Michael T. Hemann

This study identifies tumor-intrinsic stress states as modulators of CAR T cell therapy response in pancreatic cancer using CRISPR screens and single-cell genomics.

This study shows that physiological folate levels limit nucleotide synthesis in leukemia cells, making them reliant on salvage pathways for proliferation.

The paper maps CDK-drug interactions at single amino acid resolution using genome editing and computational analysis, identifying critical residues and resistance mechanisms.

This paper develops tumor-targeting gene drive vectors that eliminate drug resistance in solid tumors through systemic delivery, showing durable tumor burden reduction with minimal toxicity.

The paper identifies molecular determinants for phosphotyrosine recognition in tyrosine kinases and shows their roles in tumor promotion and suppression.

The paper uses in vivo base editing to systematically analyze the functional impact of genetic variants in cancer models, revealing context-dependent effects and limitations of CRISPR-Cas9.