David J. Feith

This study shows that inhibiting acid ceramidase (AC) enhances venetoclax's effectiveness in venetoclax-resistant AML by inducing a cytotoxic integrated stress response.

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

This study identifies two sphingolipidomic subtypes in AML, with one subtype associated with poor clinical outcomes and high-risk features.

This study evaluates the anti-leukemic effects of LCL-805, an acid ceramidase inhibitor, in AML cell lines and patient samples, showing it promotes iron-dependent cell death by antagonizing Akt signaling.

The paper analyzes LGL leukemia patient genomes to detect retrovirus integration sites but finds no new retroviruses, instead identifying polymorphic HERV-K provirus sites more prevalent in LGL patients.