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To complement the few existing AML cell lines and restricted primografts, we transplanted more than 100 primary AML samples into immunocompromised mice and generated 23 exceptionally robust patient\u2010derived xenograft (*PDX) models of AML that allow virtually unlimited serial transplantation and efficient genetic engineering. These models represent individuals of all age groups and several WHO subgroups. *PDX models substantially outperform AML cell lines in preserving leukemia biology and include AML subgroups for which no cell lines exist, such as cytogenetically normal or\n                    <jats:italic>IDH1\/2<\/jats:italic>\n                    \u2010mutant AML or simultaneous\n                    <jats:italic>NPM1<\/jats:italic>\n                    mutation and\n                    <jats:italic>FLT3\u2010<\/jats:italic>\n                    ITD. Their resilience to freeze\u2010thaw cycles supports broad dissemination across research institutions through sharing via CancerModels.org. Using lentiviruses, we stably expressed luciferase for longitudinal, noninvasive, and sensitive real\u2010time monitoring of leukemia burden and therapeutic response\n                    <jats:italic>in vivo<\/jats:italic>\n                    . This approach enabled rigorously controlled preclinical studies, including phase II\u2010like trials, which demonstrated highly variable treatment responses between different *PDX models, mimicking the heterogeneity in patient cohorts. Long\u2010term treatment, including repeated cytarabine exposure over 1 year, showed a yet undescribed decrease in leukemia's proliferation rate. These insights underscore the platform's distinctive capacity to study treatment dynamics over clinically relevant timeframes. 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