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• W2778917529 endingPage "91" @default.
• W2778917529 startingPage "74" @default.
• W2778917529 abstract "Over 99% of all gastrointestinal stromal tumors (GISTs) can be attributed to genetic or epigenetic alterations with only a few cases remaining unclassified. Succinate dehydrogenase (SDH) subunit B (SDHB) immunostaining can be used to classify GISTs, categorizing them into either a SDH-competent cluster with a normal methylation pattern or a SDH-deficient cluster with a hypermethylator phenotype. SDH-deficient GISTs are familial or syndromic in more than 90% of patients. Imatinib has limited activity in SDH-deficient GISTs. Hypermethylation of the SDHC gene promoter region is the molecular signature of the Carney triad. Hypermethylation of the SDHC gene promoter region was found by epigenetic profiling to also be present in mostly pediatric wild-type GISTs. Surveillance for paragangliomas and other tumors is indicated for patients with inherited SDH-deficient GISTs. The discovery of activated KIT mutations in gastrointestinal (GI) stromal tumors (GISTs) in 1998 triggered a sea change in our understanding of these tumors and has ushered in a new paradigm for the use of molecular genetic diagnostics to guide targeted therapies. KIT and PDGFRA mutations account for 85–90% of GISTs; subsequent genetic studies have led to the identification of mutation/epimutation of additional genes, including the succinate dehydrogenase (SDH) subunit A, B, C, and D genes. This review focuses on integrating findings from clinicopathologic, genetic, and epigenetic studies, which classify GISTs into two distinct clusters: an SDH-competent group and an SDH-deficient group. This development is important since it revolutionizes our current management of affected patients and their relatives, fundamentally, based on the GIST genotype. The discovery of activated KIT mutations in gastrointestinal (GI) stromal tumors (GISTs) in 1998 triggered a sea change in our understanding of these tumors and has ushered in a new paradigm for the use of molecular genetic diagnostics to guide targeted therapies. KIT and PDGFRA mutations account for 85–90% of GISTs; subsequent genetic studies have led to the identification of mutation/epimutation of additional genes, including the succinate dehydrogenase (SDH) subunit A, B, C, and D genes. This review focuses on integrating findings from clinicopathologic, genetic, and epigenetic studies, which classify GISTs into two distinct clusters: an SDH-competent group and an SDH-deficient group. This development is important since it revolutionizes our current management of affected patients and their relatives, fundamentally, based on the GIST genotype." @default.
• W2778917529 created "2018-01-05" @default.
• W2778917529 creator A5003947656 @default.
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• W2778917529 date "2018-01-01" @default.
• W2778917529 modified "2023-10-09" @default.
• W2778917529 title "Gastrointestinal Stromal Tumors: The GIST of Precision Medicine" @default.
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