ArticleOpen biology2021
Palbociclib-mediated cell cycle arrest can occur in the absence of the CDK inhibitors p21 and p27.
Article in Open biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 47 citations in OpenAlex.
- Targeted Folate-Chitosan Nanoformulations of Quercetin andPharmaceuticals (Basel, Switzerland) · 2026Article
- FOXO3 regulated granulosa cells apoptosis and AKT1 phosphorylation in Muscovy duck follicles (Cairina moschata).Poultry science · 2026Article
- Pseudo-senescence induced by palbociclib does not sensitise pleural mesothelioma cells to combinations with senolytics.Cell death & disease · 2026Article
- p27Kip1 regulates γ-globin production.Blood · 2026Article
- Article
- Dynamic modelling of cell cycle arrest through integrated single-cell and mathematical modelling approaches.PLoS computational biology · 2025Article
- Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations.Cell proliferation · 2025Article
- WIP1 mutations suppress DNA damage triggered bypass of the mitotic timer.The EMBO journal · 2025Article
- Reversible and effective cell cycle synchronization method for studying stage-specific processes.Life science alliance · 2025Article
- Metabolic landscape of disseminated cancer dormancy.Trends in cancer · 2025Review
- Mitochondrial priming and response to BH3 mimetics in "one-two punch" senogenic-senolytic strategies.Cell death discovery · 2025Article
- New Evidence forPharmaceuticals (Basel, Switzerland) · 2025Article
- Resistance mechanisms and therapeutic strategies of CDK4 and CDK6 kinase targeting in cancer.Nature cancer · 2025Review
- SuperFeat: Quantitative Feature Learning from Single-cell RNA-seq Data Facilitates Drug Repurposing.Genomics, proteomics & bioinformatics · 2024Article
- Reversible and effective cell cycle synchronization method for studying stage-specific investigations.bioRxiv : the preprint server for biology · 2024Article
- A Lipid-Sensitive Spider Peptide Toxin Exhibits Selective Anti-Leukemia Efficacy through Multimodal Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Genome-wide in vivo CRISPR screen identifies TGFβ3 as actionable biomarker of palbociclib resistance in triple negative breast cancer.Molecular cancer · 2024Article
- Review
- Trametinib boosts palbociclib's efficacy in breast cancer via autophagy inhibition.Oncology research · 2024Article
- Antiproliferative Activity of Gibbosic Acid H through Induction of GJournal of cancer prevention · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The use of CDK4/6 inhibitors in the treatment of a wide range of cancers is an area of ongoing investigation. Despite their increasing clinical use, there is limited understanding of the determinants of sensitivity and resistance to these drugs. Recent data have cast doubt on how CDK4/6 inhibitors arrest proliferation, provoking renewed interest in the role(s) of CDK4/6 in driving cell proliferation. As the use of CDK4/6 inhibitors in cancer therapies becomes more prominent, an understanding of their effect on the cell cycle becomes more urgent. Here, we investigate the mechanism of action of CDK4/6 inhibitors in promoting cell cycle arrest. Two main models explain how CDK4/6 inhibitors cause G1 cell cycle arrest, which differ in their dependence on the CDK inhibitor proteins p21 and p27. We have used live and fixed single-cell quantitative imaging, with inducible degradation systems, to address the roles of p21 and p27 in the mechanism of action of CDK4/6 inhibitors. We find that CDK4/6 inhibitors can initiate and maintain a cell cycle arrest without p21 or p27. This work clarifies our current understanding of the mechanism of action of CDK4/6 inhibitors and has implications for cancer treatment and patient stratification.
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.