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)

A case of a right ovarian tumor in a 64-year-old patient showing high blood levels of alpha-fetoprotein (AFP) is reported. Histologically, the tumor resembled hepatocellular carcinoma with hyaline globules. Localization of AFP was detected by the immunoperoxidase method. Electron microscopically, the rough-surfaced endoplasmic reticulum had developed into a meshwork, and the mitochondria were present within this meshwork. Because a transition from adenocarcinoma to a region resembling hepatocellular carcinoma was observed, this tumor was considered to originate as a common epithelial carcinoma. In the blood, 67% of the AFP was bound with concanavalin A (Con A), and the fraction pattern obtained by lentil agglutinin affinity chromatography (LCA) was of the germ cell type. From these results, the current case may be labeled clinicopathologically a hepatoid carcinoma of the ovary as described by Ishikura and Scully.
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PMID:Hepatoid carcinoma of the ovary: a case report. 171 89

A case of gastric adenocarcinoma with patterns resembling those of hepatocellular carcinoma is reported. The hepatoid component of the tumour was characterized by discrete masses, nests and broad bands of large polyhedral cells with central nuclei, prominent nucleoli, and abundant eosinophilic cytoplasm; single-nucleus giant cells were frequently noted. Varying numbers of tumour cells stained immunohistochemically for alpha-fetoprotein (AFP), alpha-1-antitrypsin (AAT), and albumin. Thus, in this hepatoid gastric adenocarcinoma tumour cells demonstrated both morphologic and immunohistochemical features of partial differentiation in hepatocellular carcinoma. Careful histological examination in conjunction with the immunohistochemical demonstration of AFP and other serum proteins can provide an useful contribution to the diagnosis of this rare histological type of gastric carcinoma.
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PMID:Hepatoid gastric adenocarcinoma. A histological and immunohistochemical study of a case. 172 9

Culture media conditioned by several hepatocyte derived cell lines were analyzed for their ability to stimulate adipose differentiation of the adipogenic cell line 1246. The results presented here show that culture media from HepG2 and Hep3B cell lines contain a high level of the activity, whereas media from hepatoma and hepato adenocarcinoma cell lines Huh-7, PLC/PRF/5, and SK-Hep-1 do not contain adipogenic activity. Conditioned medium from HepG2 cells also stimulated differentiation of 3T3-L1 cells and of rat epididymal adipocyte precursors in primary culture. Partial biochemical characterization of the adipogenic activity carried out using HepG2 conditioned medium indicates that the hepatocyte derived adipogenic factor has an apparent molecular weight between 445 and 232 kDa, is destroyed by treatment at 100 degrees C, with protease, with 2-mercaptoethanol and in acidic conditions. The activity is stable at alkaline pH. Culture media conditioned by normal rat hepatocytes in primary culture also contained adipogenic activity. In contrast, medium conditioned by primary culture of nonhepatocyte cell also isolated from liver was deprived of this activity. The data presented in this paper suggest that hepatocytes could be a physiological site of production of adipogenic activity.
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PMID:Adipogenic activity produced by hepatocyte-derived cell lines and by normal hepatocytes in primary culture. 174 24

We have compared by SDS-PAGE Western blotting the molecules detected by two human monoclonal antibodies, C-OU1 and 16.88. The antibodies have previously been shown to detect a cytoplasmatic antigen with an Mr of 43 kD present in colon adenocarcinoma cell lines and in colon cancer tissues. We now demonstrate that these antibodies differ significantly in their fine specificity, resulting in a quite dissimilar tumor selectivity. The antibody 16.88, in addition to reactivity with the 43-kD molecule, also recognizes a 190-kD molecule present both in melanoma cells and in cells previously reported as 16.88 antigen positive. The 16.88 antibody does not detect a 43-kD molecule in extracts of melanoma cells. The 190-kD component was not detectable in hepatoma or mamma carcinoma cells, both of which showed presence of the 43-kD molecule. The C-OU1 antibody shows no reactivity with the 190-kD molecule in any of the cells tested or with other proteins in melanoma cells. Radiolabeled 16.88 antibody shows better localization to melanoma cancer than to colon cancer xenograft transplanted onto nude mice. These findings indicate the presence of a tumor-associated antigen not previously described and have obvious implications for potential clinical uses of the antibodies.
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PMID:Antigens recognized by two human monoclonal IgM anticolon cancer antibodies, 16.88 and C-OU1 (B9165). 175 84

