ArticleOncotarget2016
Genomic characterization of pediatric T-cell acute lymphoblastic leukemia reveals novel recurrent driver mutations.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 65 citations in OpenAlex.
- Clinical and molecular characteristics ofHaematologica · 2019Trial
- The machine-learning classifier ALLCatchR2 identifies 20 T-ALL subtypes across cohorts and age groups.HemaSphere · 2026Article
- Phf6 truncating mutation drives leukemogenesis via disrupted epigenetic regulation in mice.Leukemia · 2026Article
- From Cell Lines to Avatars: Charting the Future of Preclinical Modeling in T-Cell Malignancies.Cells · 2026Review
- Pediatric T-Lymphoblastic Leukemia With Aberrant B-Cell Marker Expression: A Potential Role for Targeted Therapy.EJHaem · 2025Article
- Genetic hallmarks and clinical implications of chromothripsis in childhood T-cell acute lymphoblastic leukemia.Leukemia · 2024Article
- Rare Drivers at Low Prevalence with High Cancer Effects in T-Cell and B-Cell Pediatric Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024Article
- Integrated analysis of transcriptome and genome variations in pediatric T cell acute lymphoblastic leukemia: data from north Indian tertiary care center.BMC cancer · 2024Article
- Defining the landscape of circular RNAs in neuroblastoma unveils a global suppressive function of MYCN.Nature communications · 2023Article
- Genomics improves risk stratification of adults with T-cell acute lymphoblastic leukemia enrolled in measurable residual disease-oriented trials.Haematologica · 2023Article
- Myeloid/Lymphoid Neoplasms withJournal of inflammation research · 2023Article
- RaScALL: Rapid (Ra) screening (Sc) of RNA-seq data for prognostically significant genomic alterations in acute lymphoblastic leukaemia (ALL).PLoS genetics · 2022Article
- Identification of new ETV6 modulators through a high-throughput functional screening.iScience · 2022Article
- Bilineal evolution of a U2AF1-mutated clone associated with acquisition of distinct secondary mutations.Blood advances · 2021Article
- USP9X promotes apoptosis in cholangiocarcinoma by modulation expression of KIF1Bβ via deubiquitinating EGLN3.Journal of biomedical science · 2021Article
- DNA methylation-mediated silencing of microRNA-204 enhances T cell acute lymphoblastic leukemia by up-regulating MMP-2 and MMP-9 via NF-κB.Journal of cellular and molecular medicine · 2021Article
- lncRNAs in T lymphocytes: RNA regulation at the heart of the immune response.American journal of physiology. Cell physiology · 2021Review
- Comprehensive Overview of Gene Rearrangements in Childhood T-Cell Acute Lymphoblastic Leukaemia.International journal of molecular sciences · 2021Review
- Kdm6a deficiency restricted to mouse hematopoietic cells causes an age- and sex-dependent myelodysplastic syndrome-like phenotype.PloS one · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy with variable prognosis. It represents 15% of diagnosed pediatric ALL cases and has a threefold higher incidence among males. Many recurrent alterations have been identified and help define molecular subgroups of T-ALL, however the full range of events involved in driving transformation remain to be defined. Using an integrative approach combining genomic and transcriptomic data, we molecularly characterized 30 pediatric T-ALLs and identified common recurrent T-ALL targets such as FBXW7, JAK1, JAK3, PHF6, KDM6A and NOTCH1 as well as novel candidate T-ALL driver mutations including the p.R35L missense mutation in splicesome factor U2AF1 found in 3 patients and loss of function mutations in the X-linked tumor suppressor genes MED12 (frameshit mutation p.V167fs, splice site mutation g.chrX:70339329T>C, missense mutation p.R1989H) and USP9X (nonsense mutation p.Q117*). In vitro functional studies further supported the putative role of these novel T-ALL genes in driving transformation. U2AF1 p.R35L was shown to induce aberrant splicing of downstream target genes, and shRNA knockdown of MED12 and USP9X was shown to confer resistance to apoptosis following T-ALL relevant chemotherapy drug treatment in Jurkat leukemia cells. Interestingly, nearly 60% of novel candidate driver events were identified among immature T-ALL cases, highlighting the underlying genomic complexity of pediatric T-ALL, and the need for larger integrative studies to decipher the mechanisms that contribute to its various subtypes and provide opportunities to refine patient stratification and treatment.
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.