Eric B. Haura

The paper develops microtumor models from lung cancer samples to study EMT and metabolic changes, identifying fatty acid synthesis as a targetable vulnerability.

This study shows that stromal niches protect lung cancers from ALK inhibitors through multiple mechanisms, and targeting these mechanisms together is more effective than targeting them individually.

This paper identifies CYP3A4 hyperactivation as a tumor-extrinsic resistance mechanism in NSCLC, showing it reduces drug exposure and leads to resistance, and proposes dosing optimization and CYP3A4 inhibition as solutions.

This paper develops a computational framework combining molecular dynamics and machine learning to predict KRAS mutation-induced drug resistance with over 90% accuracy.

This study identifies that CAFs confer ALK inhibitor resistance in EML4-ALK-driven lung cancer through both MET and integrin signaling pathways, and shows that targeting both pathways improves treatment efficacy.

This study shows TAp73 regulates lipid metabolism in lung tumor microenvironment to enhance anti-tumor immunity through T-cell activation.

This study shows that combining RET and SRC inhibitors enhances anti-cancer effects in RET fusion-positive cancers by suppressing PAK signaling and restoring sensitivity in resistant cells.

This study shows that combining trastuzumab deruxtecan with sotorasib improves responses in KRASG12C-mutant NSCLC and overcomes resistance, but HER2 expression levels influence treatment effectiveness.

The paper quantifies tyrosine phosphorylation in FFPE tissues to reveal patient-specific signaling networks and identifies oncogenic kinases in cancer tumors.

This study shows that resistance to ALK inhibitors in lung cancer is unstable and dynamic, with collateral sensitivity to other drugs offering new treatment options.