Immunohistochemical techniques were used to study 177 hepatic tumors (hepatocarcinoma, cholangiocarcinoma, hepatocholangiocarcinoma, adenocarcinoma of unknown origin, and metastatic carcinoma). Phenotypes suggestive of hepatocarcinoma included keratins 8 and 18, factor XIII a, alpha-fetoprotein. C-reactive protein, carcinoembryonic antigen (CEA) cross-reacting antigen; those in effect that excluded hepatocarcinoma were keratins 1, 5, 10, 11, 19, true CEA. C-reactive protein, used for the first time, proved to be a fairly sensitive and specific marker. Factor XIII a, which was thought to be synthesized only by histiocytes, was also present in hepatocytes. Immunohistochemistry appears to be an important tool in the diagnosis of hepatic tumors. As a result of this study, 32 cases were reclassified; several were found to be intermediate between hepatocarcinoma and cholangiocarcinoma. Sixteen cases apparently were true hepatocholangiocarcinomas. In 12 cases of hepatocarcinoma, some tumor cells expressed keratins of bile duct type. It was impossible to differentiate immunohistochemically cholangiocarcinoma from metastatic carcinoma, except in two cases with breast tissue markers.
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PMID:Immunohistochemistry in the differential diagnosis of liver carcinomas. 166 Jun 78

In a prospective study, an attempt was made to determine the specificity of various imaging methods for defining tumours of the liver rather than their ability to demonstrate them. It was based on 130 patients with histologically confirmed lesions (33 haemangiomas, 17 FNH, 4 hepatocellular adenomas, 28 HCC, 36 adenocarcinoma metastases). The methods were MRT (130 cases), sonography (119), CT (122), dynamic arterial angio-CT (15), 99TC-EHIDA or blood pool scintigraphy (4 FNH, haemangiomas, HCC, 44 cases). MRT showed somewhat better results (accuracy 80%) than CT (73%) and angio-CT (73%) in demonstrating the type of lesion. The results of scintigraphy (53%) and sonography (69%) were rather worse. The range of accuracy for MRT, CT and sonography varied from 94% (haemangiomas with MRT) to 47% (FNH with sonography).
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PMID:[The accuracy of the imaging procedures (sonography, MRT, CT, angio-CT,nuclear medicine) in characterizing liver tumors]. 185 Jan 56

BCA-225 is a glycoprotein identified in human breast carcinoma cells that has been reported to show a restricted distribution in other human tissues. To further define the presence of BCA-225 in human carcinomas, the authors performed an immunohistochemical study, applying a commercially available monoclonal antibody to BCA-225 to formalin-fixed, paraffin-embedded sections of 446 adenocarcinomas from a variety of sites. BCA-225 expression was found to be common in adenocarcinomas of the breast (98%), kidney (94%), ovary (80%), and lung (74%) but was infrequent in adenocarcinomas of the gastrointestinal tract (10-16%). Adenocarcinomas of the prostate, bile ducts, thyroid, endometrium, endocervix, and pancreas showed an intermediate frequency of BCA-225 expression (36-68%). Although rare tumor cells in three hepatocellular carcinomas showed reactivity for BCA-225, staining of more than 10% of the tumor cells was not seen in any of the 23 hepatocellular carcinomas that were studied. The authors conclude that BCA-225 is expressed commonly in human adenocarcinomas and that it is not a breast-specific antigen. Antibodies to BCA-225 may have utility in helping one to exclude hepatocellular carcinoma in certain clinical settings.
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PMID:Distribution of BCA-225 in adenocarcinomas. An immunohistochemical study of 446 cases. 187 28

Guided percutaneous fine needle aspiration cytodiagnosis of the liver, retroperitoneum and pancreas was performed in 197 patients. In 42 cases, material left after the smears were prepared was embedded in paraffin wax for histological examination. Six liver tumours and seven pancreatic tumours were identified in this material. In two cases the diagnosis of liver cell carcinoma was made only after microhistological examination. Re-examination of the cytological material in both cases disclosed features of liver cell carcinoma which were underestimated in the first examination and diagnosed only broadly as cancer cells. On the other hand, in another case cancer cells were present only in the smear and absent in the microhistological preparation. Diagnosis of pancreatic tumours was generally not improved by microhistological examination. In one case cancer cells were present only in the cytological material. In another case a cytological diagnosis of suspected cancer was confirmed as adenocarcinoma by microhistology. The diagnosis of non-neoplastic material in the remaining 29 cases were identical by cytopathology and microhistology. It is concluded that the microhistology of needle aspirate material complements cytological examination and can refine diagnosis although it increases cost.
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PMID:Does microhistology improve the cytological diagnosis of liver and pancreatic tumours? 187 23

