الفهرس 
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Abstract
Hepatocellular carcinoma (HCC) is the fifth most common malignancy in the world, complicating liver cirrhosis in most cases.
There are many risk factors for HCC including the cirrhotic stage of hepatitis B, C and D virus which is the most important. However, there are some other etiologic factors like toxins (alcohol, tobacco and Aflatoxin), hereditary metabolic liver disease, autoimmune hepatitis and newer factors like overweight in males, diabetes mellitus, and non-alcoholic fatty liver disease. Hepatocarcinogenesis is generally believed to evolve from a multistep process. The stepwise transformation initiates in the normal liver or cirrhotic livers containing foci of phenotypically altered and dysplastic hepatocytes, progresses through a series of hyperplastic (large regenerative) and dysplastic (low-and high-grade dysplastic) stages, and finally results in malignancy and eventual metastasis. Dysplastic lesions are premalignant hepatic lesions that thought to be able to transform into HCC. These include dysplastic foci and dysplastic nodules. Dysplastic foci are small microscopic foci, less than 1 mm in size, of dysplastic hepatocytes recognized within the liver parenchyma in chronic liver disease, particularly at cirrhosis. Dysplastic foci are named according to the main cell type as large cell foci, small cell foci, or iron-free foci. Dysplastic nodules are more than one cm. They are classified into low grade DNs and High grade DNs. LGDNs are characterized by minimal cytologic and architectural atypia that can be mistaken for large regenerative nodule. However, HGDNs are characterized by high degree of cytologic and architectural atypia but which are insufficient for a diagnosis of malignancy.