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)

Homozygous alpha 1-antitrypsin deficiency (PiZZ phenotype) is known to be associated with increased risk of cirrhosis and primary liver cancer. Although a relationship between heterozygous alpha 1-antitrypsin deficiency and chronic liver disease was suggested recently, it is still a matter of controversy whether such patients are at increased risk of liver cancer. The goal of this study was to determine the prevalence of heterozygous alpha 1-antitrypsin deficiency of different phenotypes among patients with primary hepatobiliary cancers. We studied 82 patients with primary hepatobiliary cancer; 59 had hepatocellular carcinoma and 23 had bile duct carcinoma. alpha 1-Antitrypsin quantitation and phenotyping were performed in each patient using standard methods. The distribution of the various Pi phenotypes was compared with that found in a normal population and reported elsewhere. Odds-ratio and chi 2 tests were used to measure the relative risk and the significance of association, respectively, between primary hepatobiliary cancers and heterozygous alpha 1-antitrypsin deficiency. Four patients in each of the cancer groups were heterozygous. Among the hepatocellular carcinoma patients, three had the PiMS phenotype and one had the PiMZ phenotype. Of these four heterozygous patients, only two had cirrhosis; one had cryptogenic cirrhosis and the other had hepatitis B virus-related cirrhosis. One noncirrhotic patient with a PiMZ phenotype had a fibrolamellar carcinoma. Of the four patients with bile duct carcinoma, three had the PiMS phenotype and one had the PiMZ phenotype. Of the four heterozygous patients, two had primary sclerosing cholangitis without associated inflammatory bowel disease and one patient had had previous biliary operations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of increase in heterozygous alpha 1-antitrypsin deficiency phenotypes among patients with hepatocellular and bile duct carcinoma. 131 55

The immunohistochemical detection of the c-erbB-2 oncopeptide (p185erbB2) has been shown to be a valid marker for over-expression of this oncogene. To evaluate the possible relevance of gene expression to the proliferation of hepatocytes and bile ducts in human disease, the authors applied a monoclonal anti-p185 antibody to formalin-fixed, paraffin-embedded tissues from 67 examples of benign proliferative and neoplastic hepatic lesions and fetal liver. Focal membrane-based reactivity for the oncopeptide was detected on tumor cells in two of eight hepatocellular carcinomas and on tumor cells and adjacent bile ducts and hepatocytes in four of six cholangiocarcinomas. Each of the latter four lesions were in patients with primary sclerosing cholangitis. No reactivity was obtained in examples of hepatoblastoma, mixed cholangiocarcinoma-hepatocellular carcinoma, bile duct adenoma, or hepatocellular adenoma. Weak staining for p185erbB2 also was seen in two of seven cases of (sub)massive hepatic necrosis and two examples of postnecrotic cirrhosis, all of which were secondary to either hepatitis B or C virus infection. No other benign proliferative lesions were labeled by the anti-p185 antibody, including cases of chronic allograft rejection, necrosis secondary to hepatic artery thrombosis, metabolic-associated and nonmetabolic-associated cirrhosis, focal nodular hyperplasia, and nodular regenerative hyperplasia. The authors' results indicate that c-erbB-2 may be amplified in specific neoplastic and hepatitis B virus and hepatitis C virus infectious lesions of liver. The authors postulate that: (1) c-erbB-2 immunoreactivity may be a marker for malignant transformation in primary sclerosing cholangitis; and 2) overproduction of p185erbB2 may be an epiphenomenon of hepatitis B virus or hepatitis C virus infection.
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PMID:Immunoreactivity for c-erbB-2 oncopeptide in benign and malignant diseases of the liver. 137 19