The in vitro and in vivo growth of Con8 cells, a single cell-derived subclone of the 13762NF-transplantable rat mammary adenocarcinoma, is strongly suppressed by glucocorticoid hormones. Hybrids were formed between glucocorticoid-suppressible Con8.hD6 mammary tumor cells (Con8 transfected with the histidinol dehydrogenase selectable marker) and either glucocorticoid-resistant 8RUV7 mammary tumor cells (derived from Con8) or MCT-HTC rat hepatoma cells. Both of the glucocorticoid-resistant 8RUV7 and MCT-HTC fusion partners express functional glucocorticoid receptors, since hormone-responsive genes such as plasminogen activator inhibitor are fully dexamethasone inducible. Karyotypic analyses revealed that the hybrid cell populations possessed the appropriate number of chromosomes for a fusion between the glucocorticoid-suppressible and either of the two resistant cell types. Moreover, Northern blots showed that the intertissue hybrids expressed transcripts for both the milk fat globule membrane protein gene originating from the parental Con8.hD6 mammary tumor cells as well as mouse mammary tumor virus glycoprotein sequences which had been transfected into the MCT-HTC hepatoma cells as a molecular tag. Analysis of DNA content and [3H]thymidine incorporation demonstrated that growth of both the intratissue (Con8.hD6 x 8RUV7) and intertissue (Con8.hD6 x MCT-HTC) hybrids was glucocorticoid suppressible, even though the absolute rates of proliferation differed depending on the parental cells. Analysis of conditioned medium isolated from glucocorticoid-treated and untreated Con8.hD6 cells indicated that the growth suppression response is not mediated through the elaboration of an extracellular growth inhibitor. Taken together, our results demonstrate that the glucocorticoid-suppressible phenotype of Con8 rat mammary tumor cells is dominant, suggesting the existence of intracellular regulatory factors under glucocorticoid control that may function as trans-acting suppressors of tumor cell growth.
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PMID:Glucocorticoid growth suppression response in 13762NF adenocarcinoma-derived Con8 rat mammary tumor cells is mediated by dominant trans-acting factors. 193 66

The C57BL/6 x C3H F1 (hereafter called B6C3F1) mouse is an important animal model for long-term carcinogenesis studies. Maintained under normal laboratory conditions, these mice develop various types of spontaneous tumors during their lifetime. Activated Ha-ras genes have been detected in 66% of spontaneous hepatocellular tumors in the B6C3F1 mouse [Reynolds et al., Science (Washington DC), 237:1309, 1988]. In this study 49 spontaneous non-liver tumors were investigated for oncogene activation by DNA transfection techniques. Of the 49 tumor DNAs analyzed, only 5 yielded multiple foci in the NIH 3T3 focus assay: 2 of 10 pulmonary adenocarcinomas; 0 of 25 lymphomas; 2 of 2 Harderian gland adenomas; 0 of 1 adenocarcinoma of the small intestine; 1 of 6 malignant skin tumors; 0 of 4 hemangiosarcomas; and 0 of 1 lung metastasis of a hepatocellular carcinoma. DNA from six lymphomas which were negative in the NIH 3T3 focus assay were further analyzed for transforming genes by the nude mouse tumorigenicity assay. One of the five lymphomas tested positive with this assay. Southern blot analysis identified five activated ras genes: H-ras in two Harderian gland adenomas; K-ras in one pulmonary adenocarcinoma and in one s.c. adenocarcinoma; and N-ras in one lymphoma. The mutations involved were CG to AT and AT to TA in codon 61 of the Ha-ras genes, GC to AT or TA in codon 12 of the K-ras genes, and a GC to AT mutation in codon 12 of the N-ras gene. Transformant DNA from a pulmonary adenocarcinoma which yielded multiple foci in the transfection assay did not hybridize to DNA probes specific for the K-, H-, and N-ras, raf, neu, and met genes. Thirteen additional tumor DNAs yielded a single focus in the NIH 3T3 transfection assay. The transformant DNAs retransmitted in a second cycle transfection assay. Rearranged and/or amplified raf genes were detected in six of the transformant DNAs. At present we do not know whether these activated raf genes were present in the original tumor DNA. The other seven transformant DNAs did not hybridize with any of the above mentioned specific DNA probes utilized in Southern blot analysis. Unlike liver tumors, the activation of ras protooncogenes is not a frequent event in the development of spontaneous non-liver tumors of the B6C3F1 mouse. The results from this study should aid in understanding the neoplastic development associated with exposure to chemical carcinogens in the B6C3F1 mouse.
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PMID:Activation of protooncogenes in spontaneously occurring non-liver tumors from C57BL/6 x C3H F1 mice. 199 58


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