Seminar “Mathematical modeling helps to better understand the mechanisms B-cell lymphomas acquired resistance to BTK inhibitor treatment”

13 January at 16:30 MSK

Chronic activation of B-cell receptor (BCR) signaling via Bruton tyrosine kinase (BTK) is largely considered to be one of the primary mechanisms driving disease progression in B-cell lymphomas, particularly, ABC DLBCL. Although the BTK-targeting agent ibrutinib has shown promising clinical responses, the presence of primary or acquired resistance is common that leads to disease progression. Resistance to ibrutinib therapy can be mediated through genetic mutations, up-regulation of alternative survival pathways, or other unknown factors that are not targeted by ibrutinib therapy. In this work we did mathematical modeling of signaling pathways and transcriptional perturbations in B-cell lymphoma cells under BTK inhibitor treatment which might leads to ibrutinib resistant phenotype.

Online