Rohit Chandwani

This study investigates how different KRAS mutations drive distinct phenotypic outcomes in pancreatic tumorigenesis, revealing mutation-specific oncogenic pathways and therapeutic implications.

This paper develops a human organoid model of early PDAC that identifies genetic and epigenetic barriers to lineage plasticity, showing CDKN2A loss is essential with KRAS/TP53 mutations and TET1 suppression links ERK signaling to transcription factor silencing.

SAHA creates a multimodal, subcellular-resolution reference atlas of healthy human tissues, revealing spatial organization and disease-associated disruptions across multiple organ systems.

This study develops a pan-cancer PDO platform to preserve tumor heterogeneity and identify therapeutic vulnerabilities, finding that 58% of PDOs respond to Talazoparib and combination screens reveal resistance-overcoming drugs.