ReviewTrends in cell biology2018
CDK4/6 Inhibition in Cancer: Beyond Cell Cycle Arrest.
Review in Trends in cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 284 papers, 1 of them a synthesis that pooled 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.
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
284 citing papers in PubMed, 1 synthesis or guideline pooled it, 493 citations in OpenAlex.
- A Systematic Review of the Mechanistic Effects of Ginsenosides on Enhancing Radiotherapy and Providing Radioprotection.Anti-cancer agents in medicinal chemistry · 2026Pooled it
- Neoadjuvant Abemaciclib plus Letrozole Versus Chemotherapy in Patients with HR+/HER2- Highly Proliferative Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Trial
- Triazole-based inhibitors for breast cancer: biological activity, SAR and synthetic strategies.Molecular diversity · 2026Review
- The logarithmic phase as a therapeutic direction: evaluating pharmacological strategies against cancer progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- CDK4/6 Inhibitors in Breast Cancer Therapy: Mechanisms, Resistance, and Emerging Opportunities.Targeted oncology · 2026Review
- Harnessing machine learning, docking and molecular dynamics for the virtual screening of compounds as CDK4/6 dual inhibitors.Molecular diversity · 2026Article
- Food-Derived Natural Compounds as Molecular Targets in Cancer Prevention.Pharmaceutics · 2026Review
- The microRNA Expression Signature of Lung Adenocarcinoma HarboringInternational journal of molecular sciences · 2026Article
- CDK4/6 Inhibitor-Induced Senescence in Cancer: Mechanisms and Therapeutic Implications.Cancers · 2026Review
- The evolving landscape of CDK inhibitor use in breast cancer therapy and beyond.Nature reviews. Drug discovery · 2026Review
- Targeting CDK4/6 potentiates the efficacy of anti-CD47 therapy via modulating the suppressive function of tumor-associated macrophages.Apoptosis : an international journal on programmed cell death · 2026Article
- A PML1-CCL5-PI3K/MAPK feedback loop governs survival of endocrine-resistant breast cancer cells.Cell death and differentiation · 2026Review
- HAUS1-mediated activation of CDK4 transcription enhances proliferation, invasion and migration in hepatocellular carcinoma.Cancer gene therapy · 2026Article
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- Article
- Translational Geroscience Strategies for Delaying Multimorbidity.ACS pharmacology & translational science · 2026Review
- Comparative real-world progression free survival of CDK4/6 inhibitors in HR+/HER2- breast cancer patients with bone metastases.The oncologist · 2026Article
- Review
- Stabilization of cyclin D3 protein by CDKN1A (p21Cell communication and signaling : CCS · 2026Article
- Pyrimidine-based compounds as promising anticancer agents targeting tumor cell senescence.Molecular therapy. Oncology · 2026Article
224 more citing papers are in PubMed but not listed here.
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 at 3 institutions in 1 country.
Funding
Abstract
Pharmacologic inhibitors of cyclin-dependent kinases 4 and 6 (CDK4/6) have recently entered the therapeutic armamentarium of clinical oncologists, and show promising activity in patients with breast and other cancers. Although their chief mechanism of action is inhibition of retinoblastoma (RB) protein phosphorylation and thus the induction of cell cycle arrest, CDK4/6 inhibitors alter cancer cell biology in other ways that can also be leveraged for therapeutic benefit. These include modulation of mitogenic kinase signaling, induction of a senescence-like phenotype, and enhancement of cancer cell immunogenicity. We describe here the less-appreciated effects of CDK4/6 inhibitors on cancer cells, and suggest ways by which they might be exploited to enhance the benefits of these agents for cancer patients.
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.