Mateusz Koptyra

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BCR/ABL kinase-positive chronic myelogenous leukemia (CML) cells display genomic instability leading to point mutations in various genes including bcr/abl and p53, eventually causing resistance to imatinib and malignant progression of the disease. Mismatch repair (MMR) is responsible for detecting misincorporated nucleotides, resulting in excision repair(More)
Fanconi D2 (FANCD2) is monoubiquitinated on K561 (FANCD2-Ub) in response to DNA double-strand breaks (DSBs) to stimulate repair of these potentially lethal DNA lesions. FANCD2-Ub was upregulated in CD34+ chronic myeloid leukemia (CML) cells and in BCR-ABL1 kinase-positive cell lines in response to elevated levels of reactive oxygen species (ROS) and DNA(More)
Pr ecis: Preclinical studies validate a novel class of small molecule inhibitors of the enzyme GSK-3, which exert potent antitumor properties by blocking both tumor invasion and angiogenesis. Pr ecis: The lack of a complete cytogenetic response in chronic phase CML patients treated with the ABL kinase inhibitor imatinib can be explained by loss of the(More)
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