as novel therapeutic strategies for treating both acute and chronic leukemia patients.

Indexed as

AnimalsApoptosisCasein Kinase IICell ProliferationHumansLeukemiaProtein Kinase InhibitorsSignal TransductionCasein Kinase IIProtein Kinase Inhibitors

Identifiers

PMID28951560
PMCPMC5770594
OpenAlexW2760129444

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.