A Mind Map for Managing Minimal Residual Disease in Acute Myeloid Leukemia

  Abstract: Advances in detecting traces of leukemia that were previously unidentifiable have increasingly led to the incorporation of information about residual disease into clinical decision […]

Emerging Treatments in Acute Myeloid Leukemia: Current Standards and Unmet Challenges

  Abstract: Acute myeloid leukemia (AML) is rare and difficult to treat. Although remission is achieved in most patients with newly diagnosed disease, relapse occurs in […]

Hem/Onc News

Recombinant Factor IX Approved for Use in Adults and Children With Hemophilia B The US Food and Drug Administration (FDA) approved the recombinant coagulation factor IX […]

The Evolution of Allogeneic Stem Cell Transplant for Children and Adolescents With Acute Myeloid Leukemia

  Abstract: Survival rates in subsets of pediatric patients who have acute myeloid leukemia (AML) with favorable risk features are now greater than 90%. However, outcomes […]

FLT3 Inhibitors for the Treatment of Acute Myeloid Leukemia

Abstract: The fms-like receptor tyrosine kinase-3 (FLT3), which is important for the normal development of hematopoietic stem cells and cells of the immune system, is frequently mutated in patients with acute myeloid leukemia (AML). FLT3 is, therefore, a potential therapeutic target in AML. Recently, FLT3 inhibitors have shown therapeutic activity in AML patients with FLT3 mutations. Sorafenib and sunitinib were the first FLT3 inhibitors to be studied in the clinic and have the most clinically relevant data. Limited data are available for midostaurin (PKC412), lestaurtinib (CEP-701), tandutinib (MLN518), AC220, and KW-2449. It is likely that optimal application of these agents will involve combinations of inhibitors and combinations of inhibitors and chemotherapy, potentially with a mammalian target of rapamycin inhibitor such as everolimus or temsirolimus. This review discusses the theoretical rationale for the use of these agents and summarizes the relevant clinical data.