Aaron N. Hata

This study identifies tyrosine phosphorylation and dimerization as cooperative mechanisms activating NAMPT, enhancing NAD+ synthesis and cancer cell growth.

This study identifies M1C as a driver of sotorasib resistance in NSCLC KRAS G12C mutant tumors and shows that targeting M1C improves treatment outcomes.

The paper introduces molecular COUPLrs to systematically target protein complexes, identifying new glue classes and their interactions in cancer cell lines.

The paper identifies oxidative protein states as drivers of metastatic fitness in lung cancer by linking ROS-regulated protein modifications to mitochondrial function and metastasis.

This study shows that a dual inhibitor of KRASG12C in both ON and OFF states more effectively suppresses tumor growth than an OFF-specific inhibitor by reducing PI3K-AKT activation.

This study shows that suppressing PP2A-B56α promotes EMT in EGFR mutant NSCLC by reducing epithelial markers and increasing mesenchymal markers, leading to migratory and invasive phenotypes.

The paper introduces ApoFLARE, a luminescent reporter that quantifies APOBEC3A editing activity in living cells, enabling time-resolved analysis of its kinetics and heterogeneity.

The paper identifies MTAP loss in 18% of NSCLC specimens and shows PRMT5 inhibitors are effective in MTAP-deleted tumors, with enhanced activity when combined with TKIs.

This study shows that KRASG12C inhibition induces chromosomal instability (CIN) in NSCLC cells, which synergizes with Aurora Kinase A inhibition to enhance therapeutic efficacy.

This study develops antibody-peptide epitope conjugates (APECs) to enhance anti-tumor activity in ICB-resistant HNSCC by leveraging viral peptide-loaded MHC I proteins and protease activity.

The paper shows genomic uracil induces DNA replication stress without BER processing and identifies UNG2 upregulation as a vulnerability in cancer cells.

DrugMap quantitatively analyzes cysteine ligandability across 416 cancer cell lines, revealing redox state, conformational changes, and mutations as drivers of variability, and identifies covalent inhibitors targeting NFκB1 and SOX10.

The paper shows NRF2 activation in KEAP1 wildtype lung cancers causes NADH-reductive stress, making them vulnerable to Complex I inhibition.

The paper develops a toolbox for scRNA-Seq and snRNA-Seq of fresh and frozen human tumors, testing it across eight tumor types and optimizing protocols for different tissue characteristics.