ArticleBlood2022
Genome-wide CRISPR screen identifies CDK6 as a therapeutic target in adult T-cell leukemia/lymphoma.
Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed.
- PLK1 inhibition enhances Brentuximab vedotin efficacy in CD30-positive T-cell lymphoma via spindle assembly checkpoint activation.Leukemia · 2026Article
- Genome-wide CRISPR screens identify an RXR-MYLIP-LDLR axis regulating BH3 mimetic sensitivity in peripheral T-cell lymphomas.Oncogene · 2026Article
- Identification of a Conserved Temporal Molecular Response Signature to CDK4/6 Inhibition Through Multi-Omics Integration Across Cancer Cell Lines.International journal of molecular sciences · 2026Article
- Advances in RNA-based cancer therapeutics: pre-clinical and clinical implications.Molecular cancer · 2025Review
- JunB-HBZ nuclear translocation by TGF-β is a key driver in HTLV-1-mediated leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Article
- Super-Enhancer-Driven IRF2BP2 is Activated by Master Transcription Factors and Sustains T-ALL Cell Growth and Survival.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Multi-omics integration reveals potential stage-specific druggable targets in T-cell acute lymphoblastic leukemia.Genes & diseases · 2024Article
- Analysis of 3760 hematologic malignancies reveals rare transcriptomic aberrations of driver genes.Genome medicine · 2024Article
- Functional CRISPR screens in T cells reveal new opportunities for cancer immunotherapies.Molecular cancer · 2024Review
- Article
- Characterization of tumor microenvironment infiltration and therapeutic responses of cell cycle-related genes' signature in breast cancer.Journal of cancer research and clinical oncology · 2023Article
- CRISPR screening in hematology research: from bulk to single-cell level.Journal of hematology & oncology · 2023Review
- HTLV-1 bZIP Factor-Induced Reprogramming of Lactate Metabolism and Epigenetic Status Promote Leukemic Cell Expansion.Blood cancer discovery · 2023Article
- Investigation into the Role of Long-Non-Coding RNANon-coding RNA · 2023Article
- Targeting N-linked Glycosylation for the Therapy of Aggressive Lymphomas.Cancer discovery · 2023Article
- Treatment of Adult T-Cell Leukemia/Lymphoma: Established Paradigms and Emerging Directions.Current treatment options in oncology · 2023Review
- A gain-of-function mutation in microRNA 142 is sufficient to cause the development of T-cell leukemia in mice.Cancer science · 2023Article
- Article
Corrections and comments
- Commented on by
Authors and funding
27 authors.
Funding
Abstract
Adult T-cell leukemia/lymphoma (ATLL) is an aggressive T-cell malignancy with a poor prognosis with current therapy. Here we report genome-wide CRISPR-Cas9 screening of ATLL models, which identified CDK6, CCND2, BATF3, JUNB, STAT3, and IL10RB as genes that are essential for the proliferation and/or survival of ATLL cells. As a single agent, the CDK6 inhibitor palbociclib induced cell cycle arrest and apoptosis in ATLL models with wild-type TP53. ATLL models that had inactivated TP53 genetically were relatively resistant to palbociclib owing to compensatory CDK2 activity, and this resistance could be reversed by APR-246, a small molecule activator of mutant TP53. The CRISPR-Cas9 screen further highlighted the dependence of ATLL cells on mTORC1 signaling. Treatment of ATLL cells with palbociclib in combination with mTORC1 inhibitors was synergistically toxic irrespective of the TP53 status. This work defines CDK6 as a novel therapeutic target for ATLL and supports the clinical evaluation of palbociclib in combination with mTORC1 inhibitors in this recalcitrant malignancy.
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.