Novel therapies for chronic myelogenous leukemia Balkrishna N Jahagirdar, Jeffrey S Miller, Arun Shet, Catherine M Verfaillie  Experimental Hematology  Volume 29, Issue 5, Pages 543-556 (May 2001) DOI: 10.1016/S0301-472X(01)00633-6

Figure 1 Signal transduction pathways affected by the p210BCR-ABL oncoprotein. Activation of the Ras, Jak/Stat, and PI-3 kinase pathways results in increased proliferation, normal differentiation, and decreased apoptosis of the CML progenitors. The FAK-Paxillin-F-actin-integrin pathway impairs adhesion to the marrow stroma and causes premature release of the CML progenitors into the circulation. STK = Serine Threonine Kinase Experimental Hematology 2001 29, 543-556DOI: (10.1016/S0301-472X(01)00633-6)

Figure 2 Targets of novel therapies for CML. Antisense oligonucleotides inhibit translation. Immunotherapies evoke responses against the p210BCR-ABL peptide. Tyrosine kinase (TK) inhibitors inhibit the TK function of p210BCR-ABL. Farnesyl transferase inhibitors inhibit activation of the Ras protein Experimental Hematology 2001 29, 543-556DOI: (10.1016/S0301-472X(01)00633-6)