ArticleCancer research2011
Cyclin D1 and cdk4 mediate development of neurologically destructive oligodendroglioma.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- Phase II Trial of Palbociclib in Recurrent Retinoblastoma-Positive Anaplastic Oligodendroglioma: A Study from the Spanish Group for Research in Neuro-Oncology (GEINO).Targeted oncology · 2020Trial
- Comprehensive Characterization of the Immune Microenvironment Based on Nested Resampling Machine Learning Framework Identifies TRAF3 Interacting Protein 3 as a Promising Regulator to Improve the Resistance to Immunotherapy in Glioma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- FLASH radiation reprograms lipid metabolism and macrophage immunity and sensitizes medulloblastoma to CAR-T cell therapy.Nature cancer · 2025Article
- Oligodendrogliomas, cyclin pathway after the introduction of the molecular 2021 World Health Organization (WHO) criteria.Brain communications · 2025Article
- Therapy-Induced Senescence Contributes to the Efficacy of Abemaciclib in Patients with Dedifferentiated Liposarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Small-molecule toosendanin reverses macrophage-mediated immunosuppression to overcome glioblastoma resistance to immunotherapy.Science translational medicine · 2023Article
- High tyrosine threonine kinase expression predicts a poor prognosis: a potential therapeutic target for endometrial carcinoma.Annals of translational medicine · 2022Article
- Cyclin D1 mediates pain behaviour in a rat model of breast cancer-induced bone pain by a mechanism involving regulation of the proliferation of spinal microglia.Bone & joint research · 2022Article
- Glioma: molecular signature and crossroads with tumor microenvironment.Cancer metastasis reviews · 2022Review
- Suppression of the USP10/CCND1 axis induces glioblastoma cell apoptosis.Acta pharmacologica Sinica · 2021Article
- Targeting cell-cycle machinery in cancer.Cancer cell · 2021Review
- Article
- Targeting PAK4 to reprogram the vascular microenvironment and improve CAR-T immunotherapy for glioblastoma.Nature cancer · 2021Article
- Review
- Wnt-mediated endothelial transformation into mesenchymal stem cell-like cells induces chemoresistance in glioblastoma.Science translational medicine · 2020Article
- The CDK6-c-Jun-Sp1-MMP-2 axis as a biomarker and therapeutic target for triple-negative breast cancer.American journal of cancer research · 2020Article
- PDGF-mediated mesenchymal transformation renders endothelial resistance to anti-VEGF treatment in glioblastoma.Nature communications · 2018Article
- Review
- Temporal DNA-PK activation drives genomic instability and therapy resistance in glioma stem cells.JCI insight · 2018Article
- Cell cycle regulation and anticancer drug discovery.Cancer biology & medicine · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Although the molecular changes that characterize gliomas have been studied, the pathogenesis of tumor development remains unclear. p21 contributes to gliomagenesis by stabilizing cyclin D1-cdk4 kinase complexes, suggesting that cyclin D1 and cdk4 may also be required for glial tumor development. In this study, we used a mouse model to attempt to confirm this hypothesis, finding that cyclin D1 and cdk4 played active roles in not only the tumor but also the tumor microenvironment. Loss of cdk4 blocked tumor development, but loss of cyclin D1 did not prevent gliomas from developing. Instead, loss of cyclin D1 impeded progression to higher stages of malignancy. Enforcing expression of cyclin D1 was insufficient to correct the progression defect observed in cyclin D1-deficient animals. In contrast, restoration of cdk4 in the cdk4-deficient animals restored cell proliferation and tumor formation, although at lower tumor grades. Notably, the failure of tumors in the cyclin D1- and cdk4-deficient animals to progress to higher grades was correlated with a failure to fully activate microglia in the tumor microenvironment. Moreover, when platelet-derived growth factor-transformed glial cells were engrafted orthotopically into the mice, the tumors that formed progressed to high grades in wild-type mice but not cyclin D1-deficient animals. Together, our findings establish that the cyclin D1-cdk4 axis is not only critical in glial tumor cells but also in stromal-derived cells in the surrounding tumor microenvironment that are vital to sustain tumor outgrowth.
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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.