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Multi-omic analysis of SDHB-deficient pheochromocytomas and paragangliomas identifies metastasis and treatment-related molecular profiles

Title: Multi-omic analysis of SDHB-deficient pheochromocytomas and paragangliomas identifies metastasis and treatment-related molecular profiles
Authors: Flynn, Aidan; Pattison, Andrew David; Balachander, Shiva; Boehm, Emma; Bowen, Blake; Dwight, Trisha; Rossello, F. J.; Hofmann, Oliver M.; Martelotto, Luciano G.; Zethoven, Magnus; Kirschner, Lawrence S.; Else, Tobias; Fishbein, Lauren; Gill, Anthony J.; Tischler, Arthur S.; Giordano, Thomas J.; Prodanov, Tamara; Noble, Jane R.; Reddel, Roger R.; Trainer, Alison H.; Ghayee, Hans Kumar; Bourdeau, Isabelle; Elston, Marianne S.; Ishak, Diana; Ngeow Yuen Yie, Joanne; Hicks, Rodney J.; Crona, Joakim; Åkerström, Tobias; Stal̊berg, Peter L.H.; Dahia, Patricia; Grimmond, Sean M.; Clifton-Bligh, Roderick J.; Pacak, Karel; Tothill, Richard William
Contributors: Lee Kong Chian School of Medicine (LKCMedicine)
Publication Year: 2025
Collection: DR-NTU (Digital Repository at Nanyang Technological University, Singapore)
Subject Terms: Medicine; Health and Life Sciences
Description: Hereditary SDHB-mutant pheochromocytomas (PC) and paragangliomas (PG) are rare tumours with a high propensity to metastasize although their clinical behaviour is unpredictable. To characterize the genomic landscape of these tumours and identify metastasis biomarkers, we perform multi-omic analysis on 94 tumours from 79 patients using seven molecular methods. Sympathetic (chromaffin cell) and parasympathetic (non-chromaffin cell) PCPG have distinct molecular profiles reflecting their cell-of-origin and biochemical profile. TERT and ATRX-alterations are associated with metastatic PCPG and these tumours have an increased mutation load, and distinct transcriptional and telomeric features. Most PCPG have quiet genomes with some rare co-operative driver events, including EPAS1/HIF-2α mutations. Two mechanisms of acquired resistance to DNA alkylating chemotherapies are identifiable; MGMT overexpression and mismatch repair-deficiency causing hypermutation. Our comprehensive multi-omic analysis of SDHB-mutant PCPG therefore identifies features of metastatic disease and treatment response, expanding our understanding of these rare neuroendocrine tumours.
Document Type: article in journal/newspaper
Language: English
Relation: Nature Communications; https://hdl.handle.net/10356/209491; 16; 2632
DOI: 10.1038/s41467-025-57595-y
Availability: https://hdl.handle.net/10356/209491; https://doi.org/10.1038/s41467-025-57595-y
Rights: © 2025 Nature Research. All rights reserved.
Accession Number: edsbas.8A0EFCA2
Database: BASE