At present, there are no compounds in clinical development in the field of chronic myeloid leukemia (CML) or Philadelphia-positive (Ph+) acute lymphoblastic leukemia (ALL) that have been documented to harbor significant activity against the imatinib-resistant T315I mutation. Recent reports on the pre-clinical activity of some emerging tyrosine kinase inhibitors such as ON012380, VX-680 and PHA-739358 promise possible clinical efficacy against this specific Bcr-Abl mutant form. Here, we focus on the role of aurora kinase inhibitor VX-680 and PHA-739358 in blocking the leukemogenic pathways driven by wild-type and T315I-Bcr-Abl in CML or Ph+ ALL by reviewing recent research evidence. We also discuss the possibility of employing aurora kinase inhibitors as a promising new therapeutic approach in the treatment of CML and Ph+ ALL patients resistant to first and second generation TK inhibitors.
Aurora kinase inhibitors: which role in the treatment of chronic myelogenous leukemia patients resistant to imatinib? / Martinelli G.; Papayannidis C.; Iacobucci I.; Soverini S.; Cilloni D.; Baccarani M.. - In: HEMATOLOGY REPORTS. - ISSN 2038-8330. - ELETTRONICO. - 1:1(2009), pp. e1-e8. [10.4081/hr.2009.e1]
Aurora kinase inhibitors: which role in the treatment of chronic myelogenous leukemia patients resistant to imatinib?
MARTINELLI, GIOVANNI;PAPAYANNIDIS, CRISTINA;IACOBUCCI, ILARIA;SOVERINI, SIMONA;BACCARANI, MICHELE
2009
Abstract
At present, there are no compounds in clinical development in the field of chronic myeloid leukemia (CML) or Philadelphia-positive (Ph+) acute lymphoblastic leukemia (ALL) that have been documented to harbor significant activity against the imatinib-resistant T315I mutation. Recent reports on the pre-clinical activity of some emerging tyrosine kinase inhibitors such as ON012380, VX-680 and PHA-739358 promise possible clinical efficacy against this specific Bcr-Abl mutant form. Here, we focus on the role of aurora kinase inhibitor VX-680 and PHA-739358 in blocking the leukemogenic pathways driven by wild-type and T315I-Bcr-Abl in CML or Ph+ ALL by reviewing recent research evidence. We also discuss the possibility of employing aurora kinase inhibitors as a promising new therapeutic approach in the treatment of CML and Ph+ ALL patients resistant to first and second generation TK inhibitors.File | Dimensione | Formato | |
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