Browse
Submit Data
Databases
API
Help

Dataset Information

122 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT:

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.

PROVIDER: phs000671.v1.p1 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

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>

| phs000671 | dbGaP

Burkholderia thailandensis 34 strain:34

Project description:Burkholderia thailandensis 34 strain:34 Genome sequencing

| PRJNA178704 | ENA

RNA profiling of IL-34 overexpressing acute myeloid leukemia (AML) cells

Project description:Acute myeloid leukemia (AML) is a highly heterogeneous disease. In our study, we found that overexpressing IL-34 in AML cells accelerates the AML progression and shorten the mice survival, which is medicated by LSC level. We used one of the LSC markers, c-Kit, to divide AML cells. The goals of this study aim to reveal the mechanism mediated by IL-34 overexpression, we performed the RNAseq profiling of MA9-c-kit-, MA9-c-kit+ and MA9-IL-34 AML cells.

2022-09-16 | GSE213201 | GEO

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

Homo sapiens

Project description:Somatic mutations in variant and IGHV4-34 expressing hairy cell leukemia

| PRJNA223180 | ENA

Homo sapiens

Project description:Somatic mutations in variant and IGHV4-34 expressing hairy cell leukemia

| PRJNA223178 | ENA

Both variant and IGHV4-34-expressing hairy cell leukemia lack the BRAF V600E mutation.

Project description: Not available

| S-EPMC3321859 | biostudies-other

Somatic STAT3 mutations in large granular lymphocytic leukemia.

Project description: Not available

| S-EPMC3693860 | biostudies-literature

RNA-seq analysis of αPD-1 treatment outcomes in IL-34 expressing or not expressing CT26 cell line

Project description:Interleukin-34 (IL-34) is an alternative ligand to colony-stimulating factor-1 (CSF-1) for the CSF-1 receptor that acts as a key regulator of monocyte/macrophage lineage. In this study, we show that cancer cells-derived IL-34 mediates resistance to immune checkpoint blockade regardless of CSF-1 existence. In a therapeutic study of a programmed death-1 and cytotoxic T-lymphocyte-associated antigen-4 blocking monoclonal antibody, the expression of IL-34 in tumors was accompanied with limited benefits compared to IL-34 non-expressing tumors in various murine cancer models. Consistent with its immunosuppressive characteristics, the expression of IL-34 in tumors correlates with decreased frequencies of cellular (such as CD8+ and CD4+ T cells) and molecular (including various cytokines and chemokines) effectors at the tumor microenvironment. In addition, IL-34 blockade expands the M1-macrophage population. Then, a neutralizing antibody against IL-34 helped to reverse these effects and improved the therapeutic effects of the immune checkpoint blockade in combinatorial therapeutic models, including a patient-derived xenograft model of primary lung adenocarcinoma. Collectively, we revealed that tumor-derived IL-34 inhibits the efficacy of immune checkpoint blockade and proposed the utility of IL-34 blockade as a new strategy for cancer therapy.

2020-09-30 | GSE157602 | GEO

Surprising Phenotypic Diversity of Cancer-associated mutations at Gly 34 in the Histone H3 tail

Project description:Deep sequencing of cancer genomes has identified frequent mutation of core histones, termed oncohistones, but the role of some mutants is poorly understood. Here, using fission yeast as a model, we determine the consequences of mutation of histone H3.3 at Gly 34, a site frequently mutated in pediatric cortical high-grade glioma (G34R/V), and in virtually all giant cell tumors of bone (G34W). H3-G34 mutations cause a surprising diversity of outcomes, differentially affecting modification of the nearby H3K36 residue, subtelomeric silencing, genomic stability, sensitivity to irradiation, alkylating agents, hydroxyurea and influencing DNA repair. Since fifteen genes encode H3 isoforms, and only one allele is targeted in cancer, G34R/V/W H3 likely represents a small portion of total cellular H3. Whilst the presence of wild type H3 rescues most G34 mutant phenotypes, hydroxyurea sensitivity, subtelomeric silencing and homologous recombination defects dominate in cells expressing G34R and wild type H3. Together, these studies demonstrate the complexity associated with different substitutions at even a single residue in histone H3 and highlight the utility of genetically tractable systems for their analysis.

2021-02-08 | GSE162572 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data