Comparative computational methods for identification of inherent or acquired mechanisms of resistance to prednisolone in acute lymphoblastic leukemia cells

Lambrou, GI; Sifakis, EG; Prentza, A; Chatziioannou, A; Koutsouris, D; Koultouki, E; Tzortzatou-Stathopoulou, F

dc.contributor.author	Lambrou, GI	en
dc.contributor.author	Sifakis, EG	en
dc.contributor.author	Prentza, A	en
dc.contributor.author	Chatziioannou, A	en
dc.contributor.author	Koutsouris, D	en
dc.contributor.author	Koultouki, E	en
dc.contributor.author	Tzortzatou-Stathopoulou, F	en
dc.date.accessioned	2014-03-01T02:46:04Z
dc.date.available	2014-03-01T02:46:04Z
dc.date.issued	2009	en
dc.identifier.uri	https://dspace.lib.ntua.gr/xmlui/handle/123456789/32516
dc.subject	Acute lymphoblastic leukemia cells	en
dc.subject	Computational methods	en
dc.subject	Glucocorticoid resistance	en
dc.subject	Intrinsic vs. acquired	en
dc.subject	Microarray	en
dc.subject.other	Acquired resistance	en
dc.subject.other	Acute lymphoblastic leukemia	en
dc.subject.other	Acute lymphoblastic leukemia cells	en
dc.subject.other	Apoptotic	en
dc.subject.other	Cell state	en
dc.subject.other	Cytotoxic	en
dc.subject.other	Dose-dependent	en
dc.subject.other	Dose-dependent manner	en
dc.subject.other	Dual mechanisms	en
dc.subject.other	Feedback mechanisms	en
dc.subject.other	Glucocorticoids	en
dc.subject.other	Microarray analysis	en
dc.subject.other	Microarray data	en
dc.subject.other	Mitogenic	en
dc.subject.other	Prednisolone	en
dc.subject.other	Regulatory mechanism	en
dc.subject.other	Computational electromagnetics	en
dc.subject.other	Computational methods	en
dc.subject.other	Information technology	en
dc.subject.other	Gene expression	en
dc.title	Comparative computational methods for identification of inherent or acquired mechanisms of resistance to prednisolone in acute lymphoblastic leukemia cells	en
heal.type	conferenceItem	en
heal.identifier.primary	10.1109/ITAB.2009.5394359	en
heal.identifier.secondary	http://dx.doi.org/10.1109/ITAB.2009.5394359	en
heal.identifier.secondary	5394359	en
heal.publicationDate	2009	en
heal.abstract	It has been shown previously that glucocorticoids exert a dual mechanism of action, meaning cytotoxic and mitogenic as well as mitogenic and anti-apoptotic, in a dose-dependent manner on CCRF-CEM cells at 72h. Early gene expression response suggested also a dose-dependent dual mechanism of action of prednisolone which is apparently reflected on cell state upon 72 h of treatment. The present work applies different computational methods on microarray data in order to examine the hypothesis whether these cells have an intrinsic or acquired mechanism of resistance. Early onset gene expression at 4h was compared to 72h gene expression. Early gene expression allowed identification of genes initiating pivotal, early onset regulatory mechanisms activated by prednisolone. Late, 72h exposure, microarray analysis allowed the relative identification of feedback mechanisms. From these results, it appears that CCRF-CEM cells used in this study exhibited a combined pattern of intrinsic and acquired resistance to prednisolone. ©2009 IEEE.	en
heal.journalName	Final Program and Abstract Book - 9th International Conference on Information Technology and Applications in Biomedicine, ITAB 2009	en
dc.identifier.doi	10.1109/ITAB.2009.5394359	en