Daniel T. Starczynowski

This study shows that inhibiting UBE2N in myeloid cells reduces YUMM1.7 melanoma growth by altering immune checkpoint molecules and SPP1 expression.

This study uses single-cell multiomic analysis to reveal genotype-immunophenotype relationships and clonal evolution in NPM1-mutant AML across disease stages.

The paper introduces a fluorescence-based method to quantify drug-target engagement in temperature series using split-RNase S complementation.

This study shows MYD88 mutations in clonal hematopoiesis drive inflammation and HSPC expansion by activating NF-κB pathways and promoting myeloid bias.

The paper shows that inhibiting UBE2N in Tregs enhances anti-tumor immunity without causing autoimmunity by converting Tregs into effector-like cells.

The paper identifies a splicing mechanism in AML independent of mutations, showing it drives poor prognosis and can be targeted with PRMT5 inhibition.