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)

The effects of the differentiation-inducing polar solvent N-methylformamide (NMF) on artificially induced and spontaneous metastases from a murine hepatocarcinoma (HCA-1) in C3Hf/Kam mice were investigated. Exposure of HCA-1 cells in vitro for 6 days to 1.0% or 1.25% NMF resulted in an increase in the number of lung nodules formed in mice when these cells were injected into their tail veins. This in vitro NMF exposure increased cell volume and induced only a slight amount of cytotoxicity. Administration of NMF to mice 1 day before i.v. tumour cell inoculation resulted in a dose-dependent increase in the number of lung nodules formed, beginning at an NMF dose of 600 mg kg-1. NMF caused a similar magnitude of metastasis enhancement in immunosuppressed mice. However, when the maximum dose tested (1,800 mg kg-1) was administered as 6 daily fractions of 300 mg kg-1 each, no increase in artificial metastases was detected. Administration of NMF to mice one day after i.v. tumour cell injection resulted in a dose-dependent decrease in the number of lung nodules. In mice bearing 5-6 mm HCA-1 leg tumours, treatment with 6 daily fractions of NMF (300 mg kg-1 each) significantly reduced the number of spontaneous pulmonary metastases, yet had very little effect on the growth of the primary tumour. These data suggest that, in a clinically relevant treatment setting, NMF can reduce metastasis formation.
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PMID:The effects of N-methylformamide on artificial and spontaneous metastases from a murine hepatocarcinoma. 356 58

The effects of the differentiating agent N-methylformamide (NMF) on radiation-induced DNA damage and repair in vitro were investigated using the alkaline elution assay. Two tumor cell lines were examined: Clone A, a human colon adenocarcinoma, and HCA-1, a murine hepatocarcinoma. Both cell lines showed changes suggestive of a better differentiated phenotype when exposed to NMF. Treatment with NMF enhanced the radiation sensitivity of Clone A cells but had no effect on the radiation response of HCA-1 cells. Irradiation of NMF-treated cells, both Clone A and HCA-1, induced the formation of DNA-protein crosslinks (DPCs). The level of DPCs induced increased linearly as a function of increasing gamma-ray dose. The DPCs did not seem to be the result of NMF exposure alone, but rather an NMF-mediated modification of the spectrum of gamma-ray-induced DNA lesions. When the DPCs were removed by proteolytic digestion, no NMF effect was observed on either strand-break formation or repair.
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PMID:Enhancement of radiation-induced DNA-protein crosslinking by N-methylformamide. 357 57

N-Methylformamide (NMF), a cell-differentiating agent, was assessed for its antitumor activity against a fibrosarcoma (FSA), a hepatocarcinoma (HCA-I) and a mammary carcinoma (MCA-K), syngeneic to C3Hf/Kam mice. Tumors were grown as solitary tumors in the leg or as artificial or spontaneous micrometastases in the lung. NMF, at a dose of 300 mg/kg, was administered i.p. daily for 6 to 18 days. NMF slowed the growth of FSA and HCA-I tumors and totally inhibited the growth of the MCA-K tumor. However, the effect was transient; tumors resumed their pretreatment growth rate upon cessation of the treatment. Histologically, MCA-K tumors treated with NMF (300 mg/kg daily for six days) underwent considerable cell depopulation and reduction in mitotic activity. The number of artificial metastases, as well as the incidence and the number of spontaneous metastases, were markedly reduced by NMF. This resulted in a prolongation of the survival of mice that had artificial metastases of MCA-K tumor. The in vitro clonogenicity of MCA-K, but not of FSA or HCA-I cells, was reduced. However, in vivo reduction of MCA-K cell clonogenicity was minimal, if any. Thus, NMF is effective in restricting the growth of both solitary tumors and metastases, but the degree of response is highly dependent on tumor type.
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PMID:Antitumor and antimetastatic activity of the differentiating agent N-methylformamide in murine tumor systems. 366 21

Liver tumors developed in 2 women during pregnancy following discontinuation of hormonal contraception. Liver cell adenoma developed in a secundipara 24 years of age, and the rupture during pregnancy led to her death by bleeding after surgical intervention failed. Hepatocellular carcinoma was recorded in another secundipara 22 years of age and was surgically treated following a premature delivery. Problems of diagnosis and the need for interdisciplinary cooperation are discussed and compared with data appearing in the literature. The pathogenesis of liver tumors in the wake of exogenous hormone inflow and in the context of subsequent pregnancy are also discussed. (author's)
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PMID:[Liver tumours in pregnancy, following previous intake of hormonal contraceptives (author's transl)]. 627 Sep 31

