Lukas E. Dow

This study investigates how different KRAS mutations drive distinct phenotypic outcomes in pancreatic tumorigenesis, revealing mutation-specific oncogenic pathways and therapeutic implications.

This study identifies a stereotypic organization of pancreatic ductal adenocarcinoma cells based on WNT signaling and Notch ligand interactions, showing that disrupting this equilibrium suppresses tumor growth and metastasis.

This study identifies genetic and non-genetic resistance mechanisms to KRAS inhibition in CRC using single-cell spatial transcriptomics and exome sequencing, revealing inflammatory and fetal-like transcriptional signatures associated with resistance.

This study identifies genetic mechanisms of resistance to KRAS inhibitors by using CRISPR screens to find resistance mutations and signaling rewiring in NSCLC.

The paper identifies a TNKS2-selective inhibitor that enables tumor-selective WNT suppression by exploiting 8p loss in cancer cells.

The paper uses CRISPR-Cas9 screens in breast cancer organoids from African ancestry patients to identify essential kinases and show synergy between EGFR and FGFR1 inhibitors.

This study shows that FTSJ1-mediated tRNASec methylation enhances oxidative stress resistance and metastatic colonization in melanoma.

This study shows that loss of GPR52 in breast cancer cells increases cell clustering, EMT features, and tumor burden in zebrafish, suggesting GPR52 as a potential therapeutic target.

This study shows that KRAS inhibition in lung adenocarcinoma leads to an AT1-like cell state that drives resistance, and targeting these cells improves treatment response.

This study identifies miR-375 as a key regulator of intestinal crypt homeostasis, showing its role in stem cell proliferation, tuft cell abundance, and resistance to infection and cancer.

This study develops a rectal cancer organoid model that mimics patient tumor responses to chemoradiation and metastasis in mice.