Evidence map›Paper›PMID 42609541›Full record

ReviewMedComm2026

Cyclins and Cyclin-Dependent Kinases: Structure, Biological Functions, and Innovative Targeting Strategies in Cancer.

Suya Zheng, Zhipeng Shen, Yuanfang Wu, Xingze Huang, Zhongyuan Zhang, Jiangyu Liu, Qichun Wei, Wenhao Chen, Ye Chen, Liang Xu

Abstract readReview
In one paragraph

Review in MedComm, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Suya ZhengDepartment of Radiation Oncology (Key Laboratory of Cancer Prevention and Intervention China National Ministry of Education) The Second Affiliated Hospital Zhejiang University School of Medicine Hangzhou China.
Zhipeng ShenDepartment of Neurosurgery Children's Hospital Zhejiang University School of Medicine, National Clinical Research Center For Children and Adolescents' Health and Diseases Hangzhou China.
Yuanfang WuDepartment of Neurosurgery Children's Hospital Zhejiang University School of Medicine, National Clinical Research Center For Children and Adolescents' Health and Diseases Hangzhou China.
Xingze HuangInstitute of Biochemistry College of Life Sciences Zhejiang University Hangzhou China.
Zhongyuan ZhangDepartment of Neurosurgery Children's Hospital Zhejiang University School of Medicine, National Clinical Research Center For Children and Adolescents' Health and Diseases Hangzhou China.
Jiangyu LiuDepartment of Neurosurgery Children's Hospital Zhejiang University School of Medicine, National Clinical Research Center For Children and Adolescents' Health and Diseases Hangzhou China.
Qichun WeiDepartment of Radiation Oncology (Key Laboratory of Cancer Prevention and Intervention China National Ministry of Education) The Second Affiliated Hospital Zhejiang University School of Medicine Hangzhou China.
Wenhao ChenPediatric Cancer Research Center National Clinical Research Center for Children and Adolescents' Health and Diseases Hangzhou China.
Ye ChenDepartment of Neurosurgery Children's Hospital Zhejiang University School of Medicine, National Clinical Research Center For Children and Adolescents' Health and Diseases Hangzhou China.
Liang XuDepartment of Radiation Oncology (Key Laboratory of Cancer Prevention and Intervention China National Ministry of Education) The Second Affiliated Hospital Zhejiang University School of Medicine Hangzhou China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclins and cyclin-dependent kinases (CDKs) are frequently dysregulated in human cancers and represent compelling therapeutic targets. Beyond their well-recognized roles in cell cycle control, CDK/cyclin complexes orchestrate diverse oncogenic processes, including transcription, genome maintenance, epigenetics, metabolism, and immune regulation. Deciphering the multifaceted biology of CDK/cyclin will provide valuable insights and rationales for the development of CDK/cyclin-targeting strategies and modalities. While the clinical success of CDK4/6 inhibitors has validated CDKs as druggable targets, further efforts are urgently needed to target other CDKs and cyclins. This review critically evaluates recent mechanistic advances in CDK/cyclin biology and their pathological dysregulation across malignancies. We analyze the paradigm shift from conventional enzymatic inhibition toward proximity-induced modulation. Specifically, we highlight emerging approaches including proteolysis-targeting chimeras, HSP90-mediated targeting chimeras, hydrophobic tagging, molecular glues, and autophagy-tethering compounds that achieve selective elimination of CDKs or their cyclin partners. In parallel, we summarize strategies designed to redistribute CDK complexes and rewire transcription without enzymatic ablation, referred to as chemical inducers of proximity and transcriptional/epigenetic modulators. By integrating fundamental CDK/cyclin biology with pharmacological innovation in targeted protein degradation and kinase reprogramming, this review provides a timely roadmap for the CDK/cyclin research field and expands the frontiers of CDK/cyclin-targeted cancer therapy.

Indexed as

CDKprotein degradertargeted protein degradationTCIPtranscriptional kinase

Identifiers

PMID42609541
PMCPMC13478576

What OpenQuestion holds

Textmetadata
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.