在哺乳動物的肝組織中，含有一個相當重要的特色，即在正常的狀態之下，便會產生多倍套體的肝細胞存在於肝組織中，且因年齡增長而有多倍套體細胞比例增加的趨勢，即所謂的「年齡相關多倍套體化」現象，其被認為是肝臟為了自身保護作用而演化形成。動物研究進一步顯示，在化學致癌物的作用下，由癌前組織逐漸惡化為肝細胞癌的過程中，雙套染色體肝細胞比例會逐漸增加; 此在人體研究自慢性肝炎轉為肝癌的進程裡，也有相同的結果發現。由於雙套染色體肝細胞比例的增加易於導致致癌基因的活化與抑癌基因功能的喪失，因此被認為與肝癌的發生有密切的關係。近來，更利用染色體含量的變化來診斷臨床上癌症病患的預後狀況與探討腫瘤的單株增生。人世肝癌的產生，大多是由病看長期作用所引起，而且其產生是屬於多重因子的共同作用，與動物化學致癌作用迥異，因之本文乃對以上相關研究做一綜論，以牌了解染色體套數變化在致肝癌過程中所扮演的角色。

　　　　　In normal livers of mammals, hepatocytes proceed polyploidization whichis thought to evolve for self-protection of livers. The polyploidization isage-dependent. Animal studies showed an increase in diploid proportion grad-ually from precancerous stage to hepatocellular carcinoma (HCC) induced bychemicals; similar findings were also observed in hepatocarcinogenesis of humanstudies. Because the increasing diploid proportion is inclined to activateoncogenes and lose tumor suppressor genes, it is believed to be related to thedevelopment of cancer. Changes of DNA content has been used in predicting theprognosis of patients affected with HCC and also in studies of clonal expansionof HCC. As most human HCC is related to hepatitis viral infection andmultifactorial in origin, its ploidy changes may be different from chemical-in-duced HCC in animal models. This review summarizes the role of chromosomalploidy changes during hepatocarcinogenesis.