Acute 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.
In Western countries, chronic lymphocytic leukemia (CLL) is one of the most diagnosed leukemia types among elderly patients. CLL is described as an indolent lymphoproliferative disorder, characterized by the presence of a high number of small, mature B-cells in the peripheral blood smear, with a particular immunophenotype (CD5, CD19, CD23 positive and CD20 dim positive) and accumulation in the bone marrow and lymphoid tissue (e.g., lymph nodes, spleen). The experience of the past decades showed that CLL is clinically very heterogeneous; while some patients present a chronic clinical evolution, with a prolonged survival, in which the treatment can be delayed, others suffer from a more aggressive form, which must be treated early and is associated with many relapses. This observation led to several genomic studies that have mapped the genetic modifications involved in the disease conformations, including del(13q14), del(11q), or trisomy 12. On the other hand, certain genetic mutations such as del(17p13)–p53, NOTCH1 mutation, or ZAP70/CD38 increased expression are associated with worse clinical outcome. In order to apply the right treatment strategy, the RAI and BINET staging systems should be considered, which are based on clinical and laboratory assessment, on genetic mutations that may influence the resistance to chemotherapy, as well as the patient’s age and comorbidities. The aim of this manuscript was to present the therapeutic approaches of CLL, in order to attempt to answer the following question: to treat, or not to treat? This clinical update focuses on the managements of CLL patients in the 21st century.