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Environmental or self-antigens and homotypic interactions set off BCR and Toll-like receptor (TLR) signaling, amplifying the reaction of CLL cells to other signals in the microenvironment and raising the activation of anti-apoptotic and proliferation pathways.31,32 Genomic scientific studies have determined recurrent mutations in genes regulating tumor mobile-microenvironment interactions, that are previously demanded for tumor cell development. Thus, NOTCH1 mutations are dependent on the existence of Notch ligands in the microenvironment and activate processes for instance mobile migration, invasion and angiogenesis.
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