الفهرس 
Hepatocellular carcinomaOnly 14 pages are availabe for public view
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Abstract
HCC represents an international public health concern as one of the most common and deadly cancers worldwide. It is the third most common cause of cancer-related death worldwide. In Egypt, HCC is the second most common cancer in men and the 6th most common cancers in women.
In most cases, HCC develops within an established background of chronic liver disease (70–90% of all patients). The worldwide heterogeneous incidence reflects variations in the main risk factors which include cirrhosis, viral hepatitis (HBV and HCV), aflatoxin, exposure to pesticide and genetic host factors.
Genetic host factors play an important role in HCC development. The most common form of genetic variation between individuals is SNP which correspond to a modification of a DNA sequence due to the change of a single nucleotide. SNPs in the methylene tetrahydrofolate reductase (MTHFR) gene and epidermal growth factor (EGF) gene polymorphism seem to be associated with HCC development.
Unrepaired DNA damage is a major source of potentially mutagenic lesions that contribute in the multistep process of carcinogenesis. Cumulative genetic changes that occur as a result of active inflammation with associated oxidative stress are believed to play an important role in hepatocarcinogenesis.
Polymorphic variants that confer suboptimal DNA repair capacity could influence cancer susceptibility and prognosis. Furthermore, the anticancer activity of chemotherapy (such as alkylating agents and platinum compounds) and radiotherapy is to a large extent directly related to their ability to induce DNA damage of cancer cells.