Makiko Hayashi

This study identifies Rabgef1 as a regulator of gasdermin pore formation by controlling membrane cholesterol, showing cholesterol depletion restores pyroptosis in cancer cells and tumors.

This study identifies KEAP1 loss as a resistance mechanism to KRAS inhibitors in pancreatic and lung cancer and shows that combining glutamine inhibition with KRAS inhibitors can overcome this resistance.

This study shows that DRP-104, a glutamine antagonist, suppresses KEAP1 mutant lung tumor growth and enhances response to checkpoint blockade by inhibiting glutamine metabolism and improving T cell function.

The paper shows that inhibiting HDACs selectively targets NRF2-activated lung adenocarcinoma by altering chromatin and metabolic pathways.

This study identifies a LKB1-LIF signaling axis in tumors that promotes immune evasion by reprogramming myeloid cells, and shows that inhibiting LIF signaling reduces tumor growth.

The paper shows NRF2 activation in KEAP1 wildtype lung cancers causes NADH-reductive stress, making them vulnerable to Complex I inhibition.