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Environmental or self-antigens and homotypic interactions cause BCR and Toll-like receptor (TLR) signaling, amplifying the response of CLL cells to other signals from the microenvironment and increasing the activation of anti-apoptotic and proliferation pathways.

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mutations and complex kar yotype. It follows a linear evolution in the CLL clone through the recurrent acquisition of CDKN2A

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The existence of driver alterations is connected to speedy development. Though some alterations are enriched in CLL in comparison to MBL, the two phases share the same driver composition. (