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Hairy Cell Leukemia Cell Line JOK1 +/- RhoH Reconstitution

ABSTRACT: Hairy Cell Leukemia Cell Line JOK1 +/- RhoH Reconstitution

PROVIDER: PRJNA658103 | ENA |

REPOSITORIES: ENA

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Hairy Cell Leukemia Cell Line JOK1 +/- RhoH Reconstitution

Project description:The hairy cell leukemia line JOK1 with low RhoH expression was stably trasfected with either an empty expression vector or this same vector expressing human RhoH. The transcriptomes of these two daughter lines were then compared by differential microarray analysis The hairy cell leukemia line JOK1 with low RhoH expression was stably trasfected with either an empty expression vector or this same vector expressing human RhoH. The transcriptomes of these two daughter lines were then compared by differential microarray analysis

2021-01-03 | GSE156483 | GEO

The Adult T-Cell Leukemia/Lymphoma Cell Line KK1 +/- RhoH Reconstitution

Project description:The Adult T-Cell Leukemia/Lymphoma Cell Line KK1 +/- RhoH Reconstitution

| PRJNA947956 | ENA

The Adult T-Cell Leukemia/Lymphoma Cell Line KK1 +/- RhoH Reconstitution

Project description:The adult T-cell leukemia/lymphoma cell line KK1 with low RhoH expression was stably transfected with either an empty expression vector or this same vector expressing human RhoH. The transcriptomes of these two daughter lines were then compared by differential microarray analysis

2023-03-23 | GSE228059 | GEO

Molecular signatures for Hairy cell leukemia

Project description:Molecular signatures for Hairy cell leukemia

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Molecular signatures for Hairy cell leukemia

Project description:Analysis of the expression profile of 298 mRNA's, measured with the nCounter (Nanostring Technologies platform), in 13 samples from the peripheral blood of Hairy cell leukemia patients Hairy cell leukemia (HCL) is a rare chronic B-cell malignancy, characterized by infiltration of bone marrow, blood and spleen by typical “hairy cells” that bear the BRAFV600E mutation. However, in addition to the intrinsic activation of the MAP kinase pathway as a consequence of the BRAFV600E mutation, the potential participation of other signaling pathways to the pathophysiology of the disease remains unclear. Using mRNA gene expression profiling based on the Nanostring technology and the analysis of 290 genes with crucial roles in B-cell lymphomas, we defined a 17 gene expression signature specific for HCL. Our analysis revealed intrinsic activation of the non-canonical NF-B pathway with underexpression of BIRC2 and BIRC3, two specific non-canonical NF-B inhibitors. Western blots confirmed activation of this pathway with increased processing of p100 in primary HCL samples. Separate analysis of samples from classical and variant forms of hairy cell leukemia showed almost similar mRNA expression profiles apart from overexpression in vHCL of the immune checkpoints CD274 and PDCD1LG2 and underexpression of FAS. Our results provide a better understanding of the pathogenesis of HCL and describe new and potential targets for treatment approaches and guidance for studies in the molecular mechanisms of HCL.

2020-11-12 | GSE161279 | GEO

Single-cell transcriptional profiling of cancer cells in hairy cell leukemia (HCL) patients

Project description:This single-cell RNA sequencing (scRNA-seq) dataset profiles human HCL cells from two patients with Hairy Cell Leukemia (HCL) and varient subtype of HCL (HCLv), both expressing unmutated IGHV4-34. scRNA-seq was performed on isolated CD19⁺ and CD3⁺cells from peripheral blood mononuclear cells (PBMC) (n=2). The dataset enables the characterization of expressed mutation and transcriptional profiles of human HCL cells and supports investigations into cellular lineage and pathways associated with pathologic activation leading to HCL and variant form of HCL (HCLv).

2025-12-02 | GSE311935 | GEO

Single-cell transcriptional profiling of cancer cells in hairy cell leukemia (HCL) patients

Project description:Single-cell transcriptional profiling of cancer cells in hairy cell leukemia (HCL) patients

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Somatic Mutations in Variant and IGHV4-34 Expressing Hairy Cell Leukemia

Project description:<p>To understand the genetic mechanisms driving variant and IGHV4-34 expressing hairy-cell leukemia, we performed whole exome sequencing of tumor/normal pairs from ten patients.</p>

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Somatic Mutations in Variant and IGHV4-34 Expressing Hairy Cell Leukemia

| phs000671 | dbGaP

Braf inhibitors reverse the unique molecular signature and phenotype of hairy cell leukemia, and exert anti-leukemic activity

Project description:Hairy cell leukemia (HCL) shows unique clinico-pathological and biological features. HCL responds well to purine analogues but relapses are frequent and novel therapies are required. BRAF-V600E is the key driver mutation in HCL and distinguishes it from other B-cell lymphomas, including HCL-like leukemias/lymphomas (HCL-variant and splenic marginal zone lymphoma). The kinase-activating BRAF-V600E mutation also represents an ideal therapeutic target in HCL. Here, we investigated the biological and therapeutic importance of the activated BRAF-MEK-ERK pathway in HCL by exposing in vitro primary leukemic cells purified from 26 patients to clinically available BRAF (Vemurafenib; Dabrafenib) or MEK (Trametinib) inhibitors. Results were validated in vivo in samples from Vemurafenib-treated HCL patients within a phase-2 clinical trial. BRAF and MEK inhibitors caused, specifically in HCL (but not HCL-like) cells, marked MEK/ERK dephosphorylation, silencing of the BRAF-MEK-ERK pathway transcriptional output, loss of the HCL-specific gene expression signature, downregulation of the HCL markers CD25, TRAP and cyclin-D1, smoothening of leukemic cells' hairy surface, and, eventually, apoptosis. Apoptosis was partially blunted by co-culture with bone marrow stromal cells antagonizing MEK-ERK dephosphorylation. This protective effect could be counteracted by combined BRAF and MEK inhibition. Our results strongly support and inform the clinical use of BRAF and MEK inhibitors in HCL.

2014-12-12 | GSE63790 | GEO

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