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Modifying paclitaxel induced apoptos...

Ahmed, Wesam B.

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Modifying paclitaxel induced apoptosis by controlling signal transduction pathways in human leukemia cells.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Modifying paclitaxel induced apoptosis by controlling signal transduction pathways in human leukemia cells./
Author:	Ahmed, Wesam B.
Description:	155 p.
Notes:	Director: Steven Grant.
Contained By:	Dissertation Abstracts International64-02B.
Subject:	Biology, Cell. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3080569

Modifying paclitaxel induced apoptosis by controlling signal transduction pathways in human leukemia cells.
Ahmed, Wesam B.

Modifying paclitaxel induced apoptosis by controlling signal transduction pathways in human leukemia cells. - 155 p.

Director: Steven Grant.

Thesis (Ph.D.)--Virginia Commonwealth University, 2003.

The primary goal of this study is to investigate the underlying mechanisms of paclitaxel induced lethality in human leukemia cells as a model of p53 null human cancer cells. Based on our understanding of these proposed mechanisms, efforts were taken to modulate paclitaxel induced lethality by controlling signal transudation pathways either by using a specific pharmacological inhibitors to inhibit JNK pathway and PI3K or ectopic enforced expression of proteins using inducible systems (e.g. p21<super>cip1/WAF1</super>, MEK. AKT). Our results indicate that the CDKI p21<super>Cip1/WAF1</super> plays a significant role in the cell death response of p53-null human leukemia cells to paclitaxel-mediated lethality. Ectopic expression of p21<super>cp1/WAF1 </super> blocked the inactivation of ERK accompanying paclitaxel exposure. In addition, it attenuated, albeit modestly, paclitaxel-induced JNK activation which was accompanied by diminished phosphorylation of Bcl-2.Subjects--Topical Terms:

1017686
Biology, Cell.

Modifying paclitaxel induced apoptosis by controlling signal transduction pathways in human leukemia cells.
LDR:02466nam 2200301 a 45 001 927525
005 20110425
008 110425s2003 eng d
035 $a (UnM)AAI3080569
035 $a AAI3080569
040 $a UnM $c UnM
100 1 $a Ahmed, Wesam B. $3 1251085
245 1 0 $a Modifying paclitaxel induced apoptosis by controlling signal transduction pathways in human leukemia cells.
300 $a 155 p.
500 $a Director: Steven Grant.
500 $a Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0691.
502 $a Thesis (Ph.D.)--Virginia Commonwealth University, 2003.
520 $a The primary goal of this study is to investigate the underlying mechanisms of paclitaxel induced lethality in human leukemia cells as a model of p53 null human cancer cells. Based on our understanding of these proposed mechanisms, efforts were taken to modulate paclitaxel induced lethality by controlling signal transudation pathways either by using a specific pharmacological inhibitors to inhibit JNK pathway and PI3K or ectopic enforced expression of proteins using inducible systems (e.g. p21<super>cip1/WAF1</super>, MEK. AKT). Our results indicate that the CDKI p21<super>Cip1/WAF1</super> plays a significant role in the cell death response of p53-null human leukemia cells to paclitaxel-mediated lethality. Ectopic expression of p21<super>cp1/WAF1 </super> blocked the inactivation of ERK accompanying paclitaxel exposure. In addition, it attenuated, albeit modestly, paclitaxel-induced JNK activation which was accompanied by diminished phosphorylation of Bcl-2.
520 $a Enforced expression of MEK pathway protects Jurkat human leukemia cells from paclitaxel-induced apoptosis. In addition, paclitaxel inhibits ERK phosphorylation in human leukemia cell lines. On the other hand, Inhibition of JNK pathway significantly reduced paclitaxel induced lethality. Interestingly, JNK inhibition significantly decreased paclitaxel-induced Bcl-2 phophorylation. Finally, inhibition of PI3K potentiates paclitaxel-induced lethality. Enforced expression of AKT failed to protect the Jurkat cells from paclitaxel-induced lethality.
590 $a School code: 2383.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Chemistry, Biochemistry. $3 1017722
650 4 $a Health Sciences, Oncology. $3 1018566
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0379
690 $a 0419
690 $a 0487
690 $a 0992
710 2 0 $a Virginia Commonwealth University. $3 1018010
773 0 $t Dissertation Abstracts International $g 64-02B.
790 $a 2383
790 1 0 $a Grant, Steven, $e advisor
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3080569