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Targeting Tyrosine Kinases in Acute Myeloid Leukemia: Why, Who and How?


ABSTRACT: Acute myeloid leukemia (AML) is a myeloid malignancy carrying a heterogeneous molecular panel of mutations participating in the blockade of differentiation and the increased proliferation of myeloid hematopoietic stem and progenitor cells. The historical "3 + 7" treatment (cytarabine and daunorubicin) is currently challenged by new therapeutic strategies, including drugs depending on the molecular landscape of AML. This panel of mutations makes it possible to combine some of these new treatments with conventional chemotherapy. For example, the FLT3 receptor is overexpressed or mutated in 80% or 30% of AML, respectively. Such anomalies have led to the development of targeted therapies using tyrosine kinase inhibitors (TKIs). In this review, we document the history of TKI targeting, FLT3 and several other tyrosine kinases involved in dysregulated signaling pathways.

SUBMITTER: Fernandez S 

PROVIDER: S-EPMC6679203 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Targeting Tyrosine Kinases in Acute Myeloid Leukemia: Why, Who and How?

Fernandez Solène S   Desplat Vanessa V   Villacreces Arnaud A   Guitart Amélie V AV   Milpied Noël N   Pigneux Arnaud A   Vigon Isabelle I   Pasquet Jean-Max JM   Dumas Pierre-Yves PY  

International journal of molecular sciences 20190712 14


Acute myeloid leukemia (AML) is a myeloid malignancy carrying a heterogeneous molecular panel of mutations participating in the blockade of differentiation and the increased proliferation of myeloid hematopoietic stem and progenitor cells. The historical "3 + 7" treatment (cytarabine and daunorubicin) is currently challenged by new therapeutic strategies, including drugs depending on the molecular landscape of AML. This panel of mutations makes it possible to combine some of these new treatments  ...[more]

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