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العنوان
The association between ICOS gene polymorphism with breast cancer /
المؤلف
AbdEltawab, Ahmed Ragab.
هيئة الاعداد
باحث / احمد رجب عبدالتواب قطب
مشرف / زينب ابراهيم على عطية
مشرف / رزق أحمد الباز
مشرف / راندا عزالدين النجار
الموضوع
Zoology.
تاريخ النشر
2017.
عدد الصفحات
p 176. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
علم الحيوان والطب البيطري
تاريخ الإجازة
17/9/2017
مكان الإجازة
جامعة طنطا - كلية العلوم * - Zoology
الفهرس
Only 14 pages are availabe for public view

from 207

from 207

Abstract

Breast cancer is one of the most common malignant tumors contributing to the high mortality of females worldwide. The etiology of breast cancer is a complex combination of both environmental and genetic factors, so the determination of genetic polymorphism provided a new way to investigate the etiology of such complex genetic disease.Accordingly, significant associations have been confirmed on some gene polymorphisms with breast cancer risk. So far, accumulating evidence assure that the host immune system is involved in the regulation of cancer development and progression. T lymphocyte, whose function is central to the adaptive immune response, plays a critical role in immune surveillance of cancer cells. Therefore, the molecules, in particular the costimulatory ones, mediating regulation of T-cell activity may influence cancer susceptibility. Inducible costimulator (ICOS) molecule is a member of the CD28 family that generates essential secondary signals to determine the activation and development of the immune response.The gene encoding ICOS is located on chromosome 2q33, which contains CD28 and CTLA-4, another two numbers of CD28 family. ICOS is stimulate following T cell activation. Interaction between ICOS and its ligand (ICOS-L; CD275), a molecule highly expressed on B cells and dendritic cells, provides costimulatory signal to stimulate T cell proliferation, secretion of various cytokines and up-regulation of cell surface molecules. Blocking of ICOS with Abs or an ICOS-Ig fusion protein results in the inhibition of immune responses mediated by Th1 and Th2.