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)

Serum amyloid A (SAA) is a major acute-phase protein whose chronic production by the liver can lead to the fatal disorder of secondary amyloidosis. Control of SAA is mediated by several inflammatory cytokines, including interleukin 1 (IL-1). To study the cis-acting regulatory elements responsible for constitutive and IL-1-induced expression, DNA constructs containing varying lengths of the promoter region from the human SAA2 beta gene 5' to the bacterial reporter gene, chloramphenicol acetyltransferase (CAT), were generated and transfected into human hepatoma cells, HepG2. Both positive and negative regulatory elements were found in the 5' flanking region of the human SAA2 beta gene. The more proximal region contains an IL-1 enhancer sequence GGGACTTTCC (SAA kappa B1; between -82 and -91), the binding site for the ubiquitous transcription factor NF-kappa B. IL-1 induction of the binding of nuclear factor to this sequence is maximal between 5 min and 30 min after incubation with IL-1 and negative in cells incubated for 60 min or longer. Mutation of the SAA kappa B1 sequence to a nonbinding form of NF-kappa B (CTCACTTTCC) abolishes the IL-1 effect. The SAA 5' region also contained an upstream repressor element, shown by transfection experiments. Within this element, a second NF-kappa B binding site (SAA kappa B2; -626 to -635) was found, and mutation of SAA kappa B2 to a non-NF-kappa B-binding form results in an increase in both constitutive + IL-1 stimulated SAA transcription.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Constitutive and NF-kappa B-like proteins in the regulation of the serum amyloid A gene by interleukin 1. 175 75

Cold adaptation, apparent protein metabolism, life span, body and organ weights, organ indices, mitochondrial changes in the lymphocytes, and frequency of diseases were examined in 661 (untreated) inbred CBA/Ca male mice. The rectal temperature proved to be lower in aged mice, i.e. the rectal temperature of old animals immediately after cold exposure was more distinctly decreased than that of young ones. The apparent protein metabolism measured by 75Se-selenomethionine turnover showed that biological half-life (T 1/2) values in the aged are almost linearly elevated. In very old animals the values are decreased. Body weight decreased significantly and continuously, spleen and liver indices decreased and heart index increased with age in healthy animals. The number of diseased animals increased with age peaking at the age of 751-900 days. After 900 days the number of diseased animals decreased. The most frequent diseases in the old animals are: hepatocellular carcinoma, amyloidosis and pulmonary adenocarcinoma. The mitochondria of spleen lymphocytes showed degenerative changes not associated with diseases, thus they can be considered as age-related biological changes.
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PMID:Biological changes and diseases in aged CBA/Ca mice. 283 95

Mortality, major causes of moribundity, and spontaneous tumors in CD-1 mice were studied in 891 males and 890 females, which were used as controls in 11 different 2-year chronic and oncogenicity studies during the past 5 years. Average mortality of males and females at 83 weeks of age was 32.6% and 28.6%, respectively, and at 109 weeks of age was 66.4% and 63.3%, respectively. Mortality was significantly lowered in males and females born after 1980 in accordance with an abruptly decreased occurrence of systemic amyloidosis in these animals. The major cause of death or moribundity included systemic arteritis, systemic amyloidosis, auricular thrombosis, glomerulosclerosis, lymphoma, and pulmonary adenocarcinoma in both sexes. Dysuria and hepatocellular carcinoma in males and mammary adenocarcinoma in females were also critical lesions. The major tumors occurring at more than 3% incidence were systemic lymphoma, adenoma/adenocarcinoma of the lung, adenoma/carcinoma of the liver and adenoma/adenocarcinoma of the Harderian gland for males, and systemic lymphoma, adenoma/adenocarcinoma of the lung, adenoma/carcinoma of the liver, leiomyoma/leiomyosarcoma of the uterus, adenoma/adenocarcinoma of the pituitary (anterior), adenoma/adenocarcinoma of the mammary gland and adenoma/adenocarcinoma of the Harderian gland for females. Intralaboratory heterogeneities in the incidence were recorded as follows: systemic lymphoma in 1 of 11 control groups (1/11) and adenoma/adenocarcinoma in 1/11 for males, and systemic lymphoma in 3/11, adenoma/adenocarcinoma of the lung in 2/11, adenoma/adenocarcinoma of the liver in 1/11, and adenoma/adenocarcinoma in 1/11 for females.
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PMID:Mortality, major cause of moribundity, and spontaneous tumors in CD-1 mice. 319 56

