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Venetoclax-based therapy with decitabine noted as preferred AML-6A Footnote ww modified: This regimen is for treatment of newly diagnosed AML in patients who are ≥75 years of age, or who have significant comorbid conditions (ie, severe cardiac disease, ECOG performance status ≥2, baseline ...
Interactions may exist between these mutations, collectively promoting disease progression. In mouse models, the combination of NUP98 fusion and FLT3-ITD alterations leads to a more aggressive form of leukemia with a shorter latency period. Consistent with this, the coexistence of NUP98 fusion and ...
In particular, recurrent mutations in spliceosome machinery and genome-wide aberrant splicing events have been recognized as a prominent component of this disease. This review will focus on how these factors influence drug resistance through altered splicing of tumor suppressor and oncogenes and ...
Although the landscape for treating acute myeloid leukemia (AML) patients has changed substantially in recent years, the majority of patients will eventually relapse and succumb to their disease. Allogeneic stem cell transplantation provides the best ant
APL is a very aggressive form of AML with a rapid disease progression. Currently, APL is a highly curable disease thanks to established therapeutic protocols based on the use of all-trans retinoic acid (ATRA) in combination with anthracyclines and, more recently, arsenic trioxide4,5 ,. The ...
[1,2]. Over the past decade, advances in next-generation sequencing (NGS) have greatly improved our understanding of the molecular heterogeneity of AML [3]. Driven by these discoveries, improved disease classification and several new promising targeted therapies for AML have been developed [4,5]...
immune system and the concomitant technical developments in ex vivo cell manipulation, the vision of funding bodies, the dedication of clinical and research staff, and above all the commitment of our patients, promise substantial progress in the treatment of this disease in the year 2000 and ...
Even in the context of loss ofFLT3-ITD at R/R disease, a mechanism of resistance to FLT3 inhibition is the emergence of clones with different mutations thanFLT3mutations, such as mutations in the RAS/MAPK signaling pathways found in patients with R/R disease after treatment with midostaurin in...
We apply single-cell RNA sequencing to paired pre- and post-chemotherapy whole bone marrow samples obtained from 13 pediatric AML patients who had achieved disease remission, and distinguish AML clusters from normal cells based on their unique transcriptomic profiles. Approximately 50% of leukemic stem...