Between July 1987 and May 1989, 11 liver transplants were performed on 10 patients at the University Hospital of Geneva. Of 15 patients evaluated for elective transplantation, 10 were accepted and put on the waiting list. 5 patients were rejected because of a contraindication or because another treatment seemed preferable. 8 transplantations were eventually performed. Emergency transplantation was considered for 6 patients, but could be performed in only 3. Indications for transplantation were as follows: one hepatocellular carcinoma in a non-cirrhotic patient, 2 post-hepatitis cirrhoses (one B and one non-A-, non-B), 3 primary biliary cirrhoses, one autoimmune cirrhosis, one primary sclerosing cholangitis, one cirrhosis on alpha-1-antitrypsin deficiency, and one fulminant B-Delta hepatitis. Most of these patients had advanced liver disease and a limited life expectancy. 8 of the 10 patients transplanted are nevertheless alive and none is hospitalized at the present time. More than mere survival, however, quality of life regained after transplantation prompts us to consider transplantation early in the progress of the disease. Earlier evaluation of patients would make transplantation feasible soon after the first complication of the disease. This attitude would probably prevent patients from dying while on a waiting list and decrease operative as well as early postoperative risks. Better information and coordination regarding potential donors is necessary in Switzerland to obtain better results in organ transplantation.
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PMID:[Liver transplantation. Preliminary results in the district University Hospital of Geneva]. 237 94

Pi phenotype was determined in 335 patients with liver diseases and compared with the results in 2830 healthy blood donors. Eleven of 335 patients had phenotype MZ (3.3%, compared with 2.9% in healthy blood donors (NS]. None of 53 patients with autoimmune chronic active hepatitis had the MZ phenotype, but it was found in 2 of 18 patients (11.1%) with cryptogenic cirrhosis, 3 of 78 (3.8%) with alcoholic liver cirrhosis, 2 of 36 (5.6%) with primary sclerosing cholangitis, and 1 of 26 (3.9%) with primary biliary cirrhosis. Altogether, 3 of 335 patients were homozygous for Pi ZZ and had cirrhosis. One of them (a male) developed a hepatoma and died. We conclude that the reported association between Pi MZ phenotype and chronic non-B active hepatitis does not seem to include patients with autoimmune chronic active hepatitis, whereas the possibility of an association between cryptogenic cirrhosis and the MZ phenotype cannot be excluded.
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PMID:Heterozygous MZ alpha-1-antitrypsin deficiency in adults with chronic liver disease. 240 84

Mouse and human extracted liver tissue were examined by indirect immunofluorescent staining and transmission electron microscopy in order to study the alteration of cytokeratin intermediate filaments associated with Mallory body formation. Frozen sections of griseofulvin-fed mouse liver and human liver of primary biliary cirrhosis and primary sclerosing cholangitis were extracted by Triton X-100 and nuclease. Indirect immunofluorescent staining was performed by using anticow hoof keratin antibody for mouse liver and anti-human epidermal keratin antibody (AE1 and AE3) for human liver. Transmission electron microscopy was also performed on extracted and critical point-dried samples. The griseofulvin-fed mouse hepatoma cells showed four different types of altered staining pattern based on the indirect immunofluorescent staining of the cytoplasm and Mallory bodies: Type I--cytoplasm(+), Mallory body(-); Type II--cytoplasm(+), Mallory body(+); Type III--cytoplasm(-), Mallory body(+), and Type IV--cytoplasm(-), Mallory body(-). Types I and III were predominant, however, some hepatoma cells which contain Mallory bodies revealed bright cytoplasmic staining (Type II). The nuclear rims were strongly stained. In human liver, AE1 stained Mallory bodies and the bile duct epithelium intensely, but did not stain normal hepatocytes. AE3 mainly stained Mallory bodies and normal hepatocytes, but also stained bile duct epithelium weakly. Indirect immunofluorescent staining for human liver showed the same staining patterns as found in mouse liver, except that Type IV was not observed. Although many hepatocytes which contained Mallory bodies did not react with either of these two antibodies (Type III), some of the hepatocytes were stained, not only with AE3, but also with AE1 (Type II).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in the cytokeratin intermediate filament cytoskeleton associated with Mallory body formation in mouse and human liver. 244 43

