Paresh Vyas

The paper identifies a human HSC subset with inflammatory memory that accumulates with age and clonal hematopoiesis, potentially increasing cancer and infection risks.

This paper identifies CD180 as a marker for chemoresistant stem-like blasts in KMT2A-rearranged paediatric AML, showing its absence on normal HSCs and its role as a therapeutic target.

This study shows that resistant clones are rapidly selected in hematopoietic cell compartments with leukemic stem cell potential before relapse in patients treated with ivosidenib combination therapy.

This paper introduces EPI-clone, a method using DNA methylation to trace clonal lineages in hematopoiesis without genetic engineering, showing clonal complexity declines with age in mice and expands in humans.

This study shows that MYB activity sustains enhancer-promoter interactions and transcription by maintaining enhancer function in leukemia.

This study performs genome-wide association analyses of congenital heart defects in Down syndrome, identifying suggestive loci associated with specific heart defect subtypes.

This study identifies how DNMT3A and TET2 mutations in hematopoietic stem cells confer a selective advantage by reducing inflammation and aging effects.

The paper shows HDAC inhibitors induce AML cell differentiation via two distinct mechanisms: one through G1 arrest and another through G2 arrest via Aurora A and GSK3 inhibition.

This study shows that IDH2 mutations in AML block differentiation by altering H3K27 methylation, and that Enasidenib can reverse this block by modulating chromatin states.

The paper identifies a distinct class of enhancers in leukemia cells that depend on H3K79 methylation and shows that DOT1L inhibition disrupts their function.