ArticleCell reports2022
SDHB knockout and succinate accumulation are insufficient for tumorigenesis but dual SDHB/NF1 loss yields SDHx-like pheochromocytomas.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- PolyQ-expanded ataxin-3 is associated with mitochondrial alterations in Machado-Joseph disease.Disease models & mechanisms · 2026Article
- Genetic, cellular, and environmental factors influencing tumourigenesis in carriers of succinate dehydrogenase germline mutations.Endocrine-related cancer · 2026Review
- Gliomas with succinate dehydrogenase deficiency: A case series and brief review of the literature of oncometabolite-driven gliomagenesis.Journal of neuropathology and experimental neurology · 2026Review
- Succinate dehydrogenase loss suppresses pyrimidine biosynthesis via succinate-mediated inhibition of aspartate transcarbamylase.Nature metabolism · 2026Article
- Targeted lipidomics between hPheo1 and SDHB KD cells reveal changes in bioactive lipids and PKC with polyamine pathway inhibition.Physiological reports · 2026Article
- Succinate dehydrogenase-deficient cancer cells have increased susceptibility to Ym155-induced DNA damage.Endocrine-related cancer · 2026Article
- Mass spectrometry imaging tutorial: From cancer biomarker discovery to clinical applications.Analytica chimica acta · 2026Review
- Long-term culture of patient-derived pheochromocytoma organoids.Frontiers in endocrinology · 2026Article
- Coexisting PTEN and SDHB Mutations in a Pediatric Patient with PTEN Hamartoma Tumor Syndrome: a case report.Frontiers in pediatrics · 2026Article
- Metabolic Effects of Succinate Dehydrogenase Loss in Cancer.Journal of cellular physiology · 2025Review
- Incidence and risk factors for phaeochromocytoma diagnosis in dogs under primary veterinary care in the UK.PloS one · 2025Article
- Similar deficiencies, different outcomes: succinate dehydrogenase loss in adrenal medulla vs. fibroblast cell culture models of paraganglioma.Cancer & metabolism · 2024Article
- In-depth analysis of lymph node metastasis-related sialylated protein profiling and their clinical and biological significance in colorectal cancer using mass spectrometry and multi-omics technologies.Scientific reports · 2024Article
- Mouse developmental defects, but not paraganglioma tumorigenesis, upon conditional Complex II loss in early Sox10FASEB bioAdvances · 2024Article
- Characterisation of an Adult Zebrafish Model forInternational journal of molecular sciences · 2024Article
- Tumour immunogenicity goes with the (mitochondrial electron) flow.Molecular oncology · 2024Review
- Caution on the Use ofJCEM case reports · 2023Article
- Manipulating mitochondrial electron flow enhances tumor immunogenicity.Science (New York, N.Y.) · 2023Article
- The mitochondrial succinate dehydrogenase complex controls the STAT3-IL-10 pathway in inflammatory macrophages.iScience · 2023Article
- Proteolytic rewiring of mitochondria by LONP1 directs cell identity switching of adipocytes.Nature cell biology · 2023Article
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13 authors.
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Abstract
Inherited pathogenic succinate dehydrogenase (SDHx) gene mutations cause the hereditary pheochromocytoma and paraganglioma tumor syndrome. Syndromic tumors exhibit elevated succinate, an oncometabolite that is proposed to drive tumorigenesis via DNA and histone hypermethylation, mitochondrial expansion, and pseudohypoxia-related gene expression. To interrogate this prevailing model, we disrupt mouse adrenal medulla SDHB expression, which recapitulates several key molecular features of human SDHx tumors, including succinate accumulation but not 5hmC loss, HIF accumulation, or tumorigenesis. By contrast, concomitant SDHB and the neurofibromin 1 tumor suppressor disruption yields SDHx-like pheochromocytomas. Unexpectedly, in vivo depletion of the 2-oxoglutarate (2-OG) dioxygenase cofactor ascorbate reduces SDHB-deficient cell survival, indicating that SDHx loss may be better tolerated by tissues with high antioxidant capacity. Contrary to the prevailing oncometabolite model, succinate accumulation and 2-OG-dependent dioxygenase inhibition are insufficient for mouse pheochromocytoma tumorigenesis, which requires additional growth-regulatory pathway activation.
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