Gene duplication, rather than epigenetic changes, drives FGF4 overexpression in KIT/PDGFRA/SDH/RAS-P WT GIST

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 2045-2322

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Gene duplication, rather than epigenetic changes, drives FGF4 overexpression in KIT/PDGFRA/SDH/RAS-P WT GIST ; volume:10 ; number:1 ; day:16 ; month:11 ; year:2020 ; pages:1-7 ; date:12.2020
Scientific reports ; 10, Heft 1 (16.11.2020), 1-7, 12.2020

Creator: Urbini, Milena
Astolfi, Annalisa
Indio, Valentina
Nannini, Margherita
Schipani, Angela
Bacalini, Maria Giulia
Angelini, Sabrina
Ravegnini, Gloria
Calice, Giovanni
Del Gaudio, Massimo
Secchiero, Paola
Ulivi, Paola
Gruppioni, Elisa
Pantaleo, Maria Abbondanza

Contributor: SpringerLink (Online service)

DOI: 10.1038/s41598-020-76519-y

URN: urn:nbn:de:101:1-2020122022385576251258

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:38 AM CEST

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Associated

Urbini, Milena
Astolfi, Annalisa
Indio, Valentina
Nannini, Margherita
Schipani, Angela
Bacalini, Maria Giulia
Angelini, Sabrina
Ravegnini, Gloria
Calice, Giovanni
Del Gaudio, Massimo
Secchiero, Paola
Ulivi, Paola
Gruppioni, Elisa
Pantaleo, Maria Abbondanza
SpringerLink (Online service)

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Gene duplication, rather than epigenetic changes, drives FGF4 overexpression in KIT/PDGFRA/SDH/RAS-P WT GIST

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Other Objects (12)

Integrated genomic study of quadruple-WT GIST (KIT/PDGFRA/SDH/RAS pathway wild-type GIST)

The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST)

Succinate dehydrogenase deficiency in a PDGFRA mutated GIST

Erratum to: The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST)

The role of [68 Ga]Ga-DOTATATE PET/CT in wild-type KIT/PDGFRA gastrointestinal stromal tumours (GIST)

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

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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

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The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST)

Succinate dehydrogenase deficiency in a PDGFRA mutated GIST

Erratum to: The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST)

The role of [68 Ga]Ga-DOTATATE PET/CT in wild-type KIT/PDGFRA gastrointestinal stromal tumours (GIST)

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

Avapritinib-based SAR studies unveil a binding pocket in KIT and PDGFRA

PDGFRA, KIT, and KDR Gene Amplification in Glioblastoma: Heterogeneity and Clinical Significance

Integrated genomic study of quadruple-WT GIST (KIT/PDGFRA/SDH/RAS pathway wild-type GIST)

The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST)

Succinate dehydrogenase deficiency in a PDGFRA mutated GIST

Erratum to: The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST)

The role of [68 Ga]Ga-DOTATATE PET/CT in wild-type KIT/PDGFRA gastrointestinal stromal tumours (GIST)

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

Avapritinib-based SAR studies unveil a binding pocket in KIT and PDGFRA

PDGFRA, KIT, and KDR Gene Amplification in Glioblastoma: Heterogeneity and Clinical Significance

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