Resistance to targeted therapy in chronic lymphocytic leukemia

Targeted therapy with inhibitors of cell signaling pathways and anti-apoptotic molecules significantly improved treatment chronic lymphocytic leukemia. Inhibitors Bruton?s tyrosine kinase bcl2 protein showed significant efficacy in either treatment-na?ve or relapsed/refractory patients poor risk factors. The majority respond to have durable remissions, but some them develop resistance, which leads clinical relapse. most frequent cause resistance is mutations on the binding site targeted molecules, such as treated ibrutinib acalabrutinib, venetoclax. There are also alternative mechanisms that can lead another molecule pathway, PLCG2, overexpression protein. These been detected several months before sings relapse, therefore could serve predictive markers failure. When occurs, will be effective cases, vice versa. Other strategies for overcoming PI3K inhibitors, second third generation bispecific antiCD3/CD19 antibodies, chimeric antigen receptor T-cells allogenic stem transplantation. Several inhibit degrade different targets leukemia cells, currently under investigation, they resistant