Trial reportBlood2021
PRC2 loss of function confers a targetable vulnerability to BET proteins in T-ALL.
Trial report in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Epigenetics and One-Carbon Metabolism in Cancer: Mechanisms and Therapeutic Implications.Advances in experimental medicine and biology · 2026Review
- T-cell acute lymphoblastic leukaemia: subtype prevalence, clinical outcome, and emerging targeted treatments.Leukemia · 2025Review
- Oncogenomic profiling in infant-toddler T-ALL identifies NKX2 family genes as drivers linked to favorable outcomes.HemaSphere · 2025Article
- ATP citrate lyase is an essential player in the metabolic rewiring induced by PTEN loss during T-ALL development.Blood advances · 2025Article
- A metabolic synthetic lethality of phosphoinositide 3-kinase-driven cancer.Nature communications · 2025Article
- JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025Review
- Pharmacological Advancements of PRC2 in Cancer Therapy: A Narrative Review.Life (Basel, Switzerland) · 2024Review
- A dual role for PSIP1/LEDGF in T cell acute lymphoblastic leukemia.Science advances · 2024Article
- Enhancers in T Cell development and malignant lesions.Cell death discovery · 2024Review
- Targeted therapy and immunotherapy for T cell acute lymphoblastic leukemia/lymphoma.Annals of hematology · 2023Review
- From a drug repositioning to a structure-based drug design approach to tackle acute lymphoblastic leukemia.Nature communications · 2023Article
- The Battlefield of Chemotherapy in Pediatric Cancers.Cancers · 2023Review
- Review
- Harnessing the MYB-dependent TAL1 5'super-enhancer for targeted therapy in T-ALL.Molecular cancer · 2023Article
- Polycomb Repressive Complex 2 in Oncology.Cancer treatment and research · 2023Article
- JAK/BCL2 inhibition acts synergistically with LSD1 inhibitors to selectively target ETP-ALL.Leukemia · 2022Article
- Mechanisms of Polycomb group protein function in cancer.Cell research · 2022Review
- A Novel Risk Defining System for Pediatric T-Cell Acute Lymphoblastic Leukemia From CCCG-ALL-2015 Group.Frontiers in oncology · 2022Article
- BETter insight into PRC2-mutated T-ALL.Blood · 2021Article
- Oncogenic Cooperation Between IL7R-JAK-STAT Pathway Mutations.HemaSphere · 2021Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is a group of aggressive hematological cancers with dismal outcomes that are in need of new therapeutic options. Polycomb repressor complex 2 (PRC2) loss-of-function alterations were reported in pediatric T-ALL, yet their clinical relevance and functional consequences remain elusive. Here, we extensively analyzed PRC2 alterations in a large series of 218 adult T-ALL patients. We found that PRC2 genetic lesions are frequent events in T-ALL and are not restricted to early thymic precursor ALL. PRC2 loss of function associates with activating mutations of the IL7R/JAK/STAT pathway. PRC2-altered T-ALL patients respond poorly to prednisone and have low bone marrow blast clearance and persistent minimal residual disease. Furthermore, we identified that PRC2 loss of function profoundly reshapes the genetic and epigenetic landscapes, leading to the reactivation of stem cell programs that cooperate with bromodomain and extraterminal (BET) proteins to sustain T-ALL. This study identifies BET proteins as key mediators of the PRC2 loss of function-induced remodeling. Our data have uncovered a targetable vulnerability to BET inhibition that can be exploited to treat PRC2-altered T-ALL patients.
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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.