Associated Papers
Impact of Molecular Evaluations in the Biology, Diagnosis, and Prognostication of Patients With Mastocytosis.
Hoermann G et al.
The Journal of Allergy and Clinical Immunology. in Practice, 2026
Comprehensive molecular landscape of anal squamous cell carcinoma: analysis of tissue and liquid biopsies from 1844 patients.
Smolenschi C et al.
Npj Precision Oncology, 2025
Effects of first‑line therapies in patients with locally advanced gastrointestinal stromal tumors with KIT and PDGFRα gene mutations: A single‑center study.
Su WC et al.
Oncology Letters, 2025
ctDNA-based liquid biopsy reveals wider mutational profile with therapy resistance and metastasis susceptibility signatures in early-stage breast cancer patients.
Bharde A et al.
The Journal of Liquid Biopsy, 2025
Protein Tyrosine Phosphatase Non-Receptor 11 (PTPN11/Shp2) as a Driver Oncogene and a Novel Therapeutic Target in Non-Small Cell Lung Cancer (NSCLC).
Richards CE et al.
International Journal of Molecular Sciences, 2023
Clinicopathological and mutational characteristics of primary double mutant gastrointestinal stromal tumor: a single center study with review of the literature.
Yan J et al.
Bmc Cancer, 2023
Clinical and genomic correlates of imatinib response in melanomas with KIT alterations.
Jung S et al.
British Journal of Cancer, 2022
A literature review and database of how the primary KIT/PDGFRA variant of a gastrointestinal stromal tumour predicts for sensitivity to imatinib.
Wong NACS et al.
Cancer Genetics, 2022
Utility of plasma cell-free DNA for de novo detection and quantification of clonal hematopoiesis.
Gutierrez-Rodrigues F et al.
Haematologica, 2022
The novel KIT exon 11 germline mutation K558N is associated with gastrointestinal stromal tumor, mastocytosis, and seminoma development.
Meir M et al.
Genes, Chromosomes & Cancer, 2021
SF3B1, NRAS, KIT, and BRAF Mutation; CD117 and cMYC Expression; and Tumoral Pigmentation in Sinonasal Melanomas: An Analysis With Newly Found Molecular Alterations and Some Population-Based Molecular Differences.
Wroblewska JP et al.
The American Journal of Surgical Pathology, 2019
Circulating Cell-Free Tumor DNA Analysis of 50 Genes by Next-Generation Sequencing in the Prospective MOSCATO Trial.
Jovelet C et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2016
Morphologic shift associated with aberrant cytokeratin expression in a GIST patient after tyrosine kinase inhibitors therapy. A case report with a brief review of the literature.
Canzonieri V et al.
Pathology, Research and Practice, 2016
Small Cell Carcinoma of the Urinary Bladder: KIT and PDGFRA Gene Mutations.
Eliyakin N et al.
Rare Tumors, 2015
Frequent mono-allelic loss associated with deficient PTEN expression in imatinib-resistant gastrointestinal stromal tumors.
Quattrone A et al.
Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, 2014
Rapid relapse after resection of a sunitinib-resistant gastrointestinal stromal tumor harboring a secondary mutation in exon 13 of the c-KIT gene.
Kikuchi H et al.
Anticancer Research, 2012
Multiplex mutation screening by mass spectrometry in gastrointestinal stromal tumours.
Kang G et al.
Pathology, 2012
Tyrosine-kinase mutations in c-KIT and PDGFR-alpha genes of imatinib naïve adult patients with gastrointestinal stromal tumours (GISTs) of the stomach and small intestine: relation to tumour-biological risk-profile and long-term outcome.
Søreide K et al.
Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2012
Fresh surgical specimens yield breast stem/progenitor cells and reveal their oncogenic abnormalities.
Pommier SJ et al.
Annals of Surgical Oncology, 2012
Lack of correlation between immunohistochemical expression of CKIT and KIT mutations in atypical acral nevi.
Park E et al.
The American Journal of Dermatopathology, 2012
Anorectal melanoma with a KIT-activating mutation, which is a target for tyrosine kinase inhibitor.
Itoh M et al.
International Journal of Clinical Oncology, 2011
KIT amplification and gene mutations in acral/mucosal melanoma in Korea.
Yun J et al.
Apmis : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica, 2011
High density DNA array analysis reveals distinct genomic profiles in a subset of gastrointestinal stromal tumors.
Belinsky MG et al.
Genes, Chromosomes & Cancer, 2009
KIT gene mutations and copy number in melanoma subtypes.
Beadling C et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2008
Increased KIT signalling with up-regulation of cyclin D correlates to accelerated proliferation and shorter disease-free survival in gastrointestinal stromal tumours (GISTs) with KIT exon 11 deletions.
Haller F et al.
The Journal of Pathology, 2008
Secondary mutations in the kinase domain of the KIT gene are predominant in imatinib-resistant gastrointestinal stromal tumor.
Nishida T et al.
Cancer Science, 2008
Site-dependent differential KIT and PDGFRA expression in gastric and intestinal gastrointestinal stromal tumors.
Haller F et al.
Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, 2007
Pathologic and molecular heterogeneity in imatinib-stable or imatinib-responsive gastrointestinal stromal tumors.
Agaram NP et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2007
KIT mutations and dose selection for imatinib in patients with advanced gastrointestinal stromal tumours.
Debiec-Rychter M et al.
European Journal of Cancer (oxford, England : 1990), 2006
Polyclonal evolution of multiple secondary KIT mutations in gastrointestinal stromal tumors under treatment with imatinib mesylate.
Wardelmann E et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2006
Molecular research directions in the management of gastrointestinal stromal tumors.
Tarn C et al.
Current Treatment Options in Oncology, 2005
Activating mutations in c-KIT and PDGFRalpha are exclusively found in gastrointestinal stromal tumors and not in other tumors overexpressing these imatinib mesylate target genes.
Burger H et al.
Cancer Biology & Therapy, 2005
Prognostic role of E2F1 and members of the CDKN2A network in gastrointestinal stromal tumors.
Haller F et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2005
Changing phenotype of gastrointestinal stromal tumours under imatinib mesylate treatment: a potential diagnostic pitfall.
Pauwels P et al.
Histopathology, 2005
Analysis of KIT mutations in sporadic and familial gastrointestinal stromal tumors: therapeutic implications through protein modeling.
Tarn C et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2005
The complexity of KIT gene mutations and chromosome rearrangements and their clinical correlation in gastrointestinal stromal (pacemaker cell) tumors.
Andersson J et al.
The American Journal of Pathology, 2002