Sara J. Adair

The paper develops a method to compare multiple cell types in xenograft tumors using unique PCR tags and qPCR, enabling direct comparison within tumors without relying on tumor size.

This study identifies DRP1 reactivation as a mechanism of resistance to MEK inhibition in pancreatic cancer cells and shows that inhibiting DRP1 can restore sensitivity to trametinib.

The paper identifies genes with increased expression despite copy number reduction in cancer, highlighting mitotic genes and potential therapeutic targets.

The paper identifies ERK as a dominant driver of EMT heterogeneity in pancreas cancer cells using mutual information modeling and imaging, showing its role is independent of MEK inhibition and growth factors.

The paper shows hypoxic fibroblasts in pancreas cancer use histone methylation and ROS-mediated NF-κB activation to produce growth factors that drive epithelial-mesenchymal transition in malignant cells.

This study identifies ISL2 as an epigenetically silenced tumor suppressor in pancreatic cancer that regulates metabolism and presents therapeutic vulnerabilities.