Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and pathological analysis of 66 cases of fibromatoses are presented. The age range in our series was 1 to 72 years. Superficial fibromatoses occurred predominantly in older patients with a peak incidence in the fifties while deep fibromatoses occurred predominantly in younger patients with a peak incidence in the twenties. Male to female ratio was 1.4 to 1. The abdominal fibromatosis occurred in female while our palmar fibromatosis occurred in male. There were 17 cases (26%) of multiple fibromatoses which occurred most frequently on both palms and had a tendency to symmetric distribution. The latent period between the two fibromatoses in a patient ranged from 1 year to 36 years. Clinical presentations included a palpable nodule or mass; flexure contracture of finger; penile hypertrophy, contracture, or discomfort on erection; and soreness, tenderness, or paresthesia over the tumor. Hydronephrosis may be complicated by intraabdominal fibromatosis. Size of the tumors ranged from 0.5 cm. To 30.0 cm. Three cases were associated with diabetes mellitus, 2 with alcoholics, 1 with liver cirrhosis, 2 with pulmonary tuberculosis, and 3 with hepatocellular carcinoma, cholangiocarcinoma, and mammary papillary carcinoma, respectively. Nine cases (14%) were associated with variable types of trauma, including being hurt by a stick, intramuscular injection in the gluteal region, tying penile shaft with a plastic band, breast massage and hot applying, and operation on abdomen. The superficial fibromatoses seldom recurred after excisional biopsy or fasciectomy while the deep fibromatoses often recurred. The recurrent rate of the deep fibromatoses was 21%. Malignant transformation or spontaneous regression was not found.
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PMID:[The fibromatoses. A clinicopathological study of 66 cases]. 281 66

The purpose of this study was to investigate the natural history of adenomatous hyperplasia (AH) in liver cirrhosis, which is suspected of being a precancerous condition of hepatocellular carcinoma (HCC). Sixteen patients with 19 histologically proven AH nodules were followed-up over time with ultrasonographic (US) examinations performed every 3-4 months. The biopsy was repeated whenever the volume of the lesion increased, its US pattern changed, or there was a change in the alpha-fetoprotein values. Thirteen out of 19 AH (68.4%) evolved toward HCC after 8-31 months (mean 14.2 months). Malignant transformation was proved in 7/18 AH within 1 year of its initial detection, in 12/15 AH within 2 years, and in 13/14 AH within 4 years. Six AH remained unchanged in size and US pattern for 9-70 months (mean 29.5 months). Long term follow-up of AH confirms that this lesion is a precursor of HCC.
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PMID:Long-term follow-up study of adenomatous hyperplasia in liver cirrhosis. 752 2

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide. The major risk factors for HCC development are now well defined and some of the multiple steps involved in hepatocarcinogenesis have been elucidated in recent years. However, no clear picture of how and in what sequence these factors interact at the molecular level has emerged yet. Malignant transformation of hepatocytes may occur as a consequence of various etiologies, such as chronic viral hepatitis, alcohol, and metabolic disorders, in the context of increased cellular turnover induced by chronic liver injury, regeneration and cirrhosis. Activation of cellular oncogenes, inactivation of tumor suppressor genes, overexpression of certain growth factors, and possibly telomerase activation and DNA mismatch repair defects may contribute to the development of HCC. Finally, aflatoxins have been shown to induce specific mutations of the p53 tumor suppressor gene, thus pointing to the contribution of environmental factors to tumor development at the molecular level.
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PMID:[Molecular aspects of hepatocellular carcinoma]. 1096 Sep 67

Malignant transformation of liver cell adenoma and unequivocal hepatocellular carcinoma in resected liver cell adenomas are rare. We report two cases of liver cell adenoma with concomitant hepatocellular carcinoma. The first occurred in a 19-year-old male with an asymptomatic liver mass and was discovered incidentally. He had a history of nephrotic syndrome treated with oral prednisolone for 15 years. The second occurred in a 46-year-old female who was admitted due to right tubo-ovarian abscess. Computerized tomography scanning incidentally found a 10-cm liver mass in the right lobe. There was no history of oral contraceptive use. Both patients were negative for serum hepatitis B surface antigen and anti-hepatitis C virus antibody. Neither had cirrhosis. These two cases imply that malignant transformation of liver cell adenoma does occur, and that liver cell adenomas should be excised when malignant transformation is suspected.
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PMID:Liver cell adenoma with concomitant hepatocellular carcinoma: report of two cases. 1251 62

