A. G. Turhan

This study uses patient-derived iPSCs with in vitro mutagenesis to model genomic instability in CML, identifying aberrations linked to blast crisis progression.

This study shows that BCR-ABL expression in murine ESCs promotes the formation and maintenance of hematopoietic progenitors with a molecular signature similar to wild-type HSCs.

This study shows miR-495-3p reduces CML cell growth and TKI resistance by targeting MDR1, especially in T315I-mutant cells, and identifies it as a potential therapeutic target.

This study identifies ENOX2 as a BCR-ABL1-dependent secreted redox protein upregulated in CML, with increased expression in patient plasma and cell lines.