Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Rituximab and obinutuzumab differentially hijack the B-cell receptor and NOTCH1 signaling pathways.

ABSTRACT: An LC-MS/MS based phosphoproteomics study that characterizes the signaling processes downstream of the B-cell receptor and how they are differentially regulated following treatment with anti-CD20 monoclonal antibodies in B-cell lymphoma.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): B Cell, B-lymphocyte Cell Line, B-lymphocyte

DISEASE(S): B-cell Lymphoma,Diffuse Large B-cell Lymphoma

SUBMITTER: Arran Dokal

LAB HEAD: Pedro Cutillas

PROVIDER: PXD023572 | Pride | 2021-09-09

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	F006652.mzid.gz	Mzid
	F006653.mzid.gz	Mzid
	F006654.mzid.gz	Mzid
	F006655.mzid.gz	Mzid
	F006656.mzid.gz	Mzid

Items per page:

1 - 5 of 90

Publications

Rituximab and obinutuzumab differentially hijack the B cell receptor and NOTCH1 signaling pathways.

Edelmann Jennifer J Dokal Arran D AD Vilventhraraja Emma E Holzmann Karlheinz K Britton David D Klymenko Tetyana T Döhner Hartmut H Cragg Mark M Braun Andrejs A Cutillas Pedro P Gribben John G JG

iScience 20210122 2

The anti-CD20 monoclonal antibodies rituximab and obinutuzumab differ in their mechanisms of action, with obinutuzumab evoking greater direct B cell death. To characterize the signaling processes responsible for improved B cell killing by obinutuzumab, we undertook a phosphoproteomics approach and demonstrate that rituximab and obinutuzumab differentially activate pathways downstream of the B cell receptor. Although both antibodies induce strong ERK and MYC activation sufficient to promote cell- ...[more]

PMID: 33615197

Similar Datasets

Community detection from empirical kinase networks identifies new members of signalling pathways

Project description:We use phosphorylation sites to quantify the enrichment of kinase-kinase relationships in response to diferent kinase inhibitors, from which we construct weighted kinase networks, and assess whether the application of community detection algorithms to such networks can provide new insights on the inner workings of canonical signalling pathways

2023-06-07 | PXD026039 | Pride

Gene expression data in obinuzumab treated Karpas-1106P PMBL cell line

Project description:Primary Mediastinal large B-cell lymphoma (PMBL) is a rare form of non-Hodgkin lymphoma (NHL) representing 2% of mature B-cell NHL in patients less than 18 years of age.We compared the gene expression profiling between fully humanized anti-CD20 targeted monoclonal antibody recognizing a unique CD20 type II epitope, obinutuzumab and IgG or PBS treated Karpas Primary Mediastinal B-cell lymphoma (PMBL) cell line. -

2016-12-01 | GSE75605 | GEO

Kinase activity ranking (KAR) quantifies the contribution of protein kinases to the regulation of cell viability

Project description:New method to determine kinase activity based on phosphoproteomics data

2017-07-06 | PXD005073 | Pride

Effect of cation carriers on gene expression of Raji cell line

Project description:Our investigation uncovers that nanomolar concentrations of salinomycin, monensin, nigericin, and narasin (a group of potassium/sodium cation carriers) robustly enhance surface expression of CD20 antigen in B-cell-derived tumor cells, including primary malignant cells of chronic lymphocytic leukemia and diffuse large B-cell lymphoma. Experiments in vitro, ex vivo, and animal model reveal a novel approach of combining salinomycin or monensin with therapeutic anti-CD20 monoclonal antibodies or anti-CD20 CAR-T cells, significantly improving non-Hodgkin lymphoma (NHL) therapy. The results of RNA-seq, genetic editing, and chemical inhibition delineate the molecular mechanism of CD20 upregulation, at least partially, to the downregulation of MYC, the transcriptional repressor of the MS4A1 gene encoding CD20. Our findings propose the cation carriers as compounds targeting MYC oncogene, which can be combined with anti-CD20 antibodies or adoptive cellular therapies to treat NHL and mitigate resistance, which frequently depends on the CD20 antigen loss, offering new solutions to improve patient outcomes.

2025-07-09 | GSE282862 | GEO

eEF2K activity determines synergy to PI3K and MEK inhibitors in combination in cancer cells

Project description:To understand the mechanisms involved in synergy to PI3Ki + MEKi treatment, we performed a global phosphoproteomics analysis in 3 different cancer cell lines treated with a MEK inhibitor (Trametinib) and a PI3K inhibitor (Pictilisib) at 500 nM individually or in combination for one hour.

2022-04-25 | PXD018873 | Pride

Chemical phosphoproteomics reveals kinase network topologies associated to genotypes and phenotypes of cancer cells.

Project description:We compare the in vitro specificity profiles of several kinase inhibitors with their effects on cellular phosphoproteomes. For this aim, we developed an algorithm which utilizes information on kinase inhibitor selectivity to determine the most probable kinase(s) acting upstream of phosphorylation sites present in phosphoproteomics data obtained from cancer cells treated with kinase inhibitors.

2020-01-29 | PXD015943 | Pride

Computational analysis of cholangiocarcinoma phosphoproteomes identifies patient-specific drug targets

Project description:We used mass-spectrometry based phosphoproteomics and computational methods to identify patient-specific drug targets in primary CCA and CCA-derived cell lines. We analyzed 13 primary CCA with matched background tissue and 8 different cell lines leading to the identification and quantification of >13,000 phosphorylation sites. Application of the Drug Ranking Using Machine Learning (DRUML) algorithm identified inhibitors of HDAC and PI3K pathway members as highly ranking in primary CCA relative to background. The accuracy of drug rankings based on predicted responses was confirmed using cell line models of CCA. Together, our study uncovers frequently overactive biochemical pathways in primary CCA and provides a proof-of-concept of the use of machine learning for ranking drugs based on efficacy within individual patient tumors.

2023-03-11 | PXD027329 | Pride

Targeting LSD1 rewires kinase networks and primes leukaemia cells for kinase inhibitor treatment

Project description:We show that intrinsic resistance to kinase inhibitors may be reversed by coercing kinase networks into acquiring topologies tolerant to drug sensitivity. Using acute myeloid leukaemia (AML) as a model, we found several antagonists of chromatin modifying enzymes that sensitised cancer cells to kinase inhibitor treatments.

2022-04-25 | PXD018603 | Pride

Machine learning from large-scale proteomics accurately ranks anti-cancer drugs based on efficacy

Project description:We present an approach, named Drug Ranking Using ML (DRUML), which uses omics data to produce ordered lists of > 400 drugs based on their effectiveness in decreasing cancer cell proliferation. We trained and validated DRUML using in-house proteomics and phosphoproteomics data from a panel of 26 AML, 10 esophageal and 12 hepatocellular carcinoma cell lines in triplicate (three independent cultures per cell line) by LC-MS/MS

2021-02-22 | PXD019591 | Pride

Cancer burden is controlled by mural cell- β3-integrin regulated crosstalk with tumor cells

Project description:Phosphoproteomics analysis were performed in WT and β3-integrin-null pericytes. On the other hand, phosphoproteomics experiments were done in B16F0 melanoma cells treated for 24 hours with conditioned medium from WT and β3-integrin-null pericytes.

2020-06-01 | PXD014513 | Pride

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