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Prognosis of Patients with Acute Myeloid Leukemia Regarding the Presence FLT3 Gene Mutation – a Case Report

Prognosis of Patients with Acute Myeloid Leukemia Regarding the Presence FLT3 Gene Mutation – a... AbstractAcute myeloid leukemia (AML) is a cancerous disease affecting the myeloid line of the bone marrow cells. FLT3, also known as CD135, is a proto-oncogene, which, if mutated, leads to different types of cancer. The protein it encodes presents tyrosine-kinase activity, and its intratandem mutation, FLT3-ITD, leads to uncontrolled proliferation of myeloblasts and worse outcomes in AML patients. There are currently several pharmacological agents that can inhibit the effect of either the proteins with tyrosine-kinase activity or the mutated FLT3 gene. We present the case of a 68-year-old patient, smoker, with a history of arterial hypertension, chronic obstructive pulmonary disease, presenting with headache unresponsive to antalgics, dyspnea after physical exertion, and epistaxis, with onset 2 months prior to his presentation. The patient was diagnosed with AML with positive FTL3 mutation for which conventional induction therapy was initiated. Within the next days, the patient presented several complications related to the disease itself or caused by the treatment, which eventually led to his death. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Interdisciplinary Medicine de Gruyter

Prognosis of Patients with Acute Myeloid Leukemia Regarding the Presence FLT3 Gene Mutation – a Case Report

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Publisher
de Gruyter
Copyright
© 2017 Árpád Bzduch et al., published by De Gruyter Open
ISSN
2501-5974
eISSN
2501-8132
DOI
10.1515/jim-2017-0096
Publisher site
See Article on Publisher Site

Abstract

AbstractAcute myeloid leukemia (AML) is a cancerous disease affecting the myeloid line of the bone marrow cells. FLT3, also known as CD135, is a proto-oncogene, which, if mutated, leads to different types of cancer. The protein it encodes presents tyrosine-kinase activity, and its intratandem mutation, FLT3-ITD, leads to uncontrolled proliferation of myeloblasts and worse outcomes in AML patients. There are currently several pharmacological agents that can inhibit the effect of either the proteins with tyrosine-kinase activity or the mutated FLT3 gene. We present the case of a 68-year-old patient, smoker, with a history of arterial hypertension, chronic obstructive pulmonary disease, presenting with headache unresponsive to antalgics, dyspnea after physical exertion, and epistaxis, with onset 2 months prior to his presentation. The patient was diagnosed with AML with positive FTL3 mutation for which conventional induction therapy was initiated. Within the next days, the patient presented several complications related to the disease itself or caused by the treatment, which eventually led to his death.

Journal

Journal of Interdisciplinary Medicine – de Gruyter

Published: Dec 1, 2017

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