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On Monday 3rd April during this year’s American Association for Cancer Research (AACR) annual meeting, a poster (2686 / 15) by Eman L. Dadashian, from NIH/NHLBI, Bethesda, MD, et al. titled “Dual inhibition of BCR and TLR signaling has therapeutic potential in Chronic Lymphocytic Leukemia” was presented.
The group treated CLL PMBCs with ibrutinib and/or calbiochem (an IRAK1/4 inhibitor) for 1h and then stimulated with soluble αIgM, CpG, or both. They measured changes in phosphorylation of BTK, PLCγ2, and ERK (BCR pathway), as well as STAT3, STAT1, and total IRAK1 (TLR pathway).
The poster concluded by stating that when TLR9 signaling is activated, IRAK1 is phosphorylated by IRAK4 signaling for it to be degraded, resulting in activation of NF-kB, STAT1/3 phosphorylation, and increasing cell survival. The combination of BTK and IRAK1/4 inhibition “prevents propagation of TLR9 signaling downstream of NF-kB” and therefore reduces cell survival.
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