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العنوان
Study of Effect of Either Metformin or Acetyl Salicylic Acid versus Their Combination with Curcumin on Growth Rate of Two Different Models of Solid Tumors - Bearing Mice /
المؤلف
Mohammad, Fatma Saad Samman.
هيئة الاعداد
باحث / فاطمه سعد سمان محمد
مشرف / محمد صالح حسن
مشرف / محمد طنطاوي
مشرف / شيرين موريس
مشرف / محمد كمال
الموضوع
Clinical Pharmacology.
تاريخ النشر
2021.
عدد الصفحات
305 P. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
علم الأدوية (الطبية)
تاريخ الإجازة
1/1/2021
مكان الإجازة
جامعة قناة السويس - كلية الطب - Clinical Pharmacology
الفهرس
Only 14 pages are availabe for public view

from 324

from 324

Abstract

Breast cancer is the second leading cause of cancer mortality worldwide. Xenograft models of human cancer play an important role in the screening and evaluation of novel anticancer agents. The orthotopic mammary fat pad tumor implant model is considered a good model for breast cancer.
An Ehrlich tumor originates from spontaneous murine mammary adenocarcinoma and adapts to an ascites form by intra-peritoneal serial passages. The solid-form of Ehrlich carcinoma evolves from a subcutaneous route of inoculation and provides an efficient tool to investigate antineoplastic drugs.
Metformin is an oral hypoglycemic drug with a remarkable record of safety that has been prescribed worldwide for management of Type II diabetes. Metformin reduces tissue oxidative stress and inflammation. Metformin has been shown to exert anticancer activities in several cancers, such as breast cancer, colorectal cancer, pancreatic cancer, lung cancer and esophageal cancer. Epidemiological studies have shown that metformin use is associated with a lower incidence and mortality of numerous cancers, particularly in patients with type 2 diabetes. It has been found that metformin induces cell apoptosis and cell cycle arrest and inhibits tumor growth when used in in vitro or in vivo models.
Currently aspirin is more commonly used as an anti-thrombotic agent, in primary and secondary prevention of thromboembolic events. One obvious molecular target for aspirin is COX-2 which is the enzyme highly and rapidly induced in response to mediators of inflammation, growth factors, cytokines or endotoxins and is involved in cell proliferation and tumor promotion. This is supported by the fact that aspirin can decrease the production of potentially neoplastic prostaglandins produced from COX-2-mediated catalysis of arachidonic acid. The carcinogenic contribution of prostaglandins has generated