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Biomarkers in refractory aggressive lymphoma

ABSTRACT: Serum glutathione peroxidase 3 level as a surrogate biomarker to predict failure-treatment prior to first line in patients involved by diffuse large B-cell lymphoma

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Serum

DISEASE(S): Lymphosarcoma

SUBMITTER: Robert Winkler

LAB HEAD: Luis Mario Villela Martinez

PROVIDER: PXD001321 | Pride | 2026-04-24

REPOSITORIES: Pride

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Project description:The B cell receptor (BCR) signaling, required for the survival and maturation of B cells, is a major deregulated pathway in B cell lymphomas. Several mutations are known to enhance the tonic BCR signal in Burkitt lymphomas (BL) or to mimic an activated receptor in some diffuse large B cell lymphomas (DLBCL). While the proximal events and kinases of the BCR signaling are well studied, less is known about the interactions of downstream effector pathways. In order to reach a less abstract description of this pathway we decided to employ the Modular Response Analysis-based modelling approach STASNet on more directly connected phosphorylation data. Using a Luminex proteomics platform we measured the phosphorylation of fourteen signaling and effector proteins after activating the B cell receptor (BCR) signaling and/or using inhibitors directed against seven intracellular signaling molecules in two independent Burkitt lymphoma cells (BL-2, BL-41). Application of a novel two step STASNet modelling pipeline unveiled novel feedback and crosstalk structures in the BCR-driven signaling network, including a crosstalk from p38 which negatively regulates MEK/ERK-activity in the presence of active BCR. Using Western Blot measurements, we verified and further characterized the p38-MEK/ERK crosstalk and demonstrated that it is a general mechanism in BL cells. Global Tandem Mass Tag (TMT) phosphoproteomic analysis on BL-2 cells found PI3K to be a major mediator of B-cell receptor signaling and manifested the p38-ERK crosstalk directly on ERK phosphosites and indirectly on seven bona fide ERK targets. We also noticed that the BL-2-learned pathway network structure was transferable to perturbation data from closely related BL-41 cells. Moreover, - compared to a literature-derived network - the BL-2-developed predictive pathway proved also to be a better starting point for network development in cells with aberrant BCR signaling in two representative cell lines derived from Diffuse large B cells (HBL-1, OCI-LY3). This indicates that models trained on activated B-cells are highly informative to be transferred to closely related cancer signaling network.

			Action	DRS
	dlbcl-spot2.raw	Raw
	dlbcl-spot3.raw	Raw
	dlbcl-spot4.raw	Raw
	dlbcl-spot6.raw	Raw
	dlbcl-spot7.raw	Raw

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Biomarkers in refractory aggressive lymphoma

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