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العنوان
Genetic Mutations Associated With HCC Development /
المؤلف
Elgohary, Nahla Ahmed.
هيئة الاعداد
باحث / نهله أحمد الجوهري
مشرف / هبه الظواهري
مشرف / مجدي محمد صابر
مشرف / أحمد عبد المعبود زين الدين
مشرف / بيتر شرماخر
الموضوع
Genetics.
تاريخ النشر
2015.
عدد الصفحات
152 p. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
علم الأورام
تاريخ الإجازة
1/1/2015
مكان الإجازة
جامعة القاهرة - معهد الأورام القومى - باطنة
الفهرس
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Abstract

Hepatocellular carcinoma (HCC) is the commonest primary cancer of the liverand the second cause of cancer mortality following lung cancer in males and the sixth cause of cancer mortality in females. Geographical distribution of HCC varies throughout the world with an incidence rate ranging from 2.1 in Central America to 35.5 in Eastern Asia.The majority of cases occur indeveloping countries with more than 75% of HCC occurs in Southeast Asia and sub-Saharan Africa, with incidence rates exceeding 20 per 100,000 individuals. HCC proved tobe highly refractory to treatment. As the majority of HCCs develop in cirrhotic liver,treatment options and prognosis are determined not only by tumor but also by patient-related factors such as performance status and liver function (Major et al 2013). Egypt has the highest prevalence of HCV in the world (genotype 4), which has been attributed to previous public health eradication schemes for schistosomiasis (Yousra Mohamoud et al 2013).The burden of HCC has been increasing in Egypt with a doubling in the incidence rate in the past 10 years which may be attributed to high prevalence of HCV in Egypt. HCV and HBV infections, diabetes and smoking are the main determinants of HCC development in Egypt. Occult HBV infection may influence the outcome of HCV infection and leads to the development of HCC(Ehab Abdel-Atti 2015). Ongoing clinical trials are attempting to exploit specific biological dependencies of HCC to improve the prognosis. Overall, the future of HCC treatment will rely on an understanding of the interplay between etiological factors, molecular features of disease, and rational therapeutic intervention. Pathologically diverse forms of HCC are observed, and recent sequencing analysis has defined common events that target well-known cancer pathways including bcatenin/ Axin, TP53, and RB/CDKN2A, as well as frequent aberrations in chromatin remodeling factors.However, there are low frequency of genetic events that make each HCC case unique. Gene-expression profiling approaches have successfully been deployed for prognostic assessment of HCC and to detect the earliest stages of disease. Despite extensive research, systemic treatment for HCC is exceedingly limited, with only a handful of drugs providing benefit (Schlaeger et al2008). Genetic alterations in HCC have been identified previously, including point mutations in TP53 and beta-catenin (CTNNB1), amplifications of MYC and FGF19, and integrations.