Alina Batzilla

This study develops an iPSC-based model with enhanced endothelial identity to study malaria parasite interactions and pathogenesis in vitro.

The paper investigates how innate immune responses to Plasmodium falciparum contribute to blood-brain barrier disruption in cerebral malaria using an in vitro model.

This study shows that Plasmodium falciparum egress products disrupt BBB endothelial junctions and activate JAK-STAT signaling, leading to increased permeability and suggesting therapeutic targets.

The paper develops a method to infer tumor-specific molecular dependencies by integrating drug response assays with protein-drug affinity profiles, identifying known and novel dependencies in cancer types.