In order to evaluate geographical differences in the liver pathology of ducks infected with duck hepatitis B virus (DHBV), ducks in Chiba and Shimane, Japan, and Shanghai, China, were investigated. The numbers (DHBV positive/negative) and the maximum age of the ducks examined were 18/10 at 19 mo, 15/1 at 3 yr 4 mo, and 72/27 at 18 mo, respectively. DHBV infection was induced experimentally in ducks from Chiba and Shimane but was present congenitally in those from Shanghai. Ducks were examined regarding liver function tests, conventional histology, immunohistology, electron microscopy, and molecular hybridization for DHBV DNA in the serum and liver. There was no significant difference between DHBV-positive and -negative ducks in bilirubin and transaminase and alkaline phosphatase activities in the sera. Histologically, while the livers of ducks from Chiba and Shimane did not show necroinflammatory (hepatitis) activity, those from Shanghai frequently did (52.5%). Necroinflammatory activity of the Shanghai ducks was present almost equally in both DHBV-positive and -negative livers. The livers of Shanghai ducks but not the other two areas often (8.3%) had ground-glass inclusions which corresponded ultrastructurally to numerous virus particles in the dilated cisternae of the proliferated endoplasmic reticulum. No advanced liver disease, such as cirrhosis or hepatocellular carcinoma, was observed. There was no significant difference in the amount of DHBV DNA in the sera or in its pattern in the liver tissue among ducks of the three areas. In addition, the livers of Chiba ducks frequently had amyloidosis, while those of Shanghai ducks were contaminated with parasites. In conclusion, DHBV infection did not appear to provoke significant hepatitis activity or advanced liver disease in the examined ducks of all three areas, and the DHBV-positive livers from Shanghai ducks showed a different morphological appearance from those of the other two areas. This variation might reflect the difference in the strain of ducks, subtypes of DHBV, environmental factors, or a combination of these influences.
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PMID:Geographical pathology of duck livers infected with duck hepatitis B virus from Chiba and Shimane in Japan and Shanghai in China. 334 10

Intrahepatic cholangiography of primary sclerosing cholangitis (PSC) is characterized by stricture with or without dilation of the biliary tree. To evaluate whether this cholangiographic appearance is present in non-PSC livers as well as the histological features seen in non-PSC livers with this cholangiographic appearance, we performed postmortem intrahepatic cholangiography in 154 liver autopsy specimens. The PSC-like cholangiographic appearance was frequently found in cirrhosis with or without hepatocellular carcinoma (4 of 6, 67%), hepatocellular carcinoma (1 of 1, 100%), adult-type polycystic disease of the liver and kidneys (2 of 3, 67%), submassive hepatic necrosis (2 of 5, 40%), amyloidosis (1 of 2, 50%), and intrahepatic extensive thrombosis (1 of 1, 100%). It was also found but at lower frequency in metastatic carcinomas (3 of 13, 23%) and leukemia/lymphoma infiltration (2 of 12, 17%). Histologically, in livers with such a PSC-like cholangiographic appearance, the intrahepatic bile ducts were compressed by fibrosis, inflammatory infiltrates, liver cysts, cancer cell infiltration, amyloid deposition, or portal thrombi. Dilated ducts had less pronounced changes than strictured ducts. In these hepatobiliary diseases, the changes of intrahepatic bile ducts in the livers without the PSC-like cholangiographic appearance were much less marked than those in the livers with it. These data suggest that the PSC-like intrahepatic cholangiographic appearance is present in several hepatobiliary diseases and that clinicians should take such diseases into consideration if stricture with or without dilation is found on intrahepatic cholangiography.
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PMID:Intrahepatic cholangiographic appearance simulating primary sclerosing cholangitis in several hepatobiliary diseases: a postmortem cholangiographic and histopathological study in 154 livers at autopsy. 904 38

