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Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 1]

ABSTRACT: Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 1]

PROVIDER: PRJNA951448 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24044080_1.fastq.gz	Fastqsanger.gz
	SRR24044080_2.fastq.gz	Fastqsanger.gz
	SRR24044081_1.fastq.gz	Fastqsanger.gz
	SRR24044081_2.fastq.gz	Fastqsanger.gz
	SRR24044082_1.fastq.gz	Fastqsanger.gz

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Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 2]

Project description:Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 2]

| PRJNA951450 | ENA

Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 1]

Project description:Anti-CD38 monoclonal antibodies like Daratumumab (Dara) are effective in multiple myeloma (MM); however, drug resistance ultimately occurs and the mechanisms behind this are poorly understood. Here, we performed two in vitro genome-wide CRISPR screens to systematically discover the regulators of sensitivity to Dara-mediated antibody-dependent cellular cytotoxicity (ADCC) and identified KDM6A. The loss of KDM6A led to a marked downregulation in CD38 expression by increasing H3K27me3 on the CD38 promoter, resulting in resistance to Dara-mediated ADCC. Yet, adding back CD38 did not completely rescue this phenotype. In fact, KDM6A loss also downregulated CD48, which promoted Dara resistance by inhibiting natural killer cell activity. Lowering the H3K27me3 with an EZH2 inhibitor restored sensitivity to Dara through CD38 and CD48 upregulation. These findings suggest KDM6A loss as a mechanism of Dara resistance and explore the strategy of using an EZH2 inhibitor, one of which is already FDA-approved, to improve the response to Dara in MM.

2024-01-23 | GSE228767 | GEO

Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 2]

2024-01-23 | GSE228770 | GEO

Multiple myeloma

Project description:Multiple myeloma

| PRJNA515992 | ENA

Genome-wide screening of FOXM1 expression in multiple myeloma cells

Project description:Genome-wide screening of FOXM1 expression in multiple myeloma cells

| PRJNA1174339 | ENA

Genome-wide screening of IKZF1 binding in multiple myeloma cells.

Project description:Genome-wide screening of IKZF1 binding in multiple myeloma cells.

| PRJNA800413 | ENA

Multiple Myeloma cells

Project description:Multiple Myeloma cells

| PRJNA800411 | ENA

Genome-wide CRISPR-Cas9 knockout screening identifies NUDCD2 depletion as sensitizer for bortezomib, carfilzomib and ixazomib in multiple myeloma [CRISPR screen carfilzomib]

Project description:Genome-wide CRISPR-Cas9 knockout screening identifies NUDCD2 depletion as sensitizer for bortezomib, carfilzomib and ixazomib in multiple myeloma [CRISPR screen carfilzomib]

| PRJNA1287773 | ENA

Genome-wide CRISPR-Cas9 knockout screening identifies NUDCD2 depletion as sensitizer for bortezomib, carfilzomib and ixazomib in multiple myeloma [CRISPR screen bortezomib]

Project description:Genome-wide CRISPR-Cas9 knockout screening identifies NUDCD2 depletion as sensitizer for bortezomib, carfilzomib and ixazomib in multiple myeloma [CRISPR screen bortezomib]

| PRJNA1287776 | ENA

Serum protein N-glycosylation changes in multiple myeloma

Project description:<h4><strong>BACKGROUND:</strong> Multiple myeloma is characterized by clonal proliferation of malignant plasma cells in the bone marrow that produce monoclonal immunoglobulins. N-glycosylation changes of these monoclonal immunoglobulins have been reported in multiple myeloma, but previous studies only detected limited serum N-glycan features.</h4><h4><strong>METHODS:</strong> Here, a more detailed study of the human serum N-glycome of 91 multiple myeloma patients and 51 controls was performed. We additionally analyzed sequential samples from patients (n = 7) which were obtained at different time points during disease development as well as 16 paired blood serum and bone marrow plasma samples. N-glycans were enzymatically released and measured by mass spectrometry after linkage specific derivatization of sialic acids.</h4><h4><strong>RESULTS:</strong> A decrease in both α2,3- and α2,6-sialylation, galactosylation and an increase in fucosylation within complex-type N-glycans were found in multiple myeloma patients compared to controls, as well as a decrease in difucosylation of diantennary glycans. The observed glycosylation changes were present in all ISS stages, including the 'low-risk' ISS I. In individual patients, difucosylation of diantennary glycans decreased with development of the disease. Protein N-glycosylation features from blood and bone marrow showed strong correlation. Moreover, associations of monoclonal immunoglobulin (M-protein) and albumin levels with glycan traits were discovered in multiple myeloma patients.</h4><h4><strong>CONCLUSIONS & GENERAL SIGNIFICANCE: </strong>In conclusion, serum protein N-glycosylation analysis could successfully distinguish multiple myeloma from healthy controls. Further studies are needed to assess the potential roles of glycan trait changes and the associations of glycans with clinical parameters in multiple myeloma early detection and prognosis.</h4>

2022-04-27 | MTBLS676 | MetaboLights

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