ArticleOncogenesis2022
CCND3 is indispensable for the maintenance of B-cell acute lymphoblastic leukemia.
Article in Oncogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 20 citations in OpenAlex.
- Integrated Genomic Profiling of Pediatric Acute Lymphoblastic Leukemia: Genomic Landscape, Risk Stratification and Association of RAS Pathway Mutations with Early Treatment Response.International journal of molecular sciences · 2026Article
- Immunometabolic Dysregulation in B-Cell Acute Lymphoblastic Leukemia Revealed by Single-Cell RNA Sequencing: Perspectives on Subtypes and Potential Therapeutic Targets.International journal of molecular sciences · 2025Article
- Article
- Beyond FOXO1: AS1842856 inhibits GSK3 to enhance cytotoxic effects in B-ALL.Blood advances · 2025Article
- Genomic mutation profile and metabolic alterations in diffuse large B-cell lymphoma with abdominal bulky mass.Annals of hematology · 2025Article
- UDA-seq: universal droplet microfluidics-based combinatorial indexing for massive-scale multimodal single-cell sequencing.Nature methods · 2025Article
- Aloin protects against UVB-induced apoptosis by modulating integrated signaling pathways.Frontiers in pharmacology · 2025Article
- Analysis of CCND3 mutations in diffuse large B-cell lymphoma.Annals of hematology · 2024Article
- Complete miRNA-15/16 loss in mice promotes hematopoietic progenitor expansion and a myeloid-biased hyperproliferative state.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- IL-21 shapes germinal center polarization via light zone B cell selection and cyclin D3 upregulation.The Journal of experimental medicine · 2023Article
- D-Type Cyclins in Development and Disease.Genes · 2023Review
- The discrete roles of individual FOXO transcription factor family members in B-cell malignancies.Frontiers in immunology · 2023Review
- Super Enhancer Regulatory Gene FYB1 Promotes the Progression of T Cell Acute Lymphoblastic Leukemia by Activating IGLL1.Journal of immunology research · 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
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The D-type cyclins (CCND1, CCND2, and CCND3) in association with CDK4/6 are known drivers of cell cycle progression. We reported previously that inactivation of FOXO1 confers growth arrest and apoptosis in B-ALL, partially mediated by subsequent depletion of CCND3. Given that previously the canonical MYC target CCND2 has been considered to play the major role in B-ALL proliferation, further investigation of the role of FOXO1 in CCND3 transcription and the role of CCND3 in B-ALL is warranted. In this study, we demonstrated that CCND3 is essential for the proliferation and survival of B-ALL, independent of the mutational background. Respectively, its expression at mRNA level exceeds that of CCND1 and CCND2. Furthermore, we identified FOXO1 as a CCND3-activating transcription factor in B-ALL. By comparing the effects of CCND3 depletion and CDK4/6 inhibition by palbociclib on B-ALL cells harboring different driver mutations, we found that the anti-apoptotic effect of CCND3 is independent of the kinase activity of the CCND3-CDK4/6 complex. Moreover, we found that CCND3 contributes to CDK8 transcription, which in part might explain the anti-apoptotic effect of CCND3. Finally, we found that increased CCND3 expression is associated with the development of resistance to palbociclib. We conclude that CCND3 plays an essential role in the maintenance of B-ALL, regardless of the underlying driver mutation. Moreover, downregulation of CCND3 expression might be superior to inhibition of CDK4/6 kinase activity in terms of B-ALL treatment.
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.