G. Schwank

Treatment of a genetic liver disease in mice through transient prime editor expression

This paper demonstrates transient prime editor expression in mice to correct a genetic liver disease, reducing blood phenylalanine levels below the therapeutic threshold.

Mutant SF3B1 promotes PDAC malignancy through TGF-β resistance

This study shows that SF3B1K700E mutation in PDAC enhances tumor aggressiveness when combined with KRAS and p53 mutations by promoting TGF-β resistance.

Loss of Rnf31 and Vps4b sensitizes pancreatic cancer to T cell-mediated killing

This study identifies Rnf31 and Vps4b as factors enabling pancreatic cancer to evade T cell killing, showing their inactivation increases T cell-mediated tumor cell death.

SF3B1 promotes tumor malignancy through splicing-independent co-activation of HIF1α

This study shows SF3B1 promotes tumor malignancy by co-activating HIF1α through a splicing-independent mechanism, enhancing hypoxia response element binding and target gene expression.

Replacing the SpCas9 HNH domain by deaminases generates compact base editors with an alternative targeting scope

This study replaces the SpCas9 HNH domain with deaminases to create smaller base editors with expanded targeting scope.

Characterization of HIF-dependent alternative isoforms in pancreatic cancer

The paper identifies HIF-dependent alternative splicing events in pancreatic cancer cells under hypoxia and validates a novel long coding isoform of SLC35A3.