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An inflammatory state defines a high-risk T-lineage acute lymphoblastic leukemia subgroup [CITE-seq]

ABSTRACT: An inflammatory state defines a high-risk T-lineage acute lymphoblastic leukemia subgroup [CITE-seq]

PROVIDER: PRJNA982124 | ENA |

REPOSITORIES: ENA

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An inflammatory state defines a high-risk T-lineage acute lymphoblastic leukemia subgroup [CITE-seq]

Project description:T-cell acute lymphoblastic leukemia (T-ALL), a malignant neoplasm of immature T cells, is a particularly aggressive leukemia with diverse subtypes and limited therapeutic options. Recent studies showed that the responsiveness of drugs in preclinical models of T-ALL is linked to the specific biological characteristics exhibited by the T-ALL subtype. In order to comprehensively explore the underlying heterogeneity of T-ALL, we performed an integrative analysis of bone marrow biopsies from newly diagnosed T-ALL patients. Leveraging a combination of cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq) along with T-cell receptor sequencing (TCR-seq), we obtained a comprehensive molecular characterization of T-ALL. Our analysis uncovered a distinct subset of inflammatory T-ALLs (iT-ALLs) resembling early T-cell precursor (ETP) leukemias, characterized by enriched expression of hematopoietic stem and progenitor signatures, inflammatory gene programs, and poor survival outcomes. Furthermore, our investigation revealed a significant association between the transcription factor interferon regulatory factor 5 (IRF5) activity and the iT-ALL subgroup. Utilizing an IRF5 scoring system, we demonstrated its potential as a robust biomarker for classifying T-ALL patients and predicting disease prognosis. Our work provides a framework for identifying high-risk T-ALL patients based on the IRF5 activity and a rational for considering the inflammatory state in tailoring therapeutic interventions.

2024-12-31 | GSE234610 | GEO

An inflammatory state defines a high-risk T-lineage acute lymphoblastic leukemia subgroup

Project description:An inflammatory state defines a high-risk T-lineage acute lymphoblastic leukemia subgroup

| PRJNA982126 | ENA

An inflammatory state defines a high-risk T-lineage acute lymphoblastic leukemia subgroup [bulkRNA-Seq]

2024-12-31 | GSE234608 | GEO

An inflammatory state defines a high-risk T-lineage acute lymphoblastic leukemia subgroup [bulkRNA-Seq]

Project description:An inflammatory state defines a high-risk T-lineage acute lymphoblastic leukemia subgroup [bulkRNA-Seq]

| PRJNA982121 | ENA

IG-MYC rearrangement defines a high-risk subgroup of B-cell precursor acute lymphoblastic leukaemia

Project description:IG-MYC rearrangement defines a high-risk subgroup of B-cell precursor acute lymphoblastic leukaemia

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An inflammatory state defines a high-risk T-lineage acute lymphoblastic leukemia subgroup

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-12-31 | GSE234612 | GEO

ΔNp73 isoform defines a TP53mutant-like poor risk subgroup of acute myeloid leukemia

Project description:ΔNp73 isoform defines a TP53mutant-like poor risk subgroup of acute myeloid leukemia

| PRJNA1365095 | ENA

ΔNp73 isoform defines a TP53mutant-like poor risk subgroup of acute myeloid leukemia

Project description:Among acute myeloid leukemia (AML) patients, a subgroup remains notoriously refractory to current treatment options, with underlying mechanisms poorly understood. Here, using a multi-omics approach, we reveal that this resistant patient subgroup is characterized by high expression of the oncogenic TP73 isoform ΔNp73, exhibiting similarly poor outcomes as TP53-mutant AML. ΔNp73, which lacks a transcriptional activation domain but retains chromatin binding properties, competes with TP53 for specific gene targets, thereby downregulating TP53 signaling. We demonstrate that the transcription factor CEBPA controls ΔNp73 expression in AML cells by binding to an intragenic enhancer region. Genetic or pharmacological inhibition of the transcriptional activity of CEBPA with guanfacine reduces ΔNp73 levels and restores drug sensitivity involving ferroptosis-mediated cell death, acting synergistically with venetoclax. Our study sheds light on a previously undercharacterized poor risk subgroup of AML, which may support patient stratification and inform treatment considerations.

2026-02-01 | GSE310074 | GEO

Immune-microbiome coordination defines interferon setpoints in healthy humans [CITE-seq and WMS]

Project description:Immune-microbiome coordination defines interferon setpoints in healthy humans [CITE-seq and WMS]

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The Evolving Immune Microenvironment of Human B-cell Acute Lymphoblastic Leukemia [CITE-Seq]

Project description:The Evolving Immune Microenvironment of Human B-cell Acute Lymphoblastic Leukemia [CITE-Seq]

| PRJNA642147 | ENA