Ask about this productRelated genes to: SDHB antibody
- Gene:
- SDHB NIH gene
- Name:
- succinate dehydrogenase complex iron sulfur subunit B
- Previous symbol:
- SDH1, SDH
- Synonyms:
- -
- Chromosome:
- 1p36.13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: SDHB antibody
Related articles to: SDHB antibody
- Copyright: © 2026 Speyer et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Gastrointestinal stromal tumors (GISTs) are molecularly defined by oncogenic alterations that predict clinical behavior and response to therapy. Activating mutations in KIT or PDGFRA characterize most GISTs and confer sensitivity to imatinib, whereas succinate dehydrogenase (SDH)–deficient GISTs lack these mutations and are typically imatinib resistant. These molecular subtypes are generally considered mutually exclusive. We report a rare case of a small bowel GIST harboring both a somatic KIT exon 9 A502_Y503 duplication and a germline inactivating SDHC mutation (p.R50C). The patient received neoadjuvant high-dose imatinib with a marked radiographic and metabolic response, followed by complete surgical resection. Pathology demonstrated spindle cell GIST with significant treatment effect and retained SDHB expression. This case suggests that oncogenic KIT signaling may remain the dominant driver of GIST behavior despite the presence of a germline SDHC mutation and highlights the importance of integrated molecular interpretation in GIST management. - Source: PubMed
Speyer Cameron BKlingbeil Kyle DNakasaki ManandoDry Sarah MSingh Arun SArzoo Karo KEilber Fritz CCrompton Joseph G - PPGL are rare neuroendocrine tumors that secrete catecholamines. There are over 20 driver mutations associated with PPGL. All patients who have been diagnosed with PPGL need genetic testing. Diagnosis is made by checking either plasma or urine metanephrines. Localization studies include computed tomography, magnetic resonance imaging, and functional imaging such as positron emission tomography scans. Alpha-blockers are a central component for preparation prior to surgical removal of the tumor, which is the mainstay of therapy. For patients with metastatic disease, several different modalities can be employed from palliative surgery, chemotherapy, radionuclide therapy, HIF-2α inhibitor, and drugs in clinical trials. - Source: PubMed
Publication date: 2026/03/13
Alkaissi HussamTaieb DavidGhayee Hans K - Resveratrol (Res), a natural polyphenolic compound, exhibits multiple antitumor activities against acute myeloid leukemia (AML), though its mechanisms remain incompletely understood. In this study, CCK-8 assay, CFSE flow cytometry, Transwell assays, and flow cytometry assessed proliferation, invasion, migration, and programmed cell death in MV4-11 and MOLM-13 leukemic cell lines. Western blotting examined cell death regulatory factors (Cleaved-caspase 3/caspase 3, Bax, Bcl-2), aerobic glycolysis proteins (GLUT1, HK2, LDHA, PKM2), cuproptosis-related proteins (FDX1, DLAT, Lip-DLAT, DLST, Lip-DLST, HSP70, SDHB), and PI3K/AKT pathway proteins (p-PI3K/PI3K, p-AKT/AKT). Intracellular Cu⁺ levels were measured colorimetrically, while glucose uptake, lactate, and ATP levels were quantified to evaluate cellular metabolism. Mechanistic investigations utilized PFKFB3 overexpression, PI3K activator (740 Y-P), and inhibitor (LY294002) intervention experiments. The antitumor efficacy of Res was validated in an AML xenograft mouse model. Res significantly inhibited AML cell proliferation, invasion, and migration while promoting apoptosis. It markedly downregulated FDX1, Lip-DLAT, Lip-DLST, and SDHB while upregulating HSP70 and intracellular Cu⁺, inducing cuproptosis-an effect reversible by the cuproptosis inhibitor TTM. Res reduced glucose uptake, lactate production, ATP generation, and downregulated GLUT1, HK2, LDHA, and PKM2, thereby suppressing aerobic glycolysis-a process reversed by PFKFB3 overexpression. Furthermore, Res inhibited PI3K and AKT phosphorylation; the PI3K activator 740 Y-P counteracted Res-mediated effects while the PI3K inhibitor LY294002 enhanced them. In vivo experiments confirmed that Res treatment markedly diminished tumor size and mass, lowered Ki-67 proliferation marker, enhanced programmed cell death, suppressed PI3K/AKT signaling, decreased glycolytic enzyme levels, and elevated copper-dependent cell death mediators. Res exerts anti-AML effects by inhibiting the PI3K/AKT pathway while coordinately regulating aerobic glycolysis and cuproptosis in AML cells. - Source: PubMed
Publication date: 2026/04/30
Lian ChengLiu YanhuiLei Pingchong - Pheochromocytoma and paraganglioma (PPGL) are rare neuroendocrine tumors with unique biological behavior and remarkably high heritability, yet dedicated bioinformatics resources for these diagnoses remain limited. Existing cancer multi-omics platforms are pan-cancer in scope, often lacking the disease-specific annotations, granularity, and cross-database harmonization required for meaningful stratification and hypothesis generation. Here we introduce PPGLomics, an interactive web-based platform designed for comprehensive PPGL transcriptomics analysis. PPGLomics v1.0 integrates two major datasets, the TCGA-PCPG cohort (n=160) spanning multiple molecular subtypes, and the A5 consortium SDHB cohort (n=91) with detailed clinicopathological and molecular annotations. The platform provides basic and clinical scientists, as well as a broad range of healthcare professionals, with tools for differential expression analysis, correlation analysis, survival analysis, and visualization, including boxplots, heatmaps, volcano plots, and Kaplan-Meier survival plots, enabling exploration of gene expression patterns across PPGL subtypes without requiring bioinformatics expertise. PPGLomics v1.0 is freely available at https://alkaissilab.shinyapps.io/PPGLomics. - Source: PubMed
Publication date: 2026/02/03
Alkaissi HussamGordon Catherine MPacak Karel - Approximately 5% of pituitary adenomas (PA) are familial, linked to germline variants in AIP, or syndrome-related genes like MEN1. While somatic GNAS and USP8 variants predominate in specific subtypes, PAM and CABLES1 genes are emerging. - Source: PubMed
Martinez de Lapiscina IdoiaBaquero CandelaSantos AliciaMolina Ana RosaMoure Maria DoloresAramburu MaiteBancalari RodrigoBoronat MauroBueno GloriaCasano-Sancho PaulaFernandez-Ramos ConcepcionGarcia-Garcia EmilioGonzalez AmparoGonzalez-Rivera NatividadGuerrero-Fernandez JulioHernandez Maria IsabelPaja MiguelPortillo NancyRica ItxasoSoto-Moreno AlfonsoSuarez-Ortega LarisaVela AmaiaCastaño LuisValdes Nuria