Environmental or self-antigens and homotypic interactions cause BCR and Toll-like receptor (TLR) signaling, amplifying the reaction of CLL cells to other indicators through the microenvironment and escalating the activation of anti-apoptotic and proliferation pathways.
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The latest molecular reports have delivered a lot of insights to the processes that govern the development and progression of CLL, which includes numerous novel mutated genes clustered in various useful pathways. The CLL epigenome is reprogrammed in the modulation of regulatory locations that appear de novo