Src kinases as targets for B cell acute lymphoblastic leukaemia therapy.
The participation of Src kinases in the induction of BCR-ABL-induced B cell acute lymphoblastic leukaemia (B-ALL), but not chronic myeloid leukaemia (CML), demonstrates cell type-specific signalling in Philadelphia chromosome-positive (Ph+) leukaemias. Different therapeutic strategies are therefore needed for B-ALL and CML. Activation of Src kinases is independent of BCR-ABL kinase activity for activation. Thus, Src kinases provide a mechanism for resistance to the BCR-ABL kinase inhibitors and potential targets for B-ALL therapy. Simultaneous targeting of both BCR-ABL and Src kinases may benefit human B-ALL patients. Leukaemic stem cells may exist in Ph+ B-ALL, and eradication of this group of cells would provide a curative method for this disease.
Li
Shaoguang
S
The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609, USA. sli@jax.org
D000818:Animals; D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D002051:Burkitt Lymphoma / Q000188:drug therapy* / Q000201:enzymology*; D016503:Drug Delivery Systems / Q000379:methods*; D006801:Humans; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D019061:src-Family Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism
D000970:Antineoplastic Agents; D047428:Protein Kinase Inhibitors; D019061:src-Family Kinases