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Renal Cancer
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Sabrina H. Rossi, Grant D. Stewart
Gene function:Succinate dehydrogenase (SDH): tetrameric enzyme in the Krebs cycle, upstream to fumarate hydratase.Each four SDH subunits are encoded by four genes:SDHA, SDHB, SDHC, and SDHDMutations in the SDHB gene are the most common.
Tropical Herbs and Spices as Functional Foods with Antidiabetic Activities
Published in Megh R. Goyal, Arijit Nath, Rasul Hafiz Ansar Suleria, Plant-Based Functional Foods and Phytochemicals, 2021
Arnia Sari Mukaromah, Fitria Susilowati
Arun and Nalini [11] have reported the efficacy of turmeric and curcumin on diabetic rats. The results indicated that the injection of turmeric or curcumin reduced the blood glucose levels, Hb, and glycosylated hemoglobin levels. The supplementation of turmeric and curcumin also diminished the oxidative stress chain in diabetes-induced mice, possibly due to a decrease in the influx of blood glucose into the polyol pathway. It is associated with an increase of NADPH/NADP ratio and enhanced activity of the antioxidant enzyme, i.e., glucose peroxidase. Additionally, the activity of succinate dehydrogenase was reduced significantly due to turmeric or curcumin therapy [11].
Endocrine and Neuroendocrine Tumors
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Natasha Shrikrishnapalasuriyar, P.N. Plowman, Márta Korbonits, Ashley B. Grossman
Previously, only 10% of cases were identified as an inherited origin; however, recently some 30% of such tumors have been shown to be of a germline mutation in at least 20 genes.63 Germline mutations in different genes have been found to cause familial pheochromocytomas. Succinate dehydrogenase (SDH) mutations are frequent cause of familial pheochromocytomas. SDH mutations occur on different subunits B, D, C, A, and AF2 (Table 5.3),64 with SDHB mutations showing a particularly aggressive course and a high incidence of malignancy. Hereditary pheochromocytomas are frequently found in MEN2 and syndromes (50%) with an autosomal dominant pattern with mutations in the RET proto-oncogene, as noted earlier: These are almost always benign, and frequently bilateral.
Antioxidant activity of calcitriol reduces direct methamphetamine-induced mitochondrial dysfunction in isolated rat heart mitochondria
Published in Toxin Reviews, 2022
Ahmad Salimi, Morteza Minouei, Mohsen Niknejad, Elham Mojarad Aylar
The mitochondrial complex II or succinate dehydrogenase activity was measured through MTT reduction at 570 nm. Briefly, mitochondria (1000 µg/ml) were incubated in a 96 well plate with total volume of 100 µl/well, in assay buffer (10 mmol/L NaCl, 140 mmol/L KCL, 0.5 mmol/L KH2PO4, 2 mmol/L MgCl2, 0.5 mmol/L EGTA, 20 mmol/L HEPES; supplemented with 10 mmol/L succinate and 1 mg/mL rotenone at pH 7.4). Then isolated cardiac mitochondria were treated with different concentrations of methamphetamine (1, 5, 10, 50, 100 and 500 µM). Succinate dehydrogenase activity was evaluated after 1 h of exposure. To test the effect of calcitriol against methamphetamine-induced mitochondrial toxicity, the isolated cardiac mitochondria were treated with various concentrations of calcitriol (1, 2.5 and 5 µM) and 250 µM methamphetamine. After 1 h of incubation was added 0.4% MTT and incubated at 37 °C for 30 min. Finally, the formazan crystals were dissolved in 100 µl DMSO and the optical density was measured at 570 nm (Mersa et al.2020).
Deciding on the duration of adjuvant therapy in gastrointestinal stromal tumor
Published in Expert Review of Anticancer Therapy, 2021
Peter Whooley, Erika Correa, Margaret von Mehren
Pathologically, were first characterized as having both smooth muscle and neural features [2]. They can have a spindle, epitheliod or mixed histology [3]. Tumor cells express the KIT protein, also known as CD117, as well as CD34, DOG-1, and SMA; rarely is desmin expression observed. Most GIST are driven by activating mutations in two structurally related tyrosine kinase receptors, KIT (~85%) and Platelet Growth Factor Alpha (PDGFRA) (~5%). Alternative drivers identified include mutations in BRAF and NF-1, as well as translocations involving NTRK [4]. Tumors arising in the stomach may have abnormalities of Succinate Dehydrogenase (SDH) genes, recognized by the loss of staining for SDHB by immunohistochemistry, and are referred to as SDH deficient GIST. The loss of expression of SDHB is a consequence of either mutations in one of the SDH genes, A, B, C, or D, or due to altered methylation of the SDHC promoter [5,6].
Prevalence of succinate dehydrogenase deficiency in paragangliomas and phaeochromocytomas at a tertiary hospital in Cape Town: a retrospective review
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2021
Cassandra Bruce-Brand, Abraham C van Wyk
PGLs and PCs can occur sporadically or as hereditary tumours with up to 40% occurring as a result of germline mutations in susceptibility genes.2,3 Research conducted in the nineteenth and twentieth centuries led to the recognition of three PC/PGL-associated syndromes: von Hippel-Lindau (VHL) disease, multiple endocrine neoplasia type 2 (RET) and neurofibromatosis type 1 (NF1).4–9 Between 2000 and 2010, the molecular basis for hereditary PC/PGL syndrome was discovered to be due to mutations in succinate dehydrogenase (SDH) subunits and related genes.10–16 New susceptibility genes causing hereditary PC/PGL syndrome discovered over the past ten years included MAX, TMEM127, EGLN, HIF2α, MET and KIF1B.2 Currently these susceptibility genes are grouped into two categories: major susceptibility genes including NF1, VHL, RET and SHDB/D and minor susceptibility genes including SDHA/C, SDHAF2, MAX and TMEM127.3,17 The major susceptibility genes account for up to 90% of the hereditary tumours, the minor group accounts for the other 10%.3,17