Study
The molecular basis of T-PLL is an actionable perturbation of TCL1/ATM- and epigenetically instructed damage responses
Study ID | Alternative Stable ID | Type |
---|---|---|
EGAS00001002744 | Other |
Study Description
T-cell prolymphocytic leukemia (T-PLL) is a rare and poor-prognostic mature T-cell malignancy. To address its incomplete molecular concept, we integrated large-scale profiling data of alterations in gene expression, allelic copy number (CN), and nucleotide sequences in 111 well-characterized patients. Besides prominent signatures of T-cell activation and prevalent clonal variants, we also identified novel hot-spots for CN variability, fusion molecules, alternative transcripts, and progression-associated dynamics. The overall lesional spectrum of T-PLL is mainly annotated to axes of DNA damage responses, T-cell receptor/cytokine signaling, and histone modulation. We formulate a multi-dimensional model of T-PLL pathogenesis centered around a unique combination of TCL1 overexpression with damaging ATM aberrations as initiating core lesions. The effects imposed by TCL1 cooperate with compromised ATM towards a leukemogenic phenotype of impaired DNA damage processing. Dysfunctional ATM appears inefficient in alleviating elevated redox burdens and telomere attrition and in evoking a ... (Show More)
Study Datasets 1 dataset.
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Dataset ID | Description | Technology | Samples |
---|---|---|---|
EGAD00001003825 |
Patients with T-cell prolymphocytic leukemia (T-PLL) were profiled with
multiple OMICS approaches based on Next-Generation Sequencing (NGS). In
total, data from RNA-Seq, Whole-Exome Sequencing, Whole-Genome
Sequencing and amplicon panel analyses in 134 samples are available. All
samples were processed as paired-end libraries on Illumina sequencing
machines. The data are available as paired FastQ files.
|
Illumina HiSeq 2000,Illumina MiSeq | 134 |
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