ArticleCancer cell international2017
Molecular mechanism of G
Article in Cancer cell international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- QTc prolongation across CDK4/6 inhibitors: a systematic review and meta-analysis of randomized controlled trials.JNCI cancer spectrum · 2024Pooled it
- Upregulation of MYBL2 ameliorates senescence of nucleus pulposus cells in degenerative intervertebral discs based on RNA-sequencing analysis.Journal of molecular histology · 2026Article
- The mechanisms and therapeutic advances of interactions between breast cancer and cardiovascular diseases.Frontiers in pharmacology · 2026Review
- Comprehensive review of non-invasive-treatment-related cardiovascular toxicity in breast cancer.iScience · 2025Review
- Identification and validation of microtubule depolymerizing agent, CYT997, as a potential drug candidate for hepatocellular carcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2023Article
- Irreversible cell cycle exit associated with senescence is mediated by constitutive MYC degradation.Cell reports · 2023Article
- CDK4/6 inhibitors: basics, pros, and major cons in breast cancer treatment with specific regard to cardiotoxicity - a narrative review.Therapeutic advances in medical oncology · 2023Review
- Cardiotoxicity from neoadjuvant targeted treatment for breast cancer prior to surgery.Frontiers in cardiovascular medicine · 2023Review
- Targeting CDK4 and 6 in Cancer Therapy: Emerging Preclinical Insights Related to Abemaciclib.The oncologist · 2022Review
- Senescence of Tumor Cells in Anticancer Therapy-Beneficial and Detrimental Effects.International journal of molecular sciences · 2022Review
- The Renaissance of Cyclin Dependent Kinase Inhibitors.Cancers · 2022Review
- Senolytics: Eliminating Senescent Cells and Alleviating Intervertebral Disc Degeneration.Frontiers in bioengineering and biotechnology · 2022Review
- Possibility of inducing tumor cell senescence during therapy.Oncology letters · 2021Review
- Review
- Identification of drug combinations on the basis of machine learning to maximize anti-aging effects.PloS one · 2021Article
- SIRT1 Activation Using CRISPR/dCas9 Promotes Regeneration of Human Corneal Endothelial Cells through Inhibiting Senescence.Antioxidants (Basel, Switzerland) · 2020Article
- MDM2 inhibition in combination with endocrine therapy and CDK4/6 inhibition for the treatment of ER-positive breast cancer.Breast cancer research : BCR · 2020Article
- Review
- Stilbene Compounds Inhibit Tumor Growth by the Induction of Cellular Senescence and the Inhibition of Telomerase Activity.International journal of molecular sciences · 2019Review
- LncRNA MAGI2-AS3 is involved in cervical squamous cell carcinoma development through CDK6 up-regulation.Infectious agents and cancer · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOverexpression of cyclin D1 dependent kinases 4 and 6 (CDK4/6) is a common feature of many human cancers including leukemia. LEE011 is a novel inhibitor of both CDK4 and 6. To date, the molecular function of LEE011 in leukemia remains unclear.
methodsLeukemia cell growth and apoptosis following LEE011 treatment was assessed through CCK-8 and annexin V/propidium iodide staining assays. Cell senescence was assessed by β-galactosidase staining and p16
resultsOur studies demonstrated that LEE011 inhibited proliferation of leukemia cells and could induce apoptosis. Hoechst 33,342 staining analysis showed DNA fragmentation and distortion of nuclear structures following LEE011 treatment. Cell cycle analysis showed LEE011 significantly induced cell cycle G
conclusionsWe demonstrate for the first time that LEE011 treatment results in inhibition of cell proliferation and induction of G
Indexed as
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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.