Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Results of liver transplantation in 10 patients with tyrosinemia are reviewed. The indications for transplantation were: hepatoma in three, acute liver failure in two, and progressive chronic liver disease in five. One patient died during surgery. Of the remaining nine who survived the operation, one died at six months as a result of bronchial aspiration and aspiration pneumonia, and a second transplanted for hepatoma died five months later with metastases. Seven patients are alive 6 months to 6 1/2 years following transplantation. Of these seven patients, six have normal liver function and a good performance status. One is awaiting retransplantation for chronic rejection. Hepatocellular carcinoma (HCC) was found either preoperatively or incidentally in five patients, all older than 2 years at the time of their transplant. Four of these are alive and well without evidence of tumor with follow-ups between 3 1/2 and 6 1/2. Four of the five patients less than 2 years of age had hepatocellular dysplasia without evidence of carcinoma on histologic examination of the resected liver. This experience suggests that liver transplantation should be considered seriously for children with hereditary tyrosinemia who are more than 2 years of age because beyond that age the incidence of hepatocellular carcinoma (HCC) increases substantially.
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PMID:Liver transplantation for tyrosinemia. A review of 10 cases from the University of Pittsburgh. 215 69

Autopsy of a 4-year-old girl with hereditary tyrosinemia type I revealed a hepatocellular carcinoma in addition to cirrhosis and renal tubular dysplasia. Cytogenetic studies performed on a skin fibroblast culture demonstrated greatly increased chromosome breakage, which affected 71% of the cells. This suggests that the development of hepatoma, which is frequent in this syndrome, and the presence of dysplastic changes of hepatocytes in nontumorous liver are related to genetic instability caused by accumulation of intermediates of tyrosine catabolism, which are natural alkylating agents (e.g., maleylacetoacetate and fumarylacetoacetate). The other microscopic structural changes seen, such as renal tubular atypia, pancreatic islet cell hyperplasia, and focal necrosis of cortical neurons, may also be partly due to DNA damage caused by the accumulation of abnormal metabolites produced in patients with type 1 tyrosinemia.
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PMID:Chromosomal instability in hereditary tyrosinemia type I. 785 8

In this study, the case of a patient presenting a second hepatocellular carcinoma 13 years after resection of a first tumor of the same type is reported. In this case, etiological investigations remained negative, but an incomplete form of syndromatic Alagille syndrome with paucity of bile ducts in the nontumoral tissue was detected and associated with nodular regenerative hyperplasia and foci of dysplasia. Malignant transformation in Alagille syndrome seems to be extremely rare. The fact that such tumors evolve very slowly could be an argument for partial hepatectomy and, if necessary, liver transplantation.
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PMID:Late recurrence of a hepatocellular carcinoma in a patient with incomplete Alagille syndrome. 217 Feb 23

Two cases of hereditary tyrosinemia presented with ascites and coagulopathy in infancy. Both patients underwent liver transplantation at the age of 25 and 36 mo, respectively. Both cases had normal liver function 37 and 24 mo later. The native liver in each case showed mixed micro- and macronodular cirrhosis with hepatocellular dysplasia, including both the large and small cell varieties. One of the subjects had also shown dysplasia in a prior liver biopsy. We compared the hepatic morphology with that from two other cases from our autopsy files. One of these (a female, 9 mo old) showed dysplasia, and the other (her male sibling, 4 yr old) had a liver cell carcinoma with lung metastases. These observations confirm prior reports that neoplastic transformation occurs early in the natural history of hereditary tyrosinemia despite meticulous dietary management and other supportive treatment. With the detection of liver cell dysplasia, efforts should be intensified to find an appropriate donor. Liver transplantation cures the hepatic disease and should be performed before malignancy develops.
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PMID:Liver cell dysplasia and early liver transplantation in hereditary tyrosinemia. 217 99

Nuclear DNA content of malignant cells was measured by OPTON type III microspectrophotometry in 19 cases of hepatocellular carcinoma (HCC), as well as cells from the paraneoplastic tissue. The mean DNA value increased significantly from non liver cell dysplasia (LCD), LCD to HCC (P less than 0.05-0.01). In histograms, non-LCD hepatocyte showed a single-peak type located at 2C. HCC showed lower multi-peaks which migrated to 4C and spread widely with more aneuploid (greater than 5C) cells. The histograms of LCD were between non-LCD and HCC, and there were also some aneuploids in LCD. These results suggest that LCD is a group of proliferating cells, and those with relatively high ratio of aneuploid cells might be premalignant.
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PMID:[Analysis of DNA content of cells from liver cell dysplasia and hepatocellular carcinoma]. 217 86

