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Abstract
HCC is a multistep pathological process characterized by the progressive, sequential evolution of liver disease stages from chronic liver injury, to inflammation, hepatocellular degeneration, necrosis and hepatocellular regeneration (Farazi & DePinho, 2006). HCC-inducing aetiologies provoke continuous cycles of the destructive–regenerative process that culminates in liver cirrhosis (Farazi & DePinho, 2006). liver cirrhosis represents the most advanced stage of fibrosis including distortion of the liver parenchyma, collagen deposition and scarring of the liver associated with septae, nodule formation (regenerative nodules) and altered blood flow (Friedman, 2008). Subsequently, hyperplastic nodules are observed which have normal cytological features, and represent a potential first step towards HCC. Both genetic and epigenetic changes may occur eventually leading to the subsequent formation of small cell dysplasia (Severi et al., 2010). This is followed by the appearance of low- and high-grade dysplastic nodules which have abnormal cytological features including clear cell changes and nuclear crowding, which indicate abnormal liver architecture and eventually manifest as HCC (Figure 1.3) (Farazi & DePinho, 2006; Aravalli et al., 2013).