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      "text": "Chronic activation of the B-cell receptor (BCR) in malignant B-cells can lead to inappropriate NF-κB signalling, driving uncontrolled tumour cell proliferation and survival. MALT1 functions downstream of the BCR and also the therapeutic target, BTK, and is a critical component of tumourogenic signalling pathways in these tumour cells. Inhibition of MALT1 protease activity blocks the pathogenic signals from the BCR and, in a subset of NF-κB-addicted tumours, inhibits tumour cell proliferation. Combining MALT1 and BTK inhibitors could provide additional efficacy in these lymphomas by stronger inhibition of the pathway and by maintaining activity in tumours with target-mediated BTK inhibitor resistance.",
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