Recent developments in the pathologic assessment of several benign hepatic processes are reviewed, with particular emphasis on distinguishing these processes from malignant lesions. Liver cell dysplasia remains a controversial lesion, with mounting evidence to support its preneoplastic nature. Adenomatous hyperplastic nodules are large regenerative nodules in cirrhotic livers, and may also have malignant potential. Distinguishing these nodules from hepatocellular carcinoma by histology may become increasingly important, with the advent of more sensitive imaging techniques. Differentiating features of noncancerous biliary epithelium versus well-differentiated cholangiocarcinoma, sclerosing hemangioma versus epithelioid hemangioendothelioma, and angiomyelolipoma versus the clear cell variant of hepatocellular carcinoma are also presented and discussed.
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PMID:Pathologic assessment of liver cell dysplasia and benign liver tumors: differentiation from malignant tumors. 219 58

Two variants of dysplastic hepatocytes are revealed: small and large which are characterized by cell atypia and probably result from the disturbance of regenerative processes. The disturbance of the liver lobule architectonics is also a feature of dysplasia. The degree of hepatocyte dysplasia assessed by morphometric indices (nuclei surface, ratio of ellipticity) and its frequency increase with progression of the pathological process: chronic persistent hepatitis----chronic active hepatitis----liver cirrhosis----hepatocellular carcinoma. More frequent observation of the hepatocyte dysplasia in viral liver conditions (HBsAg in dysplastic hepatocytes) indicates the role of hepatitis B virus in the development of hepatocyte dysplasia. Increase of DNA content and nuclei polymorphism are observed in small and large dysplastic hepatocytes when the degree of dysplasia is increasing, this making these cells closer to cells of hepatocellular carcinoma and favouring the concept of hepatocellular carcinoma development in the foci of dysplastic hepatocytes, particularly in liver cirrhosis.
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PMID:[The morphological characteristics of hepatocyte dysplasia]. 228 82

Liver cell dysplasia (LCD) was investigated for hepatitis B virus (HBV) markers, alpha-fetoprotein (AFP) and ferritin by serologic and immunohistochemical methods in 101 patients with cirrhosis. LCD was found in 30 cases (29.7%), with the highest incidence in cases of posthepatitic cirrhosis (67%). In the group of dysplastic cirrhosis (DC) 46.6% of the patients had active HBV infection (hepatitis B surface antigen [HBsAg] serum positivity) compared with 7% of the patients with nondysplastic cirrhosis (NDC) (P less than 0.01). The mean serum AFP concentration was significantly raised in the DC group compared with that in the NDC group (P less than 0.05). In seven patients with LCD at the initial biopsy, the histologic followup showed the persistence of LCD in all cases, and the development of hepatocellular carcinoma (HCC) in three cases. In serologic HBsAg-positive cases, dysplastic cells, at variance with the surrounding liver parenchyma, were almost always negative for tissue HBsAg, and always negative for tissue hepatitis B core antigens (HBcAg). AFP was never detected in either normal or dysplastic cells. Ferritin was found in all cases, but dysplastic foci displayed a lesser amount of this protein. These serologic and immunohistochemical data strongly suggest a preneoplastic significance of LCD. The importance of monitoring cirrhotic patients with LCD and particularly those with HBV infection and/or increased AFP levels with more aggressive follow-up is also stressed.
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PMID:Liver cell dysplasia in cirrhosis. A serologic and immunohistochemical study. 241 42

This paper reports an autopsy case of a 78-year-old male with multiple nodules in the liver developed after long-termed administration of phosphate diethylstilbestrol (PDES) for prostatic cancer. Large part of these nodules were suspected to be well differentiated hepatocellular carcinoma with high level of serum alpha-fetoprotein (AFP) up to 3,400 ng/ml, but a part of them was evaluated to be a borderline between hepatocellular carcinoma and adenoma with mild cellular atypism. The liver other than the nodules showed liver fibrosis associated with liver cell dysplasia and peliosis hepatis-like change. This is a unique autopsy case of hepatocellular carcinoma closely related to diethylstilbestrol (DES) therapy for prostatic cancer.
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PMID:Multicentric hepatocellular carcinoma following phosphate diethylstilbestrol therapy for prostatic cancer. 244 58

Hepatocellular dysplasia, first described by Anthony et al. [J. clin. Path. 26: 217-223, 1973], is considered a peculiar pattern of proliferation process mainly observable in cirrhotic nodules in patients with hepatocellular carcinoma. Its precancerous meaning has been variously evaluated in the past. In the present study, immunohistochemical data concerning the presence of alpha-fetoprotein, alpha 1-antitrypsin, carcinoembryonic antigen, hepatitis B surface antigen and hepatitis B core antigen did not show meaningful differences between carcinomatous cells and normal and dysplastic hepatocytes. On the contrary, morphometric analysis seems to be useful to discriminate dysplastic cells by means of parametrical indexes of shape and symmetry of the nuclei and could probably offer in the future an objective evaluation of hepatocellular dysplasia.
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PMID:Hepatocellular dysplasia: immunohistochemical and morphometrical evaluation. 245 30


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