Abstract Library

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#4378 Hypoxic signalling in pancreatic NETs (pNETs)

Introduction: In a genomic profiling study conducted as part of the COMPOSE Phase III multicentre open-labelled clinical trial we assessed 9 pNET patients, 2 of which showed upregulation of CA9 and hypoxic signalling. Hypoxic tumour cells present CA9 for extracellular proton channelling, maintenance of intracellular pH and to acidify and thereby vascularise and immune-suppress the TME. In normoxia, EGLN1-3 hydroxylate proline residues of HIF1A for its subsequent ubiquitination by the VHL-complex resulting in degradation and repression of its target genes.

Conference:

Presenting Author: Walter T

Authors: Walter T, Smutna V, Srirajaskanthan R, Capdevila J, Qin Y,

Keywords: hypoxia, pNET, HIF1A, CA9, Case study, hypoxic, genomic profiling,

#1124 Correlation Between the 18F-FDG Uptake and Pathological Data in Well-Differentiated Digestive and Pulmonary Neuroendocrine Tumors (NET)

Introduction: The 18F-FDG uptake assessed by PET/CT is correlated to prognosis in most tumors.

Conference: 12th Annual ENETSConcerence (2015)

Presenting Author:

Authors: Bucau M, Laurent-Bellue A, Cros J, Hentic O, Rebours V,

Keywords: Neuroendocrine tumors, PET-scan, 18-FDG, Ki67, VHL, metabolism,

#362 Succinate Dehydrogenase (SDH) Complex Expression in Pancreatic Endocrine Tumours (PETs)

Introduction: Absence of SDH subunit D (SDHD) mutations were reported by Perren et al (Oncogene 2002) but loss of heterozigosity (LOH) was described in 29% of the PETs. Since SDHD gene may depict a form of genomic imprinting in neuroendocrine (NE) tissue, the reported LOH may drive activation of the hypoxia pathway. Taking advantage from the immunohistochemical (IHC) method for genetic triage we may deduce the mutational status of SDH subunits (A, B, C and D) based on IHC SDHB expression. These subunits are striking candidates as they are mutated in other NE neoplasias.

Conference:

Presenting Author:

Authors: Vinagre J, Preto J, Soares P, Lopes J,

Keywords: PETs SDH LOH,