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Quantitative RT-PCR study of TAp73 and xNp73 in benign and malignant lymphoid lesions / Alaa Amr Gad ; Supervised Hoda Ali Sadek , Laila Abdalrahman Hegazy , Mona Salah Aldin Hamdy

By: Contributor(s): Material type: TextTextLanguage: English Publication details: Cairo : Alaa Amr Gad , 2013Description: 210 P. : charts , facsimiles ; 25cmOther title:
  • في تضخم الغدد اللمفاوية الحميدة والخبييثة RT-PCRباستخدام TAp73 و xNp73 دراسة لكمية [Added title page title]
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Dissertation note: Thesis (Ph.D.) - Cairo University - Faculty of Medicine - Department of Clinical and Chemical Pathology Summary: Background: p73 is a member of the p53 family of tumor suppressors. Transactivating isoforms of p73 (TAp73) have p53-like, anti-proliferative and pro-apoptotic activities that are crucial for an efficient chemotherapy response. However, in contrast to p53, which is commonly inactivated in human cancer by point mutations, the TP73 gene is almost never mutated. Instead, the tumor suppressor activity of TAp73 is inhibited through a variety of mechanisms including epigenetic silencing and complex formation with inhibitory proteins. All these mechanisms have in common that they are in principle reversible and therefore amenable to therapeutic intervention. The use of 2 promoters at the N-terminus allows the expression of an isoform containing (TAp73) or not containing (xNp73) a complete N terminal transactivation domain, with the latter isoform capable of a dominant negative effect over the former
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Item type Current library Home library Call number Copy number Status Date due Barcode
Thesis Thesis قاعة الرسائل الجامعية - الدور الاول المكتبة المركزبة الجديدة - جامعة القاهرة Cai01.11.07.Ph.D.2013.Al.Q (Browse shelf(Opens below)) Not for loan 01010110063382000
CD - Rom CD - Rom مخـــزن الرســائل الجـــامعية - البدروم المكتبة المركزبة الجديدة - جامعة القاهرة Cai01.11.07.Ph.D.2013.Al.Q (Browse shelf(Opens below)) 63382.CD Not for loan 01020110063382000

Thesis (Ph.D.) - Cairo University - Faculty of Medicine - Department of Clinical and Chemical Pathology

Background: p73 is a member of the p53 family of tumor suppressors. Transactivating isoforms of p73 (TAp73) have p53-like, anti-proliferative and pro-apoptotic activities that are crucial for an efficient chemotherapy response. However, in contrast to p53, which is commonly inactivated in human cancer by point mutations, the TP73 gene is almost never mutated. Instead, the tumor suppressor activity of TAp73 is inhibited through a variety of mechanisms including epigenetic silencing and complex formation with inhibitory proteins. All these mechanisms have in common that they are in principle reversible and therefore amenable to therapeutic intervention. The use of 2 promoters at the N-terminus allows the expression of an isoform containing (TAp73) or not containing (xNp73) a complete N terminal transactivation domain, with the latter isoform capable of a dominant negative effect over the former

Issued also as CD

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