Deep learning based transcriptome model robustly predicts survival in T-cell acute lymphoblastic leukemia
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA888058 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21837354_1.fastq.gz | Fastqsanger.gz | |||
| SRR21837354_2.fastq.gz | Fastqsanger.gz | |||
| SRR21837355_1.fastq.gz | Fastqsanger.gz | |||
| SRR21837355_2.fastq.gz | Fastqsanger.gz | |||
| SRR21837356_1.fastq.gz | Fastqsanger.gz |
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Project description:Long non-coding RNAs (lncRNAs) have been found to play a role in gene regulation with dysregulated expression in various cancers. The precise role that lncRNA expression plays in the pathogenesis of B-acute lymphoblastic leukemia (B-ALL) is unknown. Therefore, unbiased microarray profiling was performed on human B-ALL specimens and it was determined that lncRNA expression correlates with cytogenetic abnormalities, which was confirmed by RT-qPCR in a large set of B-ALL cases. Importantly, high expression of BALR-2 correlated with poor overall survival and diminished response to prednisone treatment. In line with a function for this lncRNA in regulating cell survival, BALR-2 knockdown led to reduced proliferation, increased apoptosis, and increased sensitivity to prednisolone treatment. Conversely, overexpression of BALR-2 led to increased cell growth and resistance to prednisone treatment. Interestingly, BALR-2 expression was repressed by prednisolone treatment and its knockdown led to upregulation of the glucocorticoid response pathway in both human and mouse B-cells. Together, these findings indicate that BALR-2 plays a functional role in the pathogenesis and/or clinical responsiveness of B-ALL and that altering the levels of particular lncRNAs may provide a future direction for therapeutic development. B-lymphoblastic leukemia is characterized by several translocations. In this study, we hybridized patient bone marrow samples from a total of 44 patients including 14 patients with B-ALL carrying a TEL-AML1 translocation, 15 patients with E2A-PBX1 translocation, and 15 patients carrying MLL translocations. The hybridizations were carried out in two sets, a discovery set and a validation set. In addition, we utilized samples from a human cell line (NALM6) and control CD10+CD19+ cells from human bone marrow.
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