and calcuim signaling following BCR activation8. Interestingly the hypomethylation signature
is further exacerbated during ibrutinib resistance. Together, we have found that the CLL
epigenome is impacted in multiple ways, including TF-dependent reprogramming and
potentially BCR signaling activity, which occur within the global signature inherited from the
founder B cell. The combination of these effects generates a tumor-specific epigenomic
landscape that is both unique and shared among CLL patients. Understanding these patterns
will assist in predicting disease course and impact treatment decisions for patients.
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