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Statements

Subject Item
n2:RIV%2F00216224%3A14740%2F13%3A00069240%21RIV14-MSM-14740___
rdf:type
n16:Vysledek skos:Concept
rdfs:seeAlso
http://informahealthcare.com/doi/abs/10.3109/10428194.2013.796056
dcterms:description
The prognostic role of ATM defects is well documented in chronic lymphocytic leukemia. However, the predictive value of ATM inactivation is much less understood, even in response to common drugs like fludarabine. It has been demonstrated that CLL cells having inactive ATM exhibit defective phosphorylation of its downstream targets after fludarabine treatment. We performed alternative analysis focusing on fludarabine-induced p53 accumulation and induction of p53-downstream genes after artificial ATM inhibition and, in parallel, using cells with endogenous ATM inactivation. We show that after 24h fludarabine exposure: (i) 5 out of 8 ATM-deficient samples (63%) normally accumulated p53 protein, and (ii) all analyzed ATM-deficient samples (n = 7) manifested clear induction of p21, PUMA, BAX, and GADD45 genes. In all experiments, doxorubicin was used as a confined ATM inductor and confirmed effective ATM inactivation. The prognostic role of ATM defects is well documented in chronic lymphocytic leukemia. However, the predictive value of ATM inactivation is much less understood, even in response to common drugs like fludarabine. It has been demonstrated that CLL cells having inactive ATM exhibit defective phosphorylation of its downstream targets after fludarabine treatment. We performed alternative analysis focusing on fludarabine-induced p53 accumulation and induction of p53-downstream genes after artificial ATM inhibition and, in parallel, using cells with endogenous ATM inactivation. We show that after 24h fludarabine exposure: (i) 5 out of 8 ATM-deficient samples (63%) normally accumulated p53 protein, and (ii) all analyzed ATM-deficient samples (n = 7) manifested clear induction of p21, PUMA, BAX, and GADD45 genes. In all experiments, doxorubicin was used as a confined ATM inductor and confirmed effective ATM inactivation.
dcterms:title
The p53 pathway induction is not primarily dependent on Ataxia Telangiectasia Mutated (ATM) gene activity after fludarabine treatment in chronic lymphocytic leukemia cells The p53 pathway induction is not primarily dependent on Ataxia Telangiectasia Mutated (ATM) gene activity after fludarabine treatment in chronic lymphocytic leukemia cells
skos:prefLabel
The p53 pathway induction is not primarily dependent on Ataxia Telangiectasia Mutated (ATM) gene activity after fludarabine treatment in chronic lymphocytic leukemia cells The p53 pathway induction is not primarily dependent on Ataxia Telangiectasia Mutated (ATM) gene activity after fludarabine treatment in chronic lymphocytic leukemia cells
skos:notation
RIV/00216224:14740/13:00069240!RIV14-MSM-14740___
n16:predkladatel
n17:orjk%3A14740
n3:aktivita
n11:P
n3:aktivity
P(EE2.3.20.0045)
n3:cisloPeriodika
8
n3:dodaniDat
n10:2014
n3:domaciTvurceVysledku
n6:9793321 n6:9993940 n6:5626129 n6:9834761 n6:4629604
n3:druhVysledku
n8:J
n3:duvernostUdaju
n19:S
n3:entitaPredkladatele
n21:predkladatel
n3:idSjednocenehoVysledku
101112
n3:idVysledku
RIV/00216224:14740/13:00069240
n3:jazykVysledku
n4:eng
n3:klicovaSlova
ATM; fludarabine; DSBs; p53 pathway; CLL
n3:klicoveSlovo
n5:ATM n5:DSBs n5:fludarabine n5:CLL n5:p53%20pathway
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[B78D93FB9693]
n3:nazevZdroje
Leukemia & Lymphoma
n3:obor
n14:FD
n3:pocetDomacichTvurcuVysledku
5
n3:pocetTvurcuVysledku
5
n3:projekt
n7:EE2.3.20.0045
n3:rokUplatneniVysledku
n10:2013
n3:svazekPeriodika
54
n3:tvurceVysledku
Jašková, Zuzana Navrkalová, Veronika Trbušek, Martin Šebejová, Ludmila Zemanová, Jana
n3:wos
000321763800052
s:issn
1042-8194
s:numberOfPages
4
n15:doi
10.3109/10428194.2013.796056
n9:organizacniJednotka
14740