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liver neoplasms/prolina

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Proline dithiocarbamate inhibits N-nitrosodiethylamine induced liver carcinogenesis.

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A study was conducted to determine the toxicity of different dithiocarbamates and of disulfiram. In an experiment showing the cytotoxicity against murine spleen lymphocytes, proline dithiocarbamate (PDTC) and thioproline dithiocarbamate showed the lowest toxicity. Therefore one of them was selected
Large doses of dimethylnitramine (DMNM), N-nitroso-L-proline (NPRO), and sodium nitrite were administered in the drinking water to MRC Wistar rats for at least 1 year, and the rats were maintained for life. DMNM (total dose, 20 g/kg) produced liver tumors in 25 (69%) of the 36 rats and nasal cavity

The significance of proline-rich tyrosine kinase2 (Pyk2) on hepatocellular carcinoma progression and recurrence.

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Understanding the precise molecular mechanisms that trigger liver cancer cell migration and invasion could develop novel therapeutic strategies targeting cancer cell invasion to increase the sensitivity to current treatment modalities. In the current study, 49 patients with hepatocellular carcinoma
In this study, urinary metabolites from liver cancer patients and healthy volunteers were studied by a metabonomic method based on ultra performance liquid chromatography coupled to mass spectrometry. Both hydrophilic interaction chromatography (HILIC) and reversed-phase liquid chromatography (RPLC)
OBJECTIVE We aimed to investigate the effects of adiponectin on liver cancer growth and metastasis and explore the underlying mechanisms. METHODS An orthotopic liver tumor nude mice model with distant metastatic potential was applied. Either Ad-adiponectin (1 x 10(8); treatment group) or

Misregulation of the proline rich homeodomain (PRH/HHEX) protein in cancer cells and its consequences for tumour growth and invasion.

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The proline rich homeodomain protein (PRH), also known as haematopoietically expressed homeobox (HHEX), is an essential transcription factor in embryonic development and in the adult. The PRH protein forms oligomeric complexes that bind to tandemly repeated PRH recognition sequences within or at a
The aim of the current study is to elucidate the mechanism of proline-rich tyrosine kinase 2 (Pyk2)-mediated cell proliferation and invasiveness in hepatocellular carcinoma (HCC) cells. Human HCC cell lines PLC and MHCC97L were stably transfected with either full-length Pyk2 or C-terminal non-kinase

Nanoscale Coordination Polymers for Synergistic NO and Chemodynamic Therapy of Liver Cancer.

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Nitric oxide (NO) induces a multitude of antitumor activities, encompassing the induction of apoptosis, sensitization to chemo-, radio-, or immune-therapy, and inhibition of metastasis, drug resistance, angiogenesis, and hypoxia, thus attracting much attention in the area of cancer intervention. To
The Grb7 (growth factor receptor-bound 7) protein, a member of the Grb7 protein family, is found to be highly expressed in such metastatic tumors as breast cancer, esophageal cancer, liver cancer, etc. The src-homology 2 (SH2) domain in the C-terminus is reported to be mainly involved in Grb7

Hepatocellular carcinoma: Mouse models and the potential roles of proteases.

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Primary liver cancer is the second most common cause of mortality from cancer. The most common models of hepatocellular carcinoma, which use a chemical and/or metabolic insult, xenograft, or genetic manipulation, are discussed in this review. In the tumour microenvironment lymphocytes, fibroblasts,

A correlation study on urinary excretion of N-nitroso compounds and cancer mortality in China: interim results.

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Samples of 12-h overnight urine were collected from approximately 40 male adults in each of the 26 counties of China. Two urine specimens were collected from each subject--one after a loading dose of proline and ascorbic acid and another after a loading dose of proline only. Levels of N-nitrosamino

Frequent loss of p53 codon 72 Pro variant in hepatitis C virus-positive carriers with hepatocellular carcinoma.

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Codon 72 exon 4 polymorphism of the p53 gene has been implicated in cancer risk and it has been suggested that it may have an impact on the clinical outcome of the disease. Our objective was to evaluate the association between p53 polymorphism at codon 72 and hepatocellular carcinoma. The p53 codon

Abnormalities of liver regeneration: a review.

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Structural and functional changes during liver regeneration have been studied extensively in experimental animals following partial hepatectomy or hepatic injury induced by noxious substances. These observations have been extended to evaluate abnormalities of liver regeneration which contribute to

"P53 codon 72 single base substitution in viral hepatitis C and hepatocarcinoma incidences".

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Viral infection with hepatitis C virus (HCV) has a high propensity in becoming chronic and it is the major cause of hepatocellular carcinoma (HCC) worldwide. This review was basically established to illustrate the putative role of the P53 gene Arg72Pro polymorphism on various cancer models and viral
BACKGROUND Hepatocellular carcinoma (HCC) is on the rise and the sixth most common cancer worldwide. To combat HCC effectively research is directed towards its early detection and the development of targeted therapies. Given the fact that epidermal growth factor (EGF) is an important mitogen for
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