Silvia von Karstedt

This study identifies NMD inhibition as a therapeutic strategy for SCLC by enhancing immunogenicity and improving immunotherapy efficacy through increased neoantigen presentation.

The paper identifies metabolic differences between ASCL1-high and low SCLC cells, showing that ASCL1-high cells resist ferroptosis via BH4/BH2 antioxidants and are vulnerable to combined cysteine depletion and BH4/BH2 inhibition.

The paper models how population growth and ROS levels interact to determine ferroptosis sensitivity, revealing feedback loops and steady states in cellular behavior.

This study identifies GLRX3 as a vulnerability in Ewing sarcoma driven by EWSR1::FLI1 fusion oncoproteins, showing its role in oxidative stress and iron homeostasis and potential therapeutic targeting.

The paper identifies ferroptosis sensitivity as a distinguishing feature of non-neuroendocrine SCLC subtypes and shows that combining ferroptosis induction with TRX pathway inhibition can selectively kill both non-NE and NE SCLC tumors.