ArticleNature communications2025
Discrete vulnerability to pharmacological CDK2 inhibition is governed by heterogeneity of the cancer cell cycle.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed.
- Next-generation CDK inhibitors in HR+/HER2- breast cancer.The Journal of clinical investigation · 2026Review
- Targeting CDK2 ameliorates allergic asthma through suppression of epithelial chemokine production and T cell inflammatory responses.Science China. Life sciences · 2026Article
- Transcriptional Heterogeneity in Dedifferentiated Liposarcoma Reveals Distinct Cell-Cycle Subtypes.Annals of surgical oncology · 2026Article
- Adaptive mechanisms and emerging cancer therapeutics for CDK2 inhibitors.Nature chemical biology · 2026Review
- Targeting CDK2 and AURKA with Cerevisterol fromInternational journal of molecular sciences · 2026Article
- Endometriosis: Epidemiology, Risk Factors, Molecular Mechanisms, Diagnosis, and Management.MedComm · 2026Review
- The evolving landscape of CDK inhibitor use in breast cancer therapy and beyond.Nature reviews. Drug discovery · 2026Review
- Cyclin E modulates vulnerability to CDC7 kinase inhibition.Oncogenesis · 2026Article
- Cell-cycle targeted cancer therapy: clinical advances, biological gaps, and the emergence of selective CDK4 inhibitors.Journal of hematology & oncology · 2026Review
- Emerging Strategies to Inhibit the G1/S Transition for Cancer Therapy.Cancer research · 2026Review
- Frontiers in Cell-Cycle-Targeting Therapies: Addressing the Heterogeneity of the Cancer Cell Cycle.Cancers · 2026Article
- Design, Synthesis, Bioactivity, and Docking Studies of Isatin-Hydrazone Derivatives as Potential CDK-2 Inhibitors.Anti-cancer agents in medicinal chemistry · 2026Article
- Article
- Histone lysine demethylases in breast cancer: molecular mechanisms, biological functions, and therapeutic intervention.Molecular cancer · 2025Review
- CDK2 inhibition enhances CDK4/6 inhibitor antitumor activity in comprehensive breast cancer PDX model screen.NPJ breast cancer · 2025Article
- Design, synthesis, and evaluation of novel pinane-based thiazolidione derivatives with anti-glioblastoma activity.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Intrinsic RB activation induces tumoral and stromal anti-tumor responses that limit triple-negative breast cancer.NPJ breast cancer · 2025Article
- Impact of single-cell cell cycle regulation of intercellular communication on the prognosis of hepatocellular carcinoma in the tumor microenvironment.Clinical and experimental medicine · 2025Article
- p16 expression confers sensitivity to CDK2 inhibitors in cyclin E1-driven ovarian cancers.Science signaling · 2025Article
- RB loss sensitizes triple-negative breast cancer to apoptosis induced by cellular stress.Cell death discovery · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Cyclin dependent kinase 2 (CDK2) regulates cell cycle and is an emerging target for cancer therapy. There are relatively small numbers of tumor models that exhibit strong dependence on CDK2 and undergo G1 cell cycle arrest following CDK2 inhibition. The expression of P16INK4A and cyclin E1 determines this sensitivity to CDK2 inhibition. The co-expression of these genes occurs in breast cancer patients highlighting their clinical significance as predictive biomarkers for CDK2-targeted therapies. In cancer models that are genetically independent of CDK2, pharmacological inhibitors suppress cell proliferation by inducing 4N cell cycle arrest and increasing the expressions of phospho-CDK1 (Y15) and cyclin B1. CRISPR screens identify CDK2 loss as a mediator of resistance to a CDK2 inhibitor, INX-315. Furthermore, CDK2 deletion reverses the G2/M block induced by CDK2 inhibitors and restores cell proliferation. Complementary drug screens define multiple means to cooperate with CDK2 inhibition beyond G1/S. These include the depletion of mitotic regulators as well as CDK4/6 inhibitors cooperate with CDK2 inhibition in multiple phases of the cell cycle. Overall, this study underscores two fundamentally distinct features of response to CDK2 inhibitors that are conditioned by tumor context and could serve as the basis for differential therapeutic strategies in a wide range of cancers.
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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.