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Statements

Subject Item
n2:RIV%2F61989592%3A15110%2F09%3A00009742%21RIV10-MSM-15110___
rdf:type
n10:Vysledek skos:Concept
dcterms:description
Mutations of BCR-ABL tyrosine kinase domain represent the most frequently identified and best-studied mechanism of chronic myeloid leukemia (CML) resistance to the treatment with tyrosine kinase inhibitors (TKIs). In previously reported patients with F317L BCR-ABL kinasedomain mutation response to dasatinib treatment was invariably poor. We describe a CML patient in chronic phase with F317L mutation identified shortly after the initiation of dasatinib therapy,following previous imatinib failure. Despite a continual persistence of the F317L mutation, thepatient achieved a complete cytogenetic and a major molecular response after 4 and 6 months of dasatinib treatment, respectively, and maintained the response for more than 20 months of followup.Possible explanations for this long-term favourable response may include immune-mediatedeffects associated with dasatinib therapy, elimination of proliferative advantage of F317L-mutant cells through inhibition of Src family of kinases (SFK) or the presence of F3 Mutations of BCR-ABL tyrosine kinase domain represent the most frequently identified and best-studied mechanism of chronic myeloid leukemia (CML) resistance to the treatment with tyrosine kinase inhibitors (TKIs). In previously reported patients with F317L BCR-ABL kinasedomain mutation response to dasatinib treatment was invariably poor. We describe a CML patient in chronic phase with F317L mutation identified shortly after the initiation of dasatinib therapy,following previous imatinib failure. Despite a continual persistence of the F317L mutation, thepatient achieved a complete cytogenetic and a major molecular response after 4 and 6 months of dasatinib treatment, respectively, and maintained the response for more than 20 months of followup.Possible explanations for this long-term favourable response may include immune-mediatedeffects associated with dasatinib therapy, elimination of proliferative advantage of F317L-mutant cells through inhibition of Src family of kinases (SFK) or the presence of F3
dcterms:title
Major molecular response achieved with dasatinib in a CML patient with F317L BCR-ABL kinase domain mutation Major molecular response achieved with dasatinib in a CML patient with F317L BCR-ABL kinase domain mutation
skos:prefLabel
Major molecular response achieved with dasatinib in a CML patient with F317L BCR-ABL kinase domain mutation Major molecular response achieved with dasatinib in a CML patient with F317L BCR-ABL kinase domain mutation
skos:notation
RIV/61989592:15110/09:00009742!RIV10-MSM-15110___
n3:aktivita
n7:Z n7:P
n3:aktivity
P(NS9949), Z(MSM6198959205), Z(MSM6198959223)
n3:cisloPeriodika
4
n3:dodaniDat
n4:2010
n3:domaciTvurceVysledku
n8:9788662 n8:2556049 n8:8227659 n8:3461904 n8:4927354 n8:7101813 n8:8478325
n3:druhVysledku
n16:J
n3:duvernostUdaju
n15:S
n3:entitaPredkladatele
n19:predkladatel
n3:idSjednocenehoVysledku
324437
n3:idVysledku
RIV/61989592:15110/09:00009742
n3:jazykVysledku
n18:eng
n3:klicovaSlova
chronic myeloid leukemia; F317L BCR-ABL mutation; dasatinib; tyrosine kinase inhibitors
n3:klicoveSlovo
n9:dasatinib n9:F317L%20BCR-ABL%20mutation n9:tyrosine%20kinase%20inhibitors n9:chronic%20myeloid%20leukemia
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[9F7C47E59E16]
n3:nazevZdroje
Leukemia Research
n3:obor
n12:FD
n3:pocetDomacichTvurcuVysledku
7
n3:pocetTvurcuVysledku
8
n3:projekt
n17:NS9949
n3:rokUplatneniVysledku
n4:2009
n3:svazekPeriodika
34
n3:tvurceVysledku
Šťastný, Marek Indrák, Karel Mojzíková, Renáta Jarošová, Marie Plachý, Radek Faber, Edgar Rožmanová, Šárka Divoká, Martina
n3:zamer
n11:MSM6198959223 n11:MSM6198959205
s:issn
0145-2126
s:numberOfPages
3
n13:organizacniJednotka
15110