Erratum to: The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST)
- Standort
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1479-5876
- Umfang
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Online-Ressource
- Sprache
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Englisch
- Anmerkungen
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online resource.
- Erschienen in
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Erratum to: The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST) ; volume:15 ; number:1 ; day:2 ; month:6 ; year:2017 ; pages:1 ; date:12.2017
Journal of translational medicine ; 15, Heft 1 (2.6.2017), 1, 12.2017
- Schlagwort
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Krebs
Onkologie
- Urheber
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Nannini, Margherita
- Beteiligte Personen und Organisationen
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Urbini, Milena
Astolf, Annalisa
Biasco, Guido
Pantaleo, Maria A.
SpringerLink (Online service)
- DOI
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10.1186/s12967-017-1228-2
- URN
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urn:nbn:de:1111-201707019339
- Rechteinformation
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Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
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15.08.2025, 07:27 MESZ
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Beteiligte
- Nannini, Margherita
- Urbini, Milena
- Astolf, Annalisa
- Biasco, Guido
- Pantaleo, Maria A.
- SpringerLink (Online service)
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Gene duplication, rather than epigenetic changes, drives FGF4 overexpression in KIT/PDGFRA/SDH/RAS-P WT GIST
V600E BRAF mutations are alternative early molecular events in a subset of KIT/PDGFRA wild-type gastrointestinal stromal tumours
Preferential MGMT methylation could predispose a subset of KIT/PDGFRA-WT GISTs, including SDH-deficient ones, to respond to alkylating agents
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REGISTRI: Regorafenib in first-line of KIT/PDGFRA wild type metastatic GIST: a collaborative Spanish (GEIS), Italian (ISG) and French Sarcoma Group (FSG) phase II trial
Avapritinib-based SAR studies unveil a binding pocket in KIT and PDGFRA
The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST)
Integrated genomic study of quadruple-WT GIST (KIT/PDGFRA/SDH/RAS pathway wild-type GIST)
The role of [68 Ga]Ga-DOTATATE PET/CT in wild-type KIT/PDGFRA gastrointestinal stromal tumours (GIST)
Succinate dehydrogenase deficiency in a PDGFRA mutated GIST
Gene duplication, rather than epigenetic changes, drives FGF4 overexpression in KIT/PDGFRA/SDH/RAS-P WT GIST
V600E BRAF mutations are alternative early molecular events in a subset of KIT/PDGFRA wild-type gastrointestinal stromal tumours
Preferential MGMT methylation could predispose a subset of KIT/PDGFRA-WT GISTs, including SDH-deficient ones, to respond to alkylating agents
KIT exon 11 and PDGFRA exon 18 gene mutations in gastric GIST: proposal of a short panel for predicting therapeutic response
Constitutive activation of oncogenic PDGFRα-mutant proteins occurring in GIST patients induces receptor mislocalisation and alters PDGFRα signalling characteristics
Biochemische und strukturbiologische Charakterisierung der Rezeptortyrosinkinasen KIT und PDGFRA
REGISTRI: Regorafenib in first-line of KIT/PDGFRA wild type metastatic GIST: a collaborative Spanish (GEIS), Italian (ISG) and French Sarcoma Group (FSG) phase II trial