Searchable abstracts of presentations at key conferences in endocrinology

ea0089b4 | Basic Science | NANETS2022

Simultaneous Inhibition of DNA Methylation and Histone De-acetylation for Enhanced SSTR2 Expression In Vitro

Whitt Jason , Houson Hailey , Guenter Rachael , Murphy Madisen , Lapi Suzanne , Jaskula-Sztul Renata

Background: Neuroendocrine tumor (NET) patients with diminished SSTR2 expre-ssion are not eligible for any type of SSTR2-specific imaging or treatment. Herein, we propose to epigenetically enhance and enable somatostatin receptor type 2 (SSTR2)-targeted theranostics for patients with NETs. Specifically, we have found that simultaneous inhibition of DNA methylation and his-tone de-ace-tylation enhanced SSTR2 expression and in vitro binding of [68Ga]DOTATATE....

ea0098b11 | Basic Science | NANETS2023

The Notch1 pathway is a critical regulator of SSTR2 expression in neuroendocrine tumors

Guenter Rachael , Whitt Jason , Chen Weisheng , Houson Hailey , Bart Rose J. , Chen Herbert , Lapi Suzanne , Jaskula-Sztul Renata

Background: Patients with neuroendocrine tumors (NETs) have a 5-year survival rate of 30-60%. Surgery, and newly approved ‘tar-geted radionuclide therapy (TRT)’ with [177Lu]DOTATATE, are the only curative options for patients with NETs. TRT is limited to pa--tients that have high levels of somatostatin receptor subtype 2 (SSTR2) and can im-prove the survival of patients with low-grade tumors, but has little effect on high-grade NETs that express low SSTR2 ...

ea0098b12 | Basic Science | NANETS2023

Notch1 receptor-mediated metabolic flexibility promotes a survival advantage in pancreatic neuroendocrine neoplasms

Chen Weisheng , Guenter Rachael , Herring Brendon , Golivi Yuvasri , Whitt Jason , Sammy Melissa , Adams Cole , Jaskula-Sztul Renata , Chen Herbert , Rose Bart

Background: Cancer cells utilize both oxidative phosphorylation (OXPHOS) and glycolysis to generate energy. Switching between OXPHOS and glycolysis can promote tumor progression. The mechanisms governing oncogenic metabolic flexibility are largely unknown, but recent data has suggested that Notch1 dysregulation in cancer cells can contribute to altered metabolic phenotypes. We hypothesized that Notch1 signaling supports metabolic flexibility in pancreatic neuroendocrine tumor ...