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Mian et al. BMC Cancer 2012, 12:411 http://www.biomedcentral.com/1471-2407/12/RESEARCH ARTICLEOpen AccessAllosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315IAfsar Ali Mian1, Anna Metodieva1, Susanne Badura1, Mamduh Khateb2, Nili Ruimi2, Yousef Najajreh3, Oliver Gerhard Ottmann1, Jamal Mahajna2,4 and Martin Ruthardt1,5*AbstractBackground: Chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive (Ph+) acute lymphatic leukemia (Ph + ALL) are caused by the t(9;22), which fuses BCR to ABL resulting in deregulated ABL-tyrosine kinase activity. The constitutively order STI-571 activated BCR/ABL-kinase “escapes” the auto-inhibition mechanisms of c-ABL, such as allosteric inhibition. The ABL-kinase inhibitors (AKIs) Imatinib, Nilotinib or Dasatinib, which target the ATP-binding site, are effective in Ph + leukemia. Another molecular therapy approach targeting BCR/ABL restores allosteric inhibition. Given the fact that all AKIs fail to inhibit BCR/ABL harboring the `gatekeeper’ mutation T315I,.