Decoupling Lineage-Associated Genes in Acute Myeloid Leukemia Reveals Inflammatory and Metabolic Signatures Associated with Outcomes
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ABSTRACT:
PROVIDER: PRJNA695269 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13565300_1.fastq.gz | Fastqsanger.gz | |||
| SRR13565300_2.fastq.gz | Fastqsanger.gz | |||
| SRR13565301_1.fastq.gz | Fastqsanger.gz | |||
| SRR13565301_2.fastq.gz | Fastqsanger.gz | |||
| SRR13565302_1.fastq.gz | Fastqsanger.gz |
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Project description:Context: In many cancers, specific subpopulations of cells appear to be uniquely capable of initiating and maintaining tumors. The strongest support for this cancer stem cell model comes from transplantation assays in immune-deficient mice indicating that human acute myeloid leukemia (AML) is organized as a cellular hierarchy driven by self-renewing leukemia stem cells (LSC). This model has significant implications for the development of novel therapies, but its clinical significance remains unclear. Objective: To measure associations between a leukemic stem cell expression signature and clinical outcomes in AML. Design, Setting, and Patients: We defined a gene expression signature of LSC-enriched subpopulations from primary AML patient samples and xenografts, based on a functional definition in transplantation assays. 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