title: [Possibilities for inhibiting tumor-induced angiogenesis: results with multi-target tyrosine kinase inhibitors].
abstract: Functional blood vasculature is essential for tumor progression. The main signalization pathways that play a key role in the survival and growth of tumor vessels originate from the VEGF-, PDGF- and FGF tyrosine kinase receptors. In the past decade, significant results have been published on receptor tyrosine kinase inhibitors (RTKIs). In this paper, the mechanisms of action and the results so far available of experimental and clinical studies on multi-target antiangiogenic TKIs are discussed. On the one hand, notable achievements have been made recently and these drugs are already used in clinical practice in some patient populations. On the other hand, the optimal combination and dosage of these drugs, selection of the apropriate biomarker and better understanding of the conflicting role of PDGFR and FGFR signaling in angiogenesis remain future challenges.
authors.affiliation: Országos Korányi TBC és Pulmonológiai Intézet, Tumorbiológiai Osztály, Budapest, Hungary. szilvia.torok@koranyi.hu
authors.forename: Szilvia
authors.initials: S
authors.lastname: Török
authors.forename: Balázs
authors.initials: B
authors.lastname: Döme
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D000077784:Axitinib; D001557:Benzenesulfonates / Q000494:pharmacology; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D007191:Indazoles / Q000494:pharmacology; D007211:Indoles / Q000494:pharmacology; D009369:Neoplasms / Q000098:blood supply* / Q000378:metabolism; D009389:Neovascularization, Pathologic / Q000188:drug therapy* / Q000201:enzymology / Q000378:metabolism* / Q000517:prevention & control; D009536:Niacinamide / Q000031:analogs & derivatives / Q000494:pharmacology; D009841:Oligonucleotides; D010671:Phenylurea Compounds; D010793:Phthalazines / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D047428:Protein Kinase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors*; D011725:Pyridines / Q000494:pharmacology; D011743:Pyrimidines / Q000494:pharmacology; D011758:Pyrroles / Q000494:pharmacology; D011799:Quinazolines / Q000494:pharmacology; D020794:Receptor Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000187:drug effects* / Q000378:metabolism*; D017468:Receptors, Fibroblast Growth Factor / Q000187:drug effects / Q000378:metabolism; D017479:Receptors, Platelet-Derived Growth Factor / Q000187:drug effects / Q000378:metabolism; D040262:Receptors, Vascular Endothelial Growth Factor / Q000187:drug effects / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D000077157:Sorafenib; D013449:Sulfonamides / Q000494:pharmacology; D000077210:Sunitinib
chemical_list: D020533:Angiogenesis Inhibitors; D001557:Benzenesulfonates; D007093:Imidazoles; D007191:Indazoles; D007211:Indoles; D009841:Oligonucleotides; D010671:Phenylurea Compounds; D010793:Phthalazines; D010880:Piperidines; D047428:Protein Kinase Inhibitors; D011725:Pyridines; D011743:Pyrimidines; D011758:Pyrroles; D011799:Quinazolines; D017468:Receptors, Fibroblast Growth Factor; D013449:Sulfonamides; D009536:Niacinamide; C404768:vatalanib; C516667:pazopanib; D000077157:Sorafenib; D000077784:Axitinib; D011505:Protein-Tyrosine Kinases; D020794:Receptor Protein-Tyrosine Kinases; D017479:Receptors, Platelet-Derived Growth Factor; D040262:Receptors, Vascular Endothelial Growth Factor; C519562:imetelstat; C530716:nintedanib; C500926:cediranib; D000077210:Sunitinib; C452423:vandetanib