<b>Background:</b> Overexpression of dedicator of cytokinesis 1 (<i>DOCK</i>1) has been confirmed as an unfavorable prognostic marker in acute myeloid leukemia (AML).
<b>Conclusion</b>: This study indicates that melatonin, alone or in combination with sorafenib, has potential to improve the therapeutic outcome of AML patients with FLT3-ITD mutation that merits further investigation.
<b>Materials & methods:</b> The prevalence of NER genetic variants was evaluated in 67 subjects with AML and their effects on clinical outcomes were analyzed by χ<sup>2</sup> test.
<b>Objective</b>: We report the characterization of MCLA-117, a novel T cell-redirecting antibody for acute myeloid leukaemia (AML) treatment targeting CD3 on T cells and CLEC12A on leukaemic cells.
<b>Purpose:</b> c-KIT overexpression is well recognized in cancers such as gastrointestinal stromal tumors (GIST), small cell lung cancer (SCLC), melanoma, non-small cell lung cancer (NSCLC), and acute myelogenous leukemia (AML).
<b>Purpose:</b> Flotetuzumab (MGD006 or S80880) is a bispecific molecule that recognizes CD3 and CD123 membrane proteins, redirecting T cells to kill CD123-expressing cells for the treatment of acute myeloid leukemia.
<b/> AG-221 or enasidenib is a first-in-class selective inhibitor of mutated isocitrate dehydrogenase 2 (IDH2) with early demonstrated clinical efficacy in acute myeloid leukemia as a single agent, yet with persistence of mutant <i>IDH2</i> clones.
<i>RUNX1-RUNX1T1</i> transcript levels were established as a powerful marker for predicting relapse in patients with t(8;21) acute myeloid leukemia (AML).
<i>FUS-ERG</i> rearranged AML (n = 31) had no predominant French-American-British (FAB) type, whereas 76% of <i>RUNX1-CBFA2T3</i> had an M1/M2 FAB type (M1, M2), significantly different from the reference cohort (<i>P</i> = .004).
<i>FBXO9</i>, the substrate recognition component from the SCF E3 ubiquitin ligase family, is downregulated in patients with acute myeloid leukemia (AML) compared to healthy bone marrow, and this downregulation is particularly evident in patients with inv(16) AML.
<i>FBXO9</i>, the substrate recognition component from the SCF E3 ubiquitin ligase family, is downregulated in patients with acute myeloid leukemia (AML) compared to healthy bone marrow, and this downregulation is particularly evident in patients with inv(16) AML.
<i>FBXO9</i>, the substrate recognition component from the SCF E3 ubiquitin ligase family, is downregulated in patients with acute myeloid leukemia (AML) compared to healthy bone marrow, and this downregulation is particularly evident in patients with inv(16) AML.
<i>FBXO9</i>, the substrate recognition component from the SCF E3 ubiquitin ligase family, is downregulated in patients with acute myeloid leukemia (AML) compared to healthy bone marrow, and this downregulation is particularly evident in patients with inv(16) AML.
<i>FUS-ERG</i> rearranged AML (n = 31) had no predominant French-American-British (FAB) type, whereas 76% of <i>RUNX1-CBFA2T3</i> had an M1/M2 FAB type (M1, M2), significantly different from the reference cohort (<i>P</i> = .004).
<i>IDH</i> mutations seemed not to affect overall survival (OS: HR, 1.05; 95% CI, 0.89-1.23) and event-free survival (EFS: HR, 0.97; 95% CI, 0.80-1.18) when considered as a single factor, but improved accumulative incidence of relapse (CIR: HR, 1.44; 95% CI, 1.18-1.76) in patients with intermediate-risk karyotypes (IR-AML).
<i>IDH</i> mutations seemed not to affect overall survival (OS: HR, 1.05; 95% CI, 0.89-1.23) and event-free survival (EFS: HR, 0.97; 95% CI, 0.80-1.18) when considered as a single factor, but improved accumulative incidence of relapse (CIR: HR, 1.44; 95% CI, 1.18-1.76) in patients with intermediate-risk karyotypes (IR-AML).
<i>IDH</i> mutations seemed not to affect overall survival (OS: HR, 1.05; 95% CI, 0.89-1.23) and event-free survival (EFS: HR, 0.97; 95% CI, 0.80-1.18) when considered as a single factor, but improved accumulative incidence of relapse (CIR: HR, 1.44; 95% CI, 1.18-1.76) in patients with intermediate-risk karyotypes (IR-AML).