A radioimmunometric technique for the detection of autoantibodies to liver membrane antigens has been developed using Alexander cells, a human hepatocellular carcinoma cell line. After incubation of Alexander cells with serum, antimembrane antibodies were detected by addition of 125I-labeled Protein A. Binding ratios in 15 children with uncontrolled autoimmune chronic active hepatitis and in seven children with primary sclerosing cholangitis were significantly higher than in 18 age-matched normal controls. Nine patients with inactive autoimmune chronic active hepatitis, 13 with alpha 1-antitrypsin deficiency and five with fulminant hepatic failure had ratios similar to controls. In nine patients with Wilson's disease, there was a modest but significant increase in binding ratio. In four children with autoimmune chronic active hepatitis, binding ratios fell during effective immunosuppressive therapy. Sera from patients with systemic lupus erythematosus or rheumatoid arthritis gave normal results, excluding that binding derives from Fc-mediated immune complex capture. A positive correlation was found between Alexander cell binding values and anti-liver-specific protein antibody titers, suggesting that the two assays detect antibodies against shared antigenic determinants. The Alexander cell assay is a simple, rapid and sensitive technique to detect antibody to liver cell membrane antigens.
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PMID:Detection of anti-liver cell membrane antibody using a human hepatocellular carcinoma cell line. 253 48

This case report describes the previously undocumented association between fibrolamellar hepatocellular carcinoma and ulcerative colitis complicated by primary sclerosing cholangitis.
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PMID:Fibrolamellar hepatocellular carcinoma complicating ulcerative colitis with primary sclerosing cholangitis. 253 11

Postoperative jaundice is often a complex clinical problem of multifactorial origin. If underlying liver disease is present preoperatively, there is a greater likelihood of jaundice after surgery. We describe two patients: one with intrabiliary hepatocellular carcinoma and the other with primary sclerosing cholangitis. The underlying processes were unmasked after the development of jaundice in the postoperative period. These cases point out the importance of considering previously undiagnosed biliary tract obstruction in the differential diagnosis of postoperative jaundice.
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PMID:Postoperative jaundice as a clue to unrecognized biliary tract obstruction. 283 68

Hepatobiliary carcinomas were found in eight patients with chronic ulcerative colitis (CUC) and primary sclerosing cholangitis (large-duct PSC; five cases) or "pericholangitis" (small-duct PSC; three cases). The tumors were extrahepatic in five cases and intrahepatic in two; in one case the neoplasm affected both liver and gallbladder. The tumors in seven patients were glandular and, sometimes, cystic and papillary; in the remaining patient a combined hepatocellular carcinoma and cholangiocarcinoma was found. The latter tumor seemed to arise from regenerative nodules in secondary biliary cirrhosis complicating PSC. The presence of carcinoma in situ in areas of fibrous cholangitis, the multicentric origin of the tumor, the presence of tumor-free large-duct PSC or small-duct PSC (pericholangitis) at a distance from the carcinomatous areas, and the documentation, in some cases, of long-standing inflammatory hepatobiliary disease prior to the discovery of the tumors would seem to confirm the clinical impression that carcinomas may develop in pre-existing PSC. The appearance of hepatobiliary carcinomas in patients with classic PSC and in patients with pericholangitis supports previous evidence indicating that cholangiographically diagnosed large-duct PSC and histologically diagnosed small-duct PSC (pericholangitis) are manifestations of a shared condition that could be named PSC syndrome. The findings of the present study indicate that the PSC syndrome predisposes patients for the development of bile duct carcinoma. Most patients with CUC and bile duct carcinoma seem to have PSC prior to the development of the hepatobiliary tumor.
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PMID:Hepatobiliary carcinoma associated with primary sclerosing cholangitis and chronic ulcerative colitis. 400 48

The authors present the clinical and pathological data of a 28 year-old female patient, who died after several months of observation. The patient had a 15-year history of mild ulcerative colitis. On admission the diagnosis of primary sclerosing cholangitis was made, but subsequently paraneoplastic gonadotropin secretion became apparent. At autopsy a cholangio- and hepatocellular carcinoma was found and the extrahepatic bile ducts were infiltrated by the cholangiocarcinoma. Using the immunoperoxidase method, the hepatocellular part of the tumour was found to contain human choriogonadotropin.
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PMID:[Gonadotropin-secreting liver cancer in ulcerative colitis]. 632 96


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