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العنوان
Expression Of Tyrosine Kinase TIE-2 Receptor In Acute Myeloid Leukemia In Relation To Immunophenotyping.
المؤلف
Ahmed, Zahraa Ibrahim Abo Afya.
هيئة الاعداد
باحث / Zahraa Ibrahim Abo Afya Ahmed
مشرف / supervision Seham Mahrous Zaki
مشرف / Nagwa Abdelaziz Kantoush
مشرف / Hossam El-Din Salah
الموضوع
Blood- diseases. Leukemia.
تاريخ النشر
2011 .
عدد الصفحات
116 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب
الناشر
تاريخ الإجازة
1/1/2011
مكان الإجازة
جامعة الزقازيق - كلية الطب البشرى - clinical pathology
الفهرس
Only 14 pages are availabe for public view

from 135

from 135

Abstract

Acute leukemia is a cancer of white blood cells characterized by the rapid proliferation of abnormal cells which accumulate in the bone marrow and interfere with the production of normal blood cells. It most commonly affects adults and children.
Acute Myeloid Leukemia (AML) is an aggressive disease with high mortality rate and disease free survival is rare. It has been clarified that interaction between hematopoietic cells and endothelial cells is important for proliferation and differentiation of both cell lineages.
Angiogenesis is the formation of new blood vessels from preexisting vessels and plays an essential role in tumor growth, progression, and metastases; thus, focusing on the tumor endothelium rather than the genetically unstable tumor cells themselves which remains the subject of intense investigation. Tie-1 and Tie-2 constitute a distinct family of receptor tyrosine kinases found to be expressed mainly in endothelial cells.
Angiopoietins are angiogenic factors essential for vascular development and maturation. As circulating or matrix-bound molecules, Angiopoietin-1 (Ang-1) and its antagonist Angiopoietin-2 (Ang-2) bind to the extracellular domain of the receptor tyrosine kinase Tie-2, which is almost exclusively expressed on endothelial cells produced by vascular Smooth Muscle Cells (SMCs) and precursor pericytes.
Ang-1-induced activation of the Tie-2 receptor promotes quiescence and structural integrity of mature vessels, thus protecting the endothelium from activation by cytokines and growth factors. In contrast, Ang-2 disrupts the constitutive Ang-1/Tie-2 signaling by preventing Ang-1 from binding to the common receptor.
Changes in the expression of Tie-2 and angiopoietins are found in a.