Mark David Minden

This study profiles circulating hematopoietic stem and progenitor cells in MPN patients, identifying transcriptional signatures and quantitative readouts to distinguish MF from other MPNs and predict progression.

This study shows glucocorticoids eliminate AML leukemic stem cells by inducing differentiation and apoptosis, with mechanisms involving the glucocorticoid receptor and inflammatory signatures.

This study identifies CD59 as a critical regulator of Ras-MAPK signaling in AML, showing its depletion impairs leukemic growth and identifies rILYd4 as a potential therapeutic target.

This study identifies MBD1-L, an aberrantly spliced transcript in MDS, which drives epigenetic changes leading to myeloerythroid defects, and shows ASO-based targeting can restore erythroid differentiation.

This study reassesses human mitochondrial DNA methylation using multiple platforms and finds signals likely due to technical artifacts rather than biological methylation.

This paper identifies an MPO-derived epitope promiscuously presented by HLA-II molecules and develops a pan-allelic antibody that selectively targets AML cells while sparing normal myeloid cells.

This study identifies DNA methylation instability in blood cells linked to aging and disease, showing age-related instability and associations with cardiovascular disease and cancer.

This study shows that hematopoietic Tet2 inactivation improves immune checkpoint blockade response in mice and is associated with better clinical outcomes in melanoma patients with TET2-driven clonal hematopoiesis.

This study investigates how DNMT3A-R882 mutations affect HSC differentiation into immune cells, finding they drive dysfunctional neutropoiesis linked to immune dysregulation and inflammatory disease risk.

This study identifies MECOM's role in blocking differentiation via CEBPA repression, showing that targeting this regulatory element can promote differentiation and reduce leukemia burden in AMLs.

This paper develops WT1-specific CAR T cells that recognize the WT1330-348 peptide across 18 HLA-II alleles, enabling broad therapeutic application.

The paper constructs a reference atlas of human hematopoiesis and maps AML differentiation patterns, revealing genetic and non-genetic factors driving aberrant differentiation in leukemia.

This study identifies a bioenergetic mechanism in AML cells where mitochondria consume ATP to resist chemotherapy, offering a target for improving treatment.

This study shows FLT3 is essential for ITD-mutated leukemic stem cells but not for normal hematopoietic stem cells, supporting targeted therapies for AML.

This study identifies stress granules as critical for AML stem cell survival and stress adaptation, revealing their role in gene regulation and potential as therapeutic targets.

This study identifies distinct gene regulatory networks in hematopoietic stem cells and leukemia stem cells using integrated gene expression and chromatin accessibility data from AML patients and human umbilical cord blood.

This study identifies epigenetic vulnerabilities in AML and MDS/MPN with EZH2 mutations, showing increased sensitivity to EZH2 and EED inhibitors and upregulation of cell death pathways.

SmMIP-tools processes and analyzes smMIP-derived sequencing data, enabling accurate variant detection and improving accessibility to smMIP technology for genetic research.

The paper identifies microhomology-mediated end joining (MMEJ) as the mechanism behind recurrent deletions in myeloid malignancies and shows that these deletions occur in multipotent hematopoietic stem cells.