Cross-sectional imaging is playing an increasing role in diagnosis of diffuse liver diseases because it clarifies, in many cases, the overlap in clinical and laboratory manifestations often present in diffuse hepatic processes and thus may eliminate the need for a biopsy. Advances in cross-sectional imaging, particularly in magnetic resonance (MR) imaging, enable further characterization of hepatic parenchymal and architectural changes, allowing closer correlation with underlying pathologic changes. Advanced imaging techniques can be used to characterize a variety of metabolic, vascular, toxic, infectious, and neoplastic diffuse liver diseases. These include more common entities such as cirrhosis, Budd-Chiari syndrome, hemochromatosis, Wilson disease, fatty change, and diffuse neoplastic disease (hepatocellular carcinoma, metastasis, and lymphoma) and uncommon entities such as schistosomiasis, sarcoidosis, and amyloidosis. Correlation of computed tomographic and MR imaging findings with underlying pathologic features is helpful in understanding the gamut of diffuse diseases of the liver.
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PMID:Diffuse disease of the liver: radiologic-pathologic correlation. 785 42

Oxazepam is a benzodiazepine widely used as a sedative-hypnotic and antianxiety drug. In chronic studies, groups of 60 male and 60 female Swiss-Webster (SW) or B6C3F1 mice received oxazepam in feed at concentrations of 0,2500, or 5000 ppm. Additional groups of 60 male and female B6C3F1 mice received 125 ppm in feed to allow for study of mice with serum concentrations of oxazepam similar to those achieved in humans taking a therapeutic dose. At 57 weeks, treatment-related mortality of exposed SW mice caused the study to be terminated. Enhanced systemic amyloidosis contributing to heart failure was considered the principal cause of death. Hepatocellular adenomas and carcinomas were increased in exposed SW mice. Survival of B6C3F1 mice receiving 2500 and 5000 ppm oxazepam was also lower than that of controls. Early deaths were due to increased incidences of hepatoblastoma and hepatocellular carcinoma, and nearly all mice receiving 2500 or 5000 ppm developed hepatocellular neoplasia. An increase in follicular cell hyperplasia of the thyroid gland occurred in all exposed groups of B6C3F1 mice, and thyroid gland follicular cell adenoma was increased in exposed females. Further studies of the capacity of oxazepam to induce liver cell mitogenesis and an evaluation of the frequency of activated H- and K-ras oncogenes in the liver tumors of B6C3F1 mice has shown that many of the neoplastic and nonneoplastic responses of mice to oxazepam resemble those observed with phenobarbital.
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PMID:Carcinogenicity studies of oxazepam in mice. 798 36

Spontaneous hepatic bleeding is a rare condition. In the absence of trauma or anticoagulant therapy, hepatic hemorrhage may be due to underlying liver disease. The most common causes of nontraumatic hepatic hemorrhage are hepatocellular carcinoma and hepatic adenoma. Such hemorrhage can also occur in patients with other liver tumors, such as focal nodular hyperplasia, hemangiomas, and metastases. Other conditions associated with this entity include HELLP syndrome, amyloidosis, and miscellaneous causes. Imaging plays a significant role in the diagnosis and management of this potentially lethal entity. In the appropriate clinical setting, the diagnosis of a hemorrhagic liver lesion is suggested when a hyperechoic mass or a mass with hyperechoic areas is seen at ultrasonography, a hyperattenuating mass is seen at computed tomography (CT), or a mass with high-signal-intensity areas is seen at T1-weighted magnetic resonance (MR) imaging. The signal intensity of blood can be increased or decreased on MR images depending on when the hemorrhage is imaged. The presence and extent of commonly associated subcapsular hematomas and hemoperitoneum can be easily ascertained with CT. During the first 24-72 hours, acute hematomas are hyperattenuating on nonenhanced CT scans