Articles related to ACUTE MYELOID LEUKEMIA (AML)

In an integrated analysis of mutations and clinical outcomes, comprising 2,200 patients with TP53-mutated myelodysplastic syndrome (MDS) with excess blasts (EB) or TP53-mutated acute myeloid leukemia (AML), the authors state that mutant TP53 AML and MDS-EB “do not differ with respect to molecular characteristics and survival” and argue these entities should be considered a single molecular disease entity. In a commentary to the above paper, TP53 and the star-crossed lovers MDS and AML, John Welch, MD, PhD of Washington University School of Medicine writes, “As a junior Hematology/Oncology fellow, I was told there were two types of physicians: splitters and mergers. That is, clinicians either seek to diagnose increasingly homogenously narrow groups of patients based on increasingly refined, shared characteristics, or they seek to find broad, overarching patterns that unite diagnostic classifications. Hematologic malignancies have been fertile ground for the diagnostic splitters of the world. On the other hand, there have been some noteworthy exceptions. Sometimes it is a technological advance that allows for the synthesis of disparate diagnoses.”

Outcomes from the large PETHEMA registry study shows that secondary AML is common (27% of AML cases) and has a median OS of 5.6 months vs. 10.9 months for primary AML, and has various differing characteristics compared to primary AML. These include older age at diagnosis, more high-risk cytogenetics, less FMS-like tyrosine kinase three internal tandem duplication, fewer NPM1 mutations, and received a lower intensity of chemotherapy.

In this series from Blood that tackles four cases studies, the outcomes of AML pediatric patients compared to children with ALL is explored, focusing on the emerging new treatments venetoclax (Venclexta; AbbVie/Genentech), CD33- and CD123-directed CAR T-cell therapy, CD123-directed antibody therapy, and menin inhibitors.

About 75% to 80% of children with pediatric AML have clonal, acquired, somatic cytogenetic abnormalities (CAs) detected. Hematology Advisor briefs the information originally appearing in Genes, which reviews the current knowledge on evaluating pediatric patients based on cytogenetics and molecular subtypes to help match patients to risk-adapted therapies.

Key Points: In two study cohorts, less-intensive therapies increased mortality in each of three risk groups defined by age, comorbidities, and cytogenetics. The differences became nonsignificant after accounting for physician perception of cure, emphasizing the need for a randomized trial.Design: Multicenter retrospective cohort (1,292), 6 institutions, 2008-2012; prospective cohort (695), 13 institutions, 2013 – 2017Connected Content: Fitness for Intensive Chemotherapy: A Continuing Conundrum

In this Clinical Advances in Hematology & Oncology Q&A with Dr. Tapan M. Kadia, an associate professor at the MD Anderson Cancer Center, the current treatments for acute myeloid leukemia (AML) are discussed, with a specific focus on the targeted FLT3 approach, the role of the gene in AML, the differences among the approved FLT3 inhibitors, and why newer FLT3 inhibitors are needed.