{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T08:04:07Z","timestamp":1790409847107,"version":"4.1.0"},"reference-count":159,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2019,5,6]],"date-time":"2019-05-06T00:00:00Z","timestamp":1557100800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Genetics"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Succinate dehydrogenase (SDH) mutations lead to the accumulation of succinate, which acts as an oncometabolite. Germline\n                    <jats:italic>SDHx<\/jats:italic>\n                    mutations predispose to paraganglioma (PGL) and pheochromocytoma (PCC), as well as to renal cell carcinoma and gastro\u2010intestinal stromal tumors. The\n                    <jats:italic>SDHx<\/jats:italic>\n                    genes were the first tumor suppressor genes discovered which encode for a mitochondrial enzyme, thereby supporting Otto Warburg's hypothesis in 1926 that a direct link existed between mitochondrial dysfunction and cancer. Accumulation of succinate is the hallmark of tumorigenesis in PGL and PCC. Succinate accumulation inhibits several \u03b1\u2010ketoglutarate dioxygenases, thereby inducing the pseudohypoxia pathway and causing epigenetic changes. Moreover, SDH loss as a consequence of\n                    <jats:italic>SDHx<\/jats:italic>\n                    mutations can lead to reprogramming of cell metabolism. Metabolomics can be used as a diagnostic tool, as succinate and other metabolites can be measured in tumor tissue, plasma and urine with different techniques. Furthermore, these pathophysiological characteristics provide insight into therapeutic targets for metastatic disease. This review provides an overview of the pathophysiology and clinical implications of oncometabolite succinate in\n                    <jats:italic>SDHx<\/jats:italic>\n                    mutations.\n                  <\/jats:p>","DOI":"10.1111\/cge.13553","type":"journal-article","created":{"date-parts":[[2019,4,12]],"date-time":"2019-04-12T07:18:23Z","timestamp":1555053503000},"page":"39-53","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":72,"title":["Clinical implications of the oncometabolite succinate in\n                    <i>SDHx<\/i>\n                    \u2010mutation carriers"],"prefix":"10.1111","volume":"97","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3597-1803","authenticated-orcid":false,"given":"Karin","family":"Eijkelenkamp","sequence":"first","affiliation":[{"name":"Department of Endocrinology and Metabolic Diseases University Medical Center Groningen, University of Groningen  Groningen the 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