Although the study found lurbinectedin isn't promising, the presence of a chromosomal 11q21-23 abnormality may open doors in treating the disease.
Acute Myeloid Leukemia
Using mediation analysis, researchers were able to identify three gene expression markers that help explain the observed prognostic difference between certain AML patients.
Investigations into the CSF3R gene may help lead to better classification and precise treatment of AML.
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.
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.