ABL1, SRC a dalSí nereceptorové tyrozinkinázy jako nové cíle specifické protinádorové lécby
[ABL1, SRC and other non-receptor protein tyrosine kinases as new targets for specific anticancer therapy]
Language Czech Country Czech Republic Media print
Document type English Abstract, Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
20806817
- MeSH
- Adaptor Proteins, Signal Transducing metabolism MeSH
- Precursor Cell Lymphoblastic Leukemia-Lymphoma drug therapy metabolism MeSH
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive drug therapy metabolism MeSH
- Cytoskeletal Proteins metabolism MeSH
- Protein Kinase Inhibitors therapeutic use MeSH
- Humans MeSH
- Neoplasms drug therapy metabolism physiopathology MeSH
- Antineoplastic Agents therapeutic use MeSH
- Signal Transduction MeSH
- src-Family Kinases metabolism MeSH
- Protein-Tyrosine Kinases metabolism physiology MeSH
- Check Tag
- Humans MeSH
- Publication type
- English Abstract MeSH
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- ABI1 protein, human MeSH Browser
- Adaptor Proteins, Signal Transducing MeSH
- Cytoskeletal Proteins MeSH
- Protein Kinase Inhibitors MeSH
- Antineoplastic Agents MeSH
- src-Family Kinases MeSH
- Protein-Tyrosine Kinases MeSH
Non-receptor protein tyrosine kinases are responsible for signal transduction during many physiologic cellular processes, including cell growth and proliferation, apoptosis, differentiation, regulation of actin cytoskeleton, cell shape, adhesion, motility and migration. Aberrant activity of protein tyrosine kinases (acquired as a result of chromosomal translocation or point mutation) has been implicated in the stimulation of cancer growth and progression, the induction of drug-resistance, tumour neovascularization, tissue invasion, extravasation and the formation of metastases. Small molecule tyrosine kinase inhibitors interfere with these pathophysiological circuits by blocking the signalling cascades triggered by the aberrantly activated protein tyrosine kinases (e.g. BCR-ABL1, FIP1L1-PDGFRA or ETV6-PDGFRB).Tyrosine kinase inhibitors (imatinib, nilotinib, dasatinib) now belong to established anti-cancer agents with clinical activity in patients with CML, Ph+ ALL, and myeloid neoplasms with overexpression of PDGFRA, PDGFRB and wild-type KIT. New generation tyrosine kinase inhibitors (e.g. dasatinib) with extended activity against SRC and EPH kinases belong to promising anti-cancer agents with documented preclinical activity in several solid tumours (e.g. prostate cancer).
