In a large international study, pre-AML cases had greater clonal expansion and enrichment of specific gene mutations; origins of AML were detected > 5 years before it developed.
Acute Myeloid Leukemia
A preclinical study of ibrutinib provides compelling evidence that myeloid leukemias with mutated G-CSFR have abnormal activation of Btk.
Strong efficacy and safety outcomes with this agent, which targets the molecular driver of an AML subset, have led to its approval in IDH1-mutated R/R disease.
In the emerging era of personalized treatment, it may be time to rethink which surrogate markers are used in AML clinical trials.
This study is the first to show significantly improved OS from single-agent treatment in this particularly difficult to treat population.
Unconventional strategies and targeted therapeutics may be required to overcome the adverse risks associated with TP53-mutated AML.
This approach may lead to better understanding of risk-mitigation strategies, and perhaps better outcomes in patients with secondary AML.
Implications of Mutation Profiling in Myeloid Malignancies—PART 1: Myelodysplastic Syndromes and Acute Myeloid Leukemia
In this first part of our two-part review, we introduce mutation profiling as a relevant clinical tool for hematologists treating patients with myeloid malignancies.
Researchers have discovered that AML cells require high levels of cholesterol for survival, so the cholesterol pathway could represent a potential therapeutic option for the disease.
The novel agent ivosidenib is well tolerated and induces durable responses in patients with relapsed/refractory acute myeloid leukemia and other hematologic malignancies.