Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide maps of transcription in Multiple Myeloma cells treated with FHND004 or FHND008

ABSTRACT: FHND004 and FHND008 are newly synthesized epidermal growth factor receptor (EGFR) inhibitor for the treatment of non-small cell lung cancer (NSCLC), they were obtained on the basis of AZD9291. We found that FHND004 and FHND008 had a strong inhibitory effect on the proliferation of multiple myeloma cells in vitro. Genome-wide maps of transcription showed different genes change in Multiple Myeloma cells after 4μM FHND004 or FHND008 intervention.

ORGANISM(S): Homo sapiens

PROVIDER: GSE223166 | GEO | 2024/04/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Multiple myeloma

Project description:Multiple myeloma

| PRJNA515992 | ENA

Transcriptomic heterogeneity of EGFR-mutant non-small cell lung cancer evolution towards small cell lung cancer

Project description:Histological transformation from epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC) to small cell lung cancer (SCLC) is the major resistance mechanism of EGFR tyrosine kinase inhibitors (TKIs). In our analysis of 59 regions of interest from EGFR-mutant NSCLC or combined SCLC/NSCLC tumors, we compared the transcriptomic profiles before and after transformation.

2024-07-30 | GSE259387 | GEO

Multiple Myeloma cells

Project description:Multiple Myeloma cells

| PRJNA800411 | ENA

Proteomic profiling reveals CDK6 upregulation as a targetable resistance mechanism for lenalidomide in multiple myeloma

Project description:The immunomodulatory drugs (IMiDs) lenalidomide and pomalidomide are highly effective treatments for multiple myeloma. However, virtually all patients eventually relapse due to acquired drug resistance with resistance-causing genetic alterations being found only in a small subset of cases. Here, we performed integrated global quantitative tandem mass tag (TMT)-based proteomic and phosphoproteomic analyses and RNA sequencing in five paired pre-treatment and relapse samples from multiple myeloma patients to investigate non-genetic resistance mechanisms. These analyses revealed a CDK6-governed protein resistance signature that includes myeloma high-risk factors such as TRIP13 and RRM1. Overexpression of CDK6 in multiple myeloma cell lines reduced sensitivity to IMiDs while CDK6 inhibition by palbociclib or CDK6 degradation by proteolysis targeting chimeras (PROTACs) is highly synergistic with IMiDs in vitro and in vivo. In conclusion, we found upregulation of CDK6 to cause lenalidomide resistance in multiple myeloma that can be overcome by pharmacological intervention.

2021-12-17 | PXD021265 | Pride

Genome-wide maps of transcription in Multiple Myeloma cells treated with FHND004 or FHND008

Project description:Genome-wide maps of transcription in Multiple Myeloma cells treated with FHND004 or FHND008

| PRJNA925161 | ENA

Biochemical and Structural Basif for Differential Inhibitor Sensitivity of EGFR with Distinct Exon 19 Mutaions

Project description:Tyrosine kinase inhibitors (TKIs) are used to treat non-small cell lung cancers (NSCLC) driven by epidermal growth factor receptor (EGFR) mutations in the tyrosine kinase domain (TKD). We studied structural basis of differential TKI sensitivity among EGFR exon 19 mutants by HDX-MS.

2023-03-11 | PXD037374 | Pride

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

Identification of clonal neoantigens derived from driver mutations in an EGFR mutated lung cancer patient benefitting from anti-PD-1

Project description:Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) have been recommended as the first line therapy for non-small cell lung cancer (NSCLC) with EGFR mutations. However, acquired resistance to EGFR-TKIs is inevitable. Although anti- programmed cell death 1 (PD-1)/PD-ligand (PD-L1) immunotherapies have achieved great clinical success as second-line treatment for many cancer types, the clinical efficacy of anti-PD-1/PD-L1 blockades in EGFR mutated NSCLC patients has been demonstrated to be obviously lower than those without EGFR mutations. Here, we reported an advanced NSCLC patient with exon 19 deletion and T790M EGFR mutation benefitting from anti-PD-1 blockade therapy after acquiring resistance to EGFR-TKI. We characterized the mutational landscape of the patient with next-generation sequencing (NGS), and successfully identified neoantigen-specific T cell clones derived from EGFR exon 19 deletion, TP53 A116T and DENND6B R398Q mutations. Our findings support the potential application of immune checkpoint blockades in NSCLC patients with acquired resistance to EGFR-TKIs in the context of specific clonal neoantigens with high immunogenicity. Personalized immunomodulatory therapy targeting these neoantigens should be explored for better clinical outcomes in EGFR mutant NSCLC patients.

2020-06-30 | GSE150972 | GEO

The strutural dynamics of EGFR Exon 19 mutants

Project description:Tyrosine kinase inhibtors are used to treat non-small cell lung cancers (NSCLC) driven by epidermal growth factor receptor (EGFR) mutations in the tyrosine kinase domain (TKD). We characterized the dynamics of purified EGFR exon 19 kinase domain mutants by HDX-MS with or withour erlotinib, one of the first-generation TKIs.

2023-03-11 | PXD037448 | Pride

Genome-wide maps of chromatin state in YTHDF2 kockdown(KD) and wildtype(WT) cells in Multiple Myeloma

Project description:We found that the experssion of STAT5A was upregulated when the YTHDF2 was knocked down. To identify the function of STAT5A protein as a Transcription factor in YTHDF2 kockdown(KD) and wildtype(WT) cells in Multiple Myeloma. CHIP-seq was conducted to analyze changes in related signaling pathways and gene expression in Multiple Myeloma cells when YTHDF2 was knocked down.

2022-06-30 | GSE163138 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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