Alternative splicing of fibronectin pre-mRNA has been shown to be independently regulated at the EDA and EDB regions in a tissue and developmental stage-specific manner. In this study, RT-PCR approaches were developed for the detection of EDA and EDB FN mRNA isoforms in hepatocarcinoma cells (SK-Hep-I) grown in vitro and in human liver biopsies. While EDA+ and EDB+ isoforms were not present in control adult liver, they were detectable in the hepatocarcinoma cells and in fetal liver. The RT-PCR analysis, extended to biopsies of malignant and non-malignant hepatic tissues, showed that FN mRNAs containing the EDA and EDB sequences were present in the 14 hepatocellular carcinomas (HCCs) tested but absent in the non-tumorous liver tissues (i.e., normal parenchyma, non-specific reactive and chronic hepatitis, steatosis). The EDB+ FN mRNA isoforms were also detected in 3 cases of benign neoplasm (hepatocellular adenoma, HCA, I; nodular focal hyperplasia, NFH, 2), while the EDA+ was only detectable in I of the 2 cases of NFH. In addition, both EDA+ and EDB+ isoforms were expressed in 5 out of 9 cirrhotic livers surrounding the tumors. This molecular analysis, which can also be performed on small liver biopsies (2 mg), may therefore be a useful additional tool in the diagnosis of HCC.
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PMID:RT-PCR detection of fibronectin EDA+ and EDB+ mRNA isoforms: molecular markers for hepatocellular carcinoma. 750 77

The purpose of this study was to compare small and ultrasmall superparamagnetic iron oxide particles (SPIO and USPIO, respectively) as MR contrast agents for the evaluation of focal hepatic disease. In two different patient groups (SPIO [n = 53], USPIO [n = 27]), with focal liver disease (metastases, hepatocellular carcinoma [HCC], hepatocellular adenoma [HCA], and focal nodular hyperplasia [FNH]), spin-echo T1- and T2-weighted images (T1WI, T2WI) were obtained at 1.0T, before and after intravenous contrast administration. The percentage signal-to-noise ratio (SNR) change and lesion-to-liver contrast (LLC) were measured and statistically compared. The liver decreased in signal intensity (SI) after SPIO administration (-28%) and increased after USPIO administration (+16%) on T1WI. On T2WI, the liver decreased in SI on postcontrast images with both agents (-78% SPIO, -73% USPIO). This difference was not statistically significantly different (P < or = .07). Both SPIO and USPIO provided >500% improvement in LLC on T2WI. On T1WI, LLC was increased in metastases (120%) and HCC (325%) with SPIO. Post-USPIO, LLC was increased on T1WI only in metastases (>500%). Both SPIO and USPIO show excellent hepatic uptake, presumed secondary to reticuloendothelial activity, based on the degree of %SI change seen in the liver after administration of contrast on T2WI. However, USPIO preparations exhibit blood pool activity that may aid in further characterization of focal liver lesions, as is evidenced by their greater T1 effect in the liver and in some focal liver lesions.
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PMID:MRI in focal liver disease: a comparison of small and ultra-small superparamagnetic iron oxide as hepatic contrast agents. 978 44

Liver cell adenomas (LCAs) are rare tumours which may be difficult to differentiate from low-grade hepatocellular carcinomas (HCCs). This study used comparative genomic hybridization (CGH) to look for cytogenetic aberrations which would serve to distinguish between these tumours. For this purpose, ten LCAs and six well-differentiated HCCs were analysed and the results were compared with those reported previously for 15 well-differentiated HCCs. Aberrations were seen in 2/10 LCAs: a gain of chromosome 7p was observed in one and gains of 17q and 20 in a second case. In 6/6 well-differentiated HCCs, up to 13 aberrations were detectable, with a mean of 7.2 aberrations per case in chromosome sites 1q, 4p, 4q, 5p, 5q, 6p, 6q, 7p, 7q, 8p, 8q, 10q, 11p, 13q, 14q, 16p, 16q, 17p, 17q, 20p, 20q, and 21q. Aberrations focused on gains or losses of six chromosome sites, 1q, 4q, 8p, 8q, 16p, and 17p; in all HCC samples, at least two of these sites were affected. None of these aberrations occurred in any of the LCAs analysed. CGH is therefore helpful in distinguishing between LCA and well-differentiated HCC. Detection of one or more of the six most frequent aberrations in HCC supports the diagnosis of carcinoma and makes LCA unlikely.
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PMID:Differentiation of liver cell adenomas from well-differentiated hepatocellular carcinomas by comparative genomic hybridization. 1127 6

