ReviewExpert opinion on therapeutic targets2025
Targeting CDK2 and other novel cell cycle targets for breast cancer therapy.
Review in Expert opinion on therapeutic targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed.
- Metabolomics-Driven Bioactivity-Guided Isolation and Molecular Docking Reveal Antibreast Cancer Metabolome Heterogeneity in Polygonum spp.Biomedical chromatography : BMC · 2026Article
- Exploring shared biomarkers and their mechanisms in thyroid cancer and systemic lupus erythematosus via bioinformatics analysis.Discover oncology · 2026Article
- Frontiers in Cell-Cycle-Targeting Therapies: Addressing the Heterogeneity of the Cancer Cell Cycle.Cancers · 2026Article
- Efficacy and Mechanisms of CDK4/6 Inhibitors in Breast Cancer: Advancing Targeted Therapeutic Strategies.Oncology research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
introductionThe dysregulation of cyclin-dependent kinases (CDKs) is a key driver of cancer progression, making them attractive therapeutic targets. In CDK4/6 inhibitor (CDK4/6i)-resistant breast cancer, targeting CDK2 offers a promising approach. CDK2 is frequently hyperactivated due to cyclin E1 overexpression or retinoblastoma protein loss, acting as a mechanism that sustains proliferation despite CDK4/6 inhibition. CDK2 inhibitors (CDK2i) show strong anti-tumor activity, particularly in combination with CDK4/6i or immune checkpoint inhibitors. AREAS COVERED: This review explores the biological roles of CDK2 and its regulatory mechanisms. The review highlights the latest advancements in CDK2i, their mechanisms of action, and their potential in combination strategies with CDK4/6i, chemotherapy, and immunotherapies. Additionally, it examines other emerging targets, such as CDK7 and CDK5, which contribute to transcriptional regulation and immune evasion, respectively. EXPERT OPINION: Future research should focus on biomarker-driven patient selection, optimizing CDK2i combinations, and expanding CDK7 inhibitor applications. Integrating multi-omics profiling can refine patient stratification, while combination strategies with chemotherapy, DNA damaging agents, and immunotherapies may enhance efficacy. CDK7 inhibitors could also complement CDK2 targeting by modulating resistance mechanisms. Personalized, adaptive treatment approaches will be key to maximizing the clinical impact of CDK2 and CDK7 inhibitors in breast cancer therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.