Hereditary succinate dehydrogenase-deficient renal cell carcinoma

Rogala, Joanna; Zhou, Ming

doi:10.1053/j.semdp.2023.11.001

Seminars in Diagnostic Pathology

2024

DOI: 10.1053/j.semdp.2023.11.001

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Hereditary succinate dehydrogenase-deficient renal cell carcinoma

Joanna Rogala,

Ming Zhou

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2024

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Cited by 3 publications

References 70 publications

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Morphological diversity in SDH-deficient renal carcinomas: a three-case exploration of variant features and dedifferentiation

Sánta,

Dabaghian,

Pósfai

et al. 2024

Virchows Arch

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Morphological diversity in SDH-deficient renal carcinomas: a three-case exploration of variant features and dedifferentiation

Sánta,

Dabaghian,

Pósfai

et al. 2024

Virchows Arch

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Tumors with germline mutations in succinate dehydrogenase genes

Mikhaylenko,

Semyanikhinа,

Zagidullina3

2024

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Facts, Dogmas, and Unknowns About Mitochondrial Reactive Oxygen Species in Cancer

Junco,

Ventura,

Santiago Valtierra

et al. 2024

Antioxidants

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Cancer metabolism is sustained both by enhanced aerobic glycolysis, characteristic of the Warburg phenotype, and oxidative metabolism. Cell survival and proliferation depends on a dynamic equilibrium between mitochondrial function and glycolysis, which is heterogeneous between tumors and even within the same tumor. During oxidative phosphorylation, electrons from NADH and FADH2 originated in the tricarboxylic acid cycle flow through complexes of the electron transport chain. Single electron leaks at specific complexes of the electron transport chain generate reactive oxygen species (ROS). ROS are a concentration-dependent double-edged sword that plays multifaceted roles in cancer metabolism. ROS serve either as signaling molecules favoring cellular homeostasis and proliferation or damage DNA, protein and lipids, causing cell death. Several aspects of ROS biology still remain unsolved. Among the unknowns are the actual levels at which ROS become cytotoxic and if toxicity depends on specific ROS species or if it is caused by a cumulative effect of all of them. In this review, we describe mechanisms of mitochondrial ROS production, detoxification, ROS-induced cytotoxicity, and the use of antioxidants in cancer treatment. We also provide updated information about critical questions on the biology of ROS on cancer metabolism and discuss dogmas that lack adequate experimental demonstration. Overall, this review brings a comprehensive perspective of ROS as drivers of cancer progression, inducers of cell death, and the potential use of antioxidants as anticancer therapy.

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Hereditary succinate dehydrogenase-deficient renal cell carcinoma

Cited by 3 publications

References 70 publications

Morphological diversity in SDH-deficient renal carcinomas: a three-case exploration of variant features and dedifferentiation

Morphological diversity in SDH-deficient renal carcinomas: a three-case exploration of variant features and dedifferentiation

Tumors with germline mutations in succinate dehydrogenase genes

Facts, Dogmas, and Unknowns About Mitochondrial Reactive Oxygen Species in Cancer

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