Hepatocellular adenoma is a benign tumor of the liver that has a small but not negligible risk of malignant transformation into hepatocellular carcinoma. In analogy with the established role of oval cells in hepatocarcinogenesis in rodent models, human hepatic progenitor cells may have a function in the development of liver tumors. To investigate this issue, we performed immunohistochemistry on biopsies of 10 consecutively resected hepatocellular adenomas using markers for hepatic progenitor cells. Sections of paraffin-embedded and frozen biopsies were stained using antibodies against cytokeratins 7, 8, 18, and 19, chromogranin-A, OV-6, and neural cell adhesion molecule. Hepatic progenitor cells were observed in five of 10 hepatocellular adenomas. These five tumors also contained cells with an immunohistochemical phenotype intermediate between hepatic progenitor cells and hepatocytes. Hepatic progenitor cells and intermediate hepatocyte-like cells were scattered throughout the tumors with a density that varied from area to area. Ultrastructural examination confirmed the presence of hepatic progenitor cells. Our study shows that hepatic progenitor cells are present in a considerable proportion of hepatocellular adenomas, supporting the hypothesis that human hepatic progenitor cells can play a role in the development of hepatocellular tumors.
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PMID:Hepatic progenitor cells in hepatocellular adenomas. 1168 55

Glioma constitutes the most frequent brain tumour in man with glioblastoma as the most prevalent and malignant type. The average survival time of less than 16 months underlines the need for improvements in diagnosis and therapy. Here, we report the identification of a novel antigen termed glioma-expressed antigen 2 (GLEA2) causing a frequent immune response in glioma patients. Screening of 450 000 clones from a glioblastoma lambda zap expression library with autologous patient serum revealed a group of five serum-positive clones sharing a high sequence homology. Further sequence analysis showed a sequence homology to a hepatocellular carcinoma associated antigen 58 (HCA58). We localized the novel HCA homologous gene termed glioma-expressed antigen 2 (GLEA2) on chromosome 20 by somatic cell hybrid panel mapping. Using allogenic sera from 39 glioblastoma patients, we found an immune response against GLEA2 in 17 patients (43%). In addition, screening with allogenic sera from other glioma patients revealed GLEA2 directed antibodies in two out of five pilocytic astrocytomas and in one out of two astrocytomas. Unrelated tumour sera revealed no immune response and sera from healthy persons showed an immune response in two out of 14 cases (14%). Northern blot hybridization and RT-PCR showed ubiquitous GLEA2 gene expression in glioma and normal tissues. The novel HCA homologous gene, GLEA2, appears to induce a frequent immune response in glioma. In the light of the lack of useful glioma markers, it appears reasonable to consider GLEA2 as a potential future diagnostic marker.
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PMID:Glioma-expressed antigen 2 (GLEA2): a novel protein that can elicit immune responses in glioblastoma patients and some controls. 1170 62

The development of hepatic surgery involved also definition of indications for resection in primary liver tumours. Based on an analysis of a group of 76 patients with primary liver tumours operated in 1978-2001 (up to the end of October) the authors evaluated the indication criteria for resection of primary hepatic tumours. As to benign tumours most frequently haemangiomas were resected (in 35 patients) and follicular nodular hyperplasia in 10 patients. Indication for resection was the symptomatology of the tumour (40x), signs of progression during a check-up examination (13x) or doubts as regards preoperative ruling out of malignity (16x). Hepatocellular adenoma was resected in 8 patients, incl. 7 where the preoperative diagnosis was assessed by bioptic examination. The extent of resection depended on the size and site of the tumour, in haemangiomas and follicular nodular hyperplasia non-anatomical resections predominated (in 27 patients). On account of hepatocellular carcinoma resections were made in 18 patients, incl. 8 who suffered also from cirrhosis which limited the extent of resection. In patients without cirrhosis with carcinoma in one of the lobes an anatomical resection was implemented. Postoperative complications developed in 14 patients (18%), two died (3%) from hepatic failure and pulmonary embolism.
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PMID:[When is resection indicated in primary liver tumors?]. 1203 52


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