Issues
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Primary acute myeloid leukemia (AML) cells are notoriously difficult to culture, which remains a limitation in modeling the disease. In this issue, Kotini, Carcamo, Cruz-Rodriguez et al. demonstrate a large-scale approach to renewable propagation of human AML cells by reprogramming them into induced pluripotent stem cells (iPSC). With the exception of NPM1-mutant leukemia, all major genetic subtypes of the disease are amenable to reprogramming. When transplanted into mice, iPSC-derived AML cells give rise to serially transplantable leukemia mirroring immunophenotypes of the donor. These results suggest that leukemia is determined largely by the genetic lesions, as epigenetic factors were presumably erased by the reprogramming process. iPSC-AML grafts sustain multilineage hematopoiesis in vivo, currently unattainable with normal iPSC-derived hematopoietic stem and progenitor cells. The diverse range of AML-iPSC lines generated in this study is an important resource for further research in this field. For details, please see the article by Kotini, Carcamo, Cruz-Rodriguez et al. on page 318. - PDF Icon PDF LinkTable of Contents
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In This Issue
In the Spotlight
Cancer Hallmarks Reviews
Research Articles
A Phase Ib/II Study of Ivosidenib with Venetoclax ± Azacitidine in IDH1-Mutated Myeloid Malignancies
Ivodesinib and venetoclax with or without azacitidine are safe and effective against IDH1-mutated myeloid cancers, with molecular correlates illustrating potential resistance-limiting mechanisms of combination therapy.
The Polyamine–Hypusine Circuit Controls an Oncogenic Translational Program Essential for Malignant Conversion in MYC-Driven Lymphoma
Hypusination of the eIF5A translation factor is necessary for the development and maintenance of MYC-driven lymphoma, where hypusinated eIF5A controls the translation of factors that are essential for cell-cycle transit and DNA replication.
Patient-Derived iPSCs Faithfully Represent the Genetic Diversity and Cellular Architecture of Human Acute Myeloid Leukemia
A collection of iPSC lines derived from AML patients capture leukemia genomes and phenotypes and produce xenografts nearly identical to the matched primary PDXs. iPSCs from different AML clones uniquely empower the study of subclonal mutations.
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