KIT polymorphisms and mutations determine responses of neoplastic mast cells to bafetinib (INNO-406)

• Published in: Experimental hematology Vol. 38; no. 9; pp. 782 - 791
• Main Authors: Peter, Barbara, Hadzijusufovic, Emir, Blatt, Katharina, Gleixner, Karoline V., Pickl, Winfried F., Thaiwong, Tuddow, Yuzbasiyan-Gurkan, Vilma, Willmann, Michael, Valent, Peter
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 01.09.2010
• Subjects: Advanced Basic Science; Amino Acid Substitution; Animals; Dogs; Dose-Response Relationship, Drug; Drug Resistance, Neoplasm; Drug Screening Assays, Antitumor; Exons - genetics; Gene Expression Regulation, Enzymologic - drug effects; Gene Expression Regulation, Enzymologic - genetics; Gene Expression Regulation, Neoplastic - drug effects; Gene Expression Regulation, Neoplastic - genetics; Hematology, Oncology and Palliative Medicine; Humans; Mast Cells - enzymology; Mast Cells - pathology; Mastocytosis, Systemic - drug therapy; Mastocytosis, Systemic - enzymology; Mastocytosis, Systemic - genetics; Mastocytosis, Systemic - pathology; Mutation, Missense; Phosphorylation - drug effects; Phosphorylation - genetics; Polymorphism, Genetic; Protein Kinase Inhibitors - pharmacology; Proto-Oncogene Proteins c-kit - antagonists & inhibitors; Proto-Oncogene Proteins c-kit - genetics; Proto-Oncogene Proteins c-kit - metabolism; Pyrimidines - pharmacology; Species Specificity

Advanced systemic mastocytosis (SM) is characterized by uncontrolled growth of neoplastic mast cells (MC) and drug resistance. The tyrosine kinase receptor KIT is often mutated and activated and thus contributes to malignant growth of MC. Therefore, KIT-targeting drugs are currently tested for their...