Hepatocellular carcinoma (HCC) is one of the most common malignant tumours worldwide. The major aetiologies and risk factors for the development of HCC are well defined and some of the multiple steps involved in hepatocarcinogenesis have been elucidated in recent years. However, no clear picture of how and in what sequence these factors interact at the molecular level has emerged yet. Malignant transformation of hepatocytes may occur as a consequence of various aetiologies, such as chronic viral hepatitis, alcohol, and metabolic disorders, in the context of increased cellular turnover induced by chronic liver injury, regeneration and cirrhosis. Activation of cellular oncogenes, inactivation of tumour suppressor genes, genomic instability, including DNA mismatch repair defects and impaired chromosomal segregation, overexpression of growth and angiogenic factors, and telomerase activation may contribute to the development of HCC. Overall, HCCs are genetically very heterogeneous tumours. New technologies, including gene expression profiling and proteomic analyses, should allow us to further elucidate the molecular events underlying HCC development and identify novel diagnostic markers as well as therapeutic targets.
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PMID:Pathogenesis of hepatocellular carcinoma. 1582 36

Different event is a process that is dependent on stimulation of extracellular signals, signal transduction and gene express. Malignant transformation of hepatocytes may occur in cirrhosis, which is the result of extracellular matrix (ECM) remodeling. ECM could affect and maintain the differentiated phenotype of hepatocytes by regulating liver transcription factors. Moreover, ECM remodeling is correlated with dedifferentiation of hepatocellular carcinoma (HCC). Integrin-matrix adhesion system and E-cadherin/catenin adhesion complex mediate the cell-matrix interaction through focal adhesion kinase, extracellular-signal-regulated kinases and beta catenin/Wnt pathway. The different event of HCC compared with the reversion of abnormal cell-matrix interaction. New drugs that are power for regulating cell-matrix interaction may represent a novel therapeutic strategy for HCC.
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PMID:Cell-matrix talks: effects on differentiation of hepatocellular carcinoma. 1710 70

The liver is the main storage site for iron in the body. Excess accumulation of iron in the liver has been well-documented in two human diseases, hereditary hemochromatosis and dietary iron overload in the African. Hepatic iron overload in these conditions often results in fibrosis and cirrhosis and may be complicated by the development of hepatocellular carcinoma. Malignant transformation usually occurs in the presence of cirrhosis, suggesting that free iron-induced chronic necroinflammatory hepatic disease plays a role in the hepatocarcinogenesis. However, the supervention of hepatocellular carcinoma in the absence of cirrhosis raises the possibility that ionic iron may also be directly hepatocarcinogenic. Support for this possibility is provided by a recently described animal model of dietary iron overload in which iron-free preneoplastic nodules and hepatocellular carcinoma developed in the absence of fibrosis or cirrhosis. The mechanisms by which iron induces malignant transformation have yet to be fully characterized but the most important appears to be the generation of oxidative stress. Free iron generates reactive oxygen intermediates that disrupt the redox balance of the cells and cause chronic oxidative stress. Oxidative stress leads to lipid peroxidation of unsaturated fatty acids in membranes of cells and organelles. Cytotoxic by-products of lipid peroxidation, such as malondialdehyde and 4-hydroxy-2'-nonenal, are produced and these impair cellular function and protein synthesis and damage DNA. Deoxyguanosine residues in DNA are also hydroxylated by reactive oxygen intermediates to form 8-hydroxy-2'-deoxyguanosine, a major promutagenic adduct that causes G:C to T:A transversions and DNA unwinding and strand breaks. Free iron also induces immunologic abnormalities that may decrease immune surveillance for malignant transformation.
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PMID:Hepatic iron overload and hepatocellular carcinoma. 1908 72