Abstract Oncogenic KIT or PDGFRA receptor tyrosine kinase mutations are compelling therapeutic targets in gastrointestinal stromal tumor (GIST), and treatment with the KIT/PDGFRA inhibitor imatinib is standard of care for patients advanced GIST. Polyclonal emergence secondary main mechanism progression, making it challenging to overcome KIT/PDGFRA-inhibitor resistance. It unclear whether there ...

Soil thickness, intended as depth to bedrock, is a key input parameter for many environmental models. Nevertheless, it often difficult obtain reliable spatially exhaustive soil thickness map in wide-area applications, and existing prediction models have been extensively applied only test sites with shallow depths. This study addresses this limitation by showing the results of an application sec...

BACKGROUND Imatinib, a selective tyrosine kinase inhibitor, has been used as a standard first-line therapy for irresectable and metastasized gastrointestinal stromal tumor (GIST) patients. Unfortunately, most patients responding to imatinib will eventually exhibit imatinib-resistance, the cause of which is not fully understood. The serious clinical problem of imatinib-resistance demands alterna...

Purpose: KIT is the major oncogenic driver of gastrointestinal stromal tumors (GIST). Imatinib, sunitinib, and regorafenib are approved therapies; however, efficacy is often limited by the acquisition of polyclonal secondary resistancemutations inKIT,with those located in the activation (A) loop (exons 17/ 18) being particularly problematic. Here, we explore the KIT-inhibitory activity of ponat...

BACKGROUND DOG1 is a novel gene on gastrointestinal stromal tumors (GISTs) that encodes the chloride channel protein anoctamin 1, also known as discovered on GIST-1 (DOG1) protein. DOG1 antibodies are a sensitive and specific marker against GIST positive for CD117 and CD34 and negative for CD117 and CD34. DOG1 is also independent of KIT or PDGFRA mutation status and considered specific for GIST...

Gastrointestinal stromal tumors (GIST) are thought to derive from the interstitial cells of Cajal (ICC) or an ICC precursor. Oncogenic mutations of the KIT or PDGFRA receptor tyrosine kinases are present in the majority of GIST, leading to ligand-independent activation of the intracellular signal transduction pathways. We previously investigated the gene expression profile in the murine Kit(K64...

OBJECTIVE To investigate the relationship between gene mutations and protein expressions of PDGFR α and C-kit in gastrointestinal stromal tumors (GIST) and its significance in tumorigenesis. METHODS Single strand conformation polymorphism-polymerase chain reaction (PCR-SSCP), immunohistochemistry and Western blot were used to detect the gene mutations in PDGFR α and C-kit and their protein ex...

Gastrointestinal stromal tumor (GIST) is a rare and therefore often neglected disease. Introduction of the kinase inhibitor imatinib mesylate radically improved the clinical response of patients with GIST; however, its effects are often short-lived, with GISTs demonstrating a median time-to-progression of approximately two years. Although many investigational drugs, approved first for other can...

BACKGROUND The diagnosis of gastrointestinal stromal tumors is based on documentation of c-KIT and platelet-derived growth factor-alpha receptors or specific c-KIT mutations. Before the diagnosis of GIST was possible, all cases had been classified as sarcomas or benign tumors. OBJECTIVES To identify cases of GIST formerly diagnosed as abdominal or retroperitoneal mesenchymal tumors. METHODS...

BACKGROUND Circulating tumor cells (CTC) are prognostic and predictive for several cancer types. Only limited data exist regarding prognostic or predictive impact of CTC on gastrointestinal stromal tumor (GIST) patients. The aim of our study was to elucidate the role of CTC in GIST patients. RESULTS A total of 121 GIST patients and 54 non-GIST samples were enrolled in the study. The cutoff va...