Evidence map›Paper›PMID 40581698›Full record

ReviewNPJ precision oncology2025

Targeting CDKs in cancer therapy: advances in PROTACs and molecular glues.

Hany E Marei, Khaled Bedair, Anwarul Hasan, Layla Al-Mansoori, Alice Gaiba, Andrea Morrione, Carlo Cenciarelli, Antonio Giordano

Abstract readReview
In one paragraph

Review in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  5. Thieno[3,2-International journal of molecular sciences · 2026
    Review
  6. Mechanisms of breast cancer dormancy in bone metastasis.Clinical & experimental metastasis · 2026
    Review
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  9. 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

8 authors.

Hany E MareiDepartment of Cytology and Histology, Faculty of Veterinary Medicine, Mansoura University, Mansoura, Egypt. hanymarei@mans.edu.eg.
Khaled BedairDepartment of Social Sciences, College of Arts and Sciences, Qatar University, Doha, P.O. Box 2713, Qatar.
Anwarul HasanDepartment of Mechanical and Industrial Engineering, College of Engineering, Qatar University, Doha, Qatar.
Layla Al-MansooriBiomedical Research Center, Qatar University, Doha, P.O. Box 2713, Qatar.
Alice GaibaInstitute of Translational Pharmacology-CNR, Rome, Italy.
Andrea MorrioneSbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Department of Biology, College of Science and Technology, Temple University, Philadelphia, PA, 19122, USA.
Carlo CenciarelliInstitute of Translational Pharmacology-CNR, Rome, Italy.
Antonio GiordanoSbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Department of Biology, College of Science and Technology, Temple University, Philadelphia, PA, 19122, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Essential transcription and cell cycle progression controllers are CDKs, whose dysregulation is a defining trait of many human cancers. CDKs have grown to be very crucial therapeutic targets in cancer. Although traditional CDK inhibitors have demonstrated therapeutic efficacy, they frequently encounter limitations due to resistance mechanisms and off-target effects. Recent developments in targeted protein degradation, like proteolysis-targeting chimeras (PROTACs) and molecular glues, offer creative ways to destroy CDK proteins specifically. These techniques reduce scaffolding activities and slow down kinase activity, hence more completely blocking oncogenic CDK signaling. This paper highlights the clinical and preclinical developments of PROTACs and molecular glues, investigates the current CDK-targeting therapeutic landscape, and studies the molecular basis of CDK dysregulation in cancer. We also address their benefits over conventional inhibitors, current issues, and possibilities for inclusion into precision oncology. These new approaches taken together represent a change in CDK-targeted cancer therapy.

Identifiers

PMID40581698
PMCPMC12206236

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.