الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Hepatocellular carcinoma (HCC) is one of the most frequent and lethal human cancers, and its incidence is rising worldwide. The burden of HCC has been increasing in Egypt with a doubling in the incidence rate in 10 years. HCC was found to constitute about 4.7% of chronic liver disease (CLD) patients.
HCC is multifactorial in origin and results from a complex series of genetic and other events occurring against a background of host factors. Cirrhosis of whatever cause is the main risk factor for the development of HCC as the majority of patients (80%-90%) with HCC have underlying cirrhosis.
The diagnosis of HCC can be established, and treatment rendered, based on noninvasive imaging without the need for a confirmatory biopsy. Even when biopsy is needed, imaging usually is required for guidance. Alpha-fetoprotein (AFP) and other serum biomarkers generally have a minor role in the diagnosis of HCC. Surveillance for HCC is recommended in patients with cirrhosis using liver ultrasound (US) with or without alpha-fetoprotein (AFP) every 6 months.
Although surveillance programs of HCC have been improved, a significant percentage of patients have vascular invasion or extrahepatic metastasis (advanced stage) on diagnosis and HCC mortality rate worldwide is close to its incidence rate despite the current availability of several advanced therapies, as cases are mostly detected at an advanced, non-resectable stage. Therefore, more screening as well as surveillance strategies are needed to aid in the process of early diagnosis of HCC in the population at risk.
SIRT1 is a modulator of epigenetics as it directly and indirectly affects histone acetylation besides chromatin compaction. Although SIRT1 roles in mediating genomic stability normally protect cells from oncogenic transformation; its enzymatic activity may promote cancer growth through inactivating some proapoptotic factors. Whether SIRT1 acts as a cancer promoter or tumor suppressor remains controversial, because of the temporal in addition to the characteristic distribution of SIRT1 up and downstream multiple targets and factors within different tissue contexts as well as the unclear explanations of the complex mechanisms underlying SIRT1 signaling during carcinogenesis.