ArticleJournal of Cancer2011
Succinate Dehydrogenase Subunit B (SDHB) Is Expressed in Neurofibromatosis 1-Associated Gastrointestinal Stromal Tumors (Gists): Implications for the SDHB Expression Based Classification of Gists.
Article in Journal of Cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Gastrointestinal stromal tumors associated with neurofibromatosis 1: a single centre experience and systematic review of the literature including 252 cases.International journal of surgical oncology · 2013Pooled it
- Systems Biology Approaches Reveal Potential Phenotype-Modifier Genes in Neurofibromatosis Type 1.Cancers · 2020Article
- Abdominal neoplastic manifestations of neurofibromatosis type 1.Neuro-oncology advances · 2020Review
- Advanced pharmacological therapies for neurofibromatosis type 1-related tumors.Acta bio-medica : Atenei Parmensis · 2020Article
- A Huge Pelvic-Abdominal Malignant GIST Tumour in a Patient with Neurofibromatosis Type 1: Case Report and Literature Review.Case reports in oncological medicine · 2020Article
- Oncogene mutational analysis in Chinese gastrointestinal stromal tumor patients.OncoTargets and therapy · 2018Article
- Succinate dehydrogenase deficiency in a PDGFRA mutated GIST.BMC cancer · 2017Review
- Somatic loss of function mutations in neurofibromin 1 and MYC associated factor X genes identified by exome-wide sequencing in a wild-type GIST case.BMC cancer · 2015Article
- Novel oncogene and tumor suppressor mutations in KIT and PDGFRA wild type gastrointestinal stromal tumors revealed by next generation sequencing.Genes, chromosomes & cancer · 2015Article
- The genetic landscape of gastrointestinal stromal tumor lacking KIT and PDGFRA mutations.Endocrine · 2014Review
- Succinate dehydrogenase deficient gastrointestinal stromal tumors (GISTs) - a review.The international journal of biochemistry & cell biology · 2014Review
- Analysis of all subunits, SDHA, SDHB, SDHC, SDHD, of the succinate dehydrogenase complex in KIT/PDGFRA wild-type GIST.European journal of human genetics : EJHG · 2014Article
- cAMP/PKA signaling defects in tumors: genetics and tissue-specific pluripotential cell-derived lesions in human and mouse.Molecular and cellular endocrinology · 2013Review
- Rapid diagnosis of combined multifocal gastrointestinal stromal tumours and coeliac disease in a patient with type 1 neurofibromatosis.JRSM short reports · 2013Article
- Gastrointestinal manifestations of neurofibromatosis type 1 (Recklinghausen's disease): clinicopathological spectrum with pathogenetic considerations.International journal of clinical and experimental pathology · 2012Review
- Succinate dehydrogenase-deficient GISTs: a clinicopathologic, immunohistochemical, and molecular genetic study of 66 gastric GISTs with predilection to young age.The American journal of surgical pathology · 2011Article
- Multifocal gastric gastrointestinal stromal tumors (GISTs) with lymph node metastases in children and young adults: a comparative clinical and histomorphological study of three cases including a new case of Carney triad.Diagnostic pathology · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastrointestinal Stromal Tumor (GIST) is the most common mesenchymal tumor of the digestive tract. GISTs develop with relatively high incidence in patients with Neurofibromatosis-1 syndrome (NF1). Mutational activation of KIT or PDGFRA is believed to be a driving force in the pathogenesis of familial and sporadic GISTs. Unlike those tumors, NF1-associated GISTs do not have KIT or PGDFRA mutations. Similarly, no mutational activation of KIT or PDGFRA has been identified in pediatric GISTs and in GISTs associated with Carney Triad and Carney-Stratakis Syndrome. KIT and PDGFRA-wild type tumors are expected to have lesser response to imatinib treatment. Recently, Carney Triad and Carney-Stratakis Syndrome -associated GISTs and pediatric GISTs have been shown to have a loss of expression of succinate dehydrogenase subunit B (SDHB), a Krebs cycle/electron transport chain interface protein. It was proposed that GISTs can be divided into SDHB- positive (type 1), and SDHB-negative (type 2) tumors because of similarities in clinical features and response to imatinib treatment. In this study, SDHB expression was examined immunohistochemically in 22 well-characterized NF1-associated GISTs. All analyzed tumors expressed SDHB. Based on SDHB-expression status, NF1-associated GISTs belong to type 1 category; however, similarly to SDHB type 2 tumors, they do not respond well to imatinib treatment. Therefore, a simple categorization of GISTs into SDHB-positive and-negative seems to be incomplete. A classification based on both SDHB expression status and KIT and PDGFRA mutation status characterize GISTs more accurately and allow subdivision of SDHB-positive tumors into different clinico-genetic categories.
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