Abstract Library

#4194 Temozolomide treatment induces an MMR-dependent hypermutator phenotype in well-differentiated pancreatic neuroendocrine tumors

Introduction: Temozolomide (TMZ), an alkylating agent, is an effective treatment used in multiple tumor types including advanced pancreatic neuroendocrine tumors (PanNET). In glioblastomas, TMZ induces a hypermutator and hyperprogressor phenotype in a subset of patients through MMR deficiency. In advanced colon cancer, TMZ priming increases tumor mutational burden (TMB), favouring immunotherapy efficacy.

Conference:

Presenting Author: de Mestier L

Authors: de Mestier L, Cohen D, de Rycke O, Masliah Planchon J, Fleischmann Z,

Keywords: temozolomide, hypermutation, pancreatic neuroendocrine tumor,

#3471 A novel in vitro spheroid model enables multi-modality assessment of the anti-tumoral immune response in pancreatic neuroendocrine neoplasms

Introduction: Patients harbouring pancreatic neuroendocrine neoplasms (PNENs) often present as a non-resectable disease due to distant metastases, hence, efficacy of the current medical intervention is limited. Activation of the mammalian target of rapamycin (mTOR) pathway is a known tumorigenic driver in PNENs. mTOR inhibition by Everolimus (EVE) delays PNEN progression, but the mechanism is not clear. EVE is also used as an immunosuppressant, thus we hypothesized that it may suppress the anti-tumoral immune response.

Conference:

Presenting Author:

Authors: Nasirov S, Zaig E, Mor-Cohen R, Telerman A, Tirosh A,

Keywords: PNEN, spheroid, Everolimus, mTOR,

#3188 mTOR pathway inhibitors differently effect proliferation and gene expression in pancreatic and pulmonary NET cell lines

Introduction: The mammalian target of rapamycin (mTOR) is part of the PI3K/Akt/mTOR signalling pathway which has a central role in the oncogenesis of neuroendocrine tumors (NETs). Everolimus (EVE), an mTOR inhibitor, has shown effective in delaying progression of advanced NETs, but with a limited long-term efficacy, possibly due to a compensatory activation of the PI3K/AKT signalling. BYL719, a PI3K inhibitor, was shown to inhibit growth of several NET cell line models.

Conference: 18th Annual ENETS Concerence (2021)

Presenting Author: Mor-Cohen R

Authors: Mor-Cohen R, Braiman N, Tirosh A,

Keywords: NET cell lines, PI3K/Akt/mTOR signalling, Wnt signalling, everolimus, BYL719,

#2217 Prognostic Impact of CHOI Response Criteria Compared to RECIST in Grade 1-2 Advanced Pancreatic Neuroendocrine Tumors (CRIPNET-GETNE Study-NCT02841865)

Introduction: Response Evaluation Criteria In Solid Tumors (RECIST) are not presumably the most optimal option for predicting the benefit of antiangiogenic drugs in neuroendocrine tumors (NETs), given that tumor shrinkage is not frequent, and qualitative changes in tumor tissues are to be expected.

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author:

Authors: Carmona-Bayonas A, Fernandez del Valle A, Solis M, Matos I, Garcia-Carbonero R,

Keywords: CHOI criteria, pancreatic neuroendocrine tumor, RECIST, response, survival,

#838 Succinate Dehydrogenase Subunit B (SDHB) Immunohistochemistry Should Not Replace Clinical Genetic Testing for SDHx Mutations in Patients with Pheochromocytoma and Paraganglioma

Introduction: Mutations in any of the subunits of the succinate dehydrogenase (SDH) complex predispose to PCC/PGL. Knowing the germline mutation is important for surveillance for recurrence, metastatic disease or more primary tumors and for screening affected family members. Expression of SDHB protein by immunohistochemistry (IHC) has been proposed as a surrogate marker for SDHx mutation status, with absent or decreased expression of SDHB suggesting the presence of a germline SDHB mutation or disruption of the SDH complex by mutation in another subunit.

Conference: 11th Annual ENETSConcerence (2014)

Presenting Author:

Authors: Fishbein L, Bennett B, Merrill S, Cohen D, LiVolsi V,

Keywords: Pheo, succinate dehydrogenase,