Associated Papers
Monitoring Circulating Tumor DNA During Surgical Treatment in Patients with Gastrointestinal Stromal Tumors.
Johansson G et al.
Molecular Cancer Therapeutics, 2021
34552011 (PubMed )
Supplement: 15357163mct210403-sup-264922_2_supp_7338541_qy3h8n.xlsx › Supplementary_Table_S5
Pathogenic and diagnostic relevance of KIT in primary mast cell activation disorders.
Muñoz-González JI et al.
Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology, 2021
Is high-risk cutaneous squamous cell carcinoma of the head and neck a suitable candidate for current targeted therapies?
Zilberg C et al.
Journal of Clinical Pathology, 2020
The Immunogenic Potential of Recurrent Cancer Drug Resistance Mutations: An In Silico Study.
Punta M et al.
Frontiers in Immunology, 2020
33133066 (PubMed )
Supplement: Table_1.xlsx › Resistance-no-BCR-ABL1
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
Detection of KIT and PDGFRA mutations in the plasma of patients with gastrointestinal stromal tumor.
Kang G et al.
Targeted Oncology, 2015
Prevalence of c-KIT mutations in gonadoblastoma and dysgerminomas of patients with disorders of sex development (DSD) and ovarian dysgerminomas.
Hersmus R et al.
Plos One, 2012
Comparative analysis of mutation of tyrosine kinase kit in mast cells from patients with systemic mast cell activation syndrome and healthy subjects.
Molderings GJ et al.
Immunogenetics, 2010
c-KIT is frequently mutated in bilateral germ cell tumours and down-regulated during progression from intratubular germ cell neoplasia to seminoma.
Biermann K et al.
The Journal of Pathology, 2007
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