Linde A. Miles

This study identifies a resistance mechanism in AML leukemic stem cells to PI3K inhibition and shows that combining PI3K and EZH1/2 inhibitors overcomes resistance.

This study identifies BRAF mutations in AML, showing poor outcomes and unique co-mutation patterns, suggesting potential targeted therapies.

This study shows that genetic activation of ERK2 in mice models key neurodevelopmental features of Rasopathy syndromes, including cognitive impairments and facial dysmorphology.

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

This study identifies PTPN11 mutations as potential initiating events in AML when paired with NPM1 mutations, revealing their co-driver role and immune diversity in patient samples.

scDNA is a toolkit for analyzing single-cell DNA data to identify subclonal structures, mutation trajectories, and sample quality, with applications in cancer research.

This study identifies TTLL4 as a therapeutic target in NPM1-mutated AML by showing its role in stabilizing NPM1c and promoting differentiation block, with a small molecule inhibitor demonstrating efficacy.

The paper identifies changes in the bone marrow microenvironment during preleukemic stages of AML, including an expanded CD55+ fibroblast population that supports preleukemic stem cells over normal HSCs.

The paper identifies TMEM41B as a host factor required for flavivirus infection and shows SNPs in TMEM41B reduce infection in East Asian populations.