Identification of the APE1-redox function as a critical post-translational stabilizer of the SOX9 transcription factor in esophageal adenocarcinoma (EAC).
Mechanistic discovery that acidic bile salts, mimicking gastroesophageal reflux disease (GERD), activate the APE1-SOX9-ALDH1A1 signaling cascade.
Pharmacological inhibition of APE1’s redox activity using the small molecule APX2009 successfully reverses oxaliplatin resistance in patient-derived xenograft (PDX) models.
Clinical validation confirms that a high SOX9 molecular signature is a potent predictor of poor relapse-free survival in patients with EAC.
