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Nature Medicine 13, 1144 - 1145 (2007)
doi:10.1038/nm1007-1144
Where lies the blame for resistance—tumor or host?
Charles L Sawyers1
- Charles L. Sawyers is in the Human Oncology and Pathogenesis Program at the Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA. e-mail: sawyersc@mskcc.org
Abstract
Cytokine signaling from the tumor microenvironment can allow leukemia cells to survive targeted imatinib therapy, in the first report of a non-autonomous resistance mechanism.
Targeted cancer therapy, as showcased by the Abelson murine leukemia viral oncogene homolog-1 (ABL) kinase inhibitor imatinib in the treatment of chronic myeloid leukemia (CML)1, has captivated the attention of the cancer world. Because they specifically attack the molecular underpinnings of a tumor, such as an oncogenic mutant kinase, these targeted drugs promise remarkable efficacy with minimal toxicity.
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