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Ivosidenib monotherapy demonstrates substantial efficacy and safety in IDH1 mutated myelodysplastic neoplasm, especially in treatment-naïve high-risk patients, offering a new therapeutic option.
Mutant IDH1 in acute myeloid leukemia causes a reversible block in neutrophil differentiation by repressing myeloid progenitor transcriptional programs, highlighting a preleukemic defect with therapeutic implications.
A comprehensive longitudinal ctDNA analysis of patients from the ClarIDHy phase III trial reveals that MAPK pathway alterations, including KRAS and NRAS mutations, are primary drivers of acquired resistance to ivosidenib by suppressing crit
