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001-es BibID:	BIBFORM001935
Első szerző:	Kappelmayer János (laboratóriumi szakorvos)
Cím:	Pgp and FLT3 : identification and modulation of two proteins that lead to chemotherapy resistance in acute myeloid leukemia / Kappelmayer János, Udvardy Miklós, Antal-Szalmás Péter
Dátum:	2007
Megjegyzések:	Acute myeloid leukaemia (AML) comprises 80% of acute adult leukaemias and the disease has mostly an unfavourable outcome. Diagnostic criteria rely primarily on morphological classification, while prognostic evaluation is determined by cytogenetic methods. Survival is highly variable and it is a matter of debate, whether alternative therapeutic approaches may improve the effectiveness of conventional cytotoxic drug treatment. Two transmembrane proteins undoubtedly contribute to worse prognosis: P-glycoprotein (Pgp) and FLT3. Pgp is a transmembrane, ATP-cassette binding efflux pump that efficiently removes structurally unrelated xenobiotics from leukaemic blasts. This leads to inefficiency towards several cytotoxic drugs, hence the phenomenon is called multidrug resistance. FLT3 is a transmembrane tyrosine kinase and an internal tandem duplication can considerably augment its kinase activity. Both mechanisms lead to chemotherapy resistance and significantly shorter survival; thus several studies have been designed to treat patients via therapeutic measures that neutralize these proteins. This review focuses on the pathophysiological phenomena and the detection methods of Pgp and FLT3 as well as on novel therapeutic strategies that are offered by their inhibition.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban acute myeloid leukaemia p-glycoprotein FLT-3 mutation
Megjelenés:	Current Medical Chemistry. - 14 : 5 (2007), p. 519-530. -
További szerzők:	Udvardy Miklós (1947-) (belgyógyász, haematológus) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos)
Internet cím:	elektronikus változat
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001-es BibID:	BIBFORM028396
Első szerző:	Nagy Béla Jr. (labordiagnosztikai szakorvos)
Cím:	Potential therapeutic targeting of platelet-mediated cellular interactions in atherosclerosis and inflammation / B. Nagy Jr., K. Miszti-Blasius, A. Kerényi, K. J. Clemetson, J. Kappelmayer
Dátum:	2012
ISSN:	0929-8673
Megjegyzések:	Cellular interactions among platelets, leukocytes and endothelial cells are considered as a major cause of inflammation and atherosclerosis in many diseases. Via exposed surface receptors and released soluble substances, activated platelets play a crucial role in the initiation of inflammatory processes, resulting in endothelial injury and leading to formation of atherosclerotic plaque with possible thrombotic complications. Classic anti-platelet treatments (e.g. cyclooxygenase inhibitor or ADP-receptor antagonist) have favorable effects in patients with vascular diseases, but they also have several limitations such as increased bleeding risk or non-responsiveness. Thus, the need and opportunities for developing novel therapeutic inhibitors for platelet-mediated events are obvious. Animal and (pre)clinical human studies have suggested that some recently produced specific antagonists of P-selectin from α-granules, as well as its main ligand/receptor P-selectin Glycoprotein Ligand-1, the two major platelet chemokines CXCL4 and CCL5, as well as CD40L, may be considered potential new candidates in the treatment of atherogenesis and inflammation. In this review, we summarize the pathophysiological roles of these effectors in platelet activation and acute or chronic inflammation, and discuss the latest findings on promising antagonistic agents in basic and clinical studies in the prevention of platelet-mediated cellular interaction.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Molekuláris Medicina atherosclerosis CD40L chemokine endothelial cell inflammation leukocyte platelet P-selectin
Megjelenés:	Current Medicinal Chemistry. - 19 : 4 (2012), p. 518-531. -
További szerzők:	Miszti-Blasius Kornél (1977-) (laboratóriumi szakorvos) Kerényi Adrienne (1970-) (laboratóriumi szakorvos) Clemetson, Kenneth J. Kappelmayer János (1960-) (laboratóriumi szakorvos)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Celluláris hematológia - immunológia OTKA T75199 OTKA
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM077899
035-os BibID:	(PMID)29278207 (WoS)000432247500002 (Scopus)85048878557
Első szerző:	Nánási Péter Pál ifj. (sejtbiológus)
Cím:	Omecamtiv Mecarbil : a Myosin Motor Activator Agent with Promising Clinical Performance and New in vitro Results / Péter Nánási Jr., István Komáromi, Marta Gaburjakova, János Almássy
Dátum:	2018
ISSN:	0929-8673
Megjegyzések:	Abstract: Background: Clinical treatment of heart failure is still suffering from limited efficacy and unfavorable side effects. The recently developed group of agents, the myosin motor activators, act directly on cardiac myosin resulting in an increased force generation and prolongation of contraction. The lead molecule, omecamtiv mecarbil is now in human 3 stage. In addition tothe promising clinical data published so far, there are new in vitro results indicating that the effect of omecamtiv mecarbil on contractility is rate-dependent. Furthermore, omecamtiv mecarbilwas shown to activate cardiac ryanodine receptors, an effect that may carry proarrhythmic risk. Methods: These new results, together with the controversial effects of the drug on cardiac oxygen consumption, are critically discussed in this review in light of the current literature on omecamtiv mecarbil. Results: In therapeutically relevant concentrations the beneficial inotropic effect of the agent isnot likely affected by these new results - in accordance with the good clinical data. At supratherapeutic concentrations, however, activation of cardiac ryanodine receptors may increasearrhythmia propensity, and the stronger effect on diastolic than systolic cell shortening, observed at higher pacing frequencies, may decrease or offset the inotropic effect of omecamtivmecarbil. Conclusion: Further studies with definitely supratherapeutical concentrations of omecamtivmecarbil should be designed to map the actual risk of these potentially harmful side-effects.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Heart failure inotropic agents myosin activators Omecamtiv mecarbil Ryanodine receptor Cytosolic Ca 2+
Megjelenés:	Current Medicinal Chemistry. - 25 : 15 (2018), p. 1720-1728. -
További szerzők:	Komáromi István (1957-) (vegyész, molekuláris biológus, biokémikus) Gaburjakova, Marta Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító)
Pályázati támogatás:	NKFIH PD112199 NKFIH Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences MTA Szodoray Scholarship of the University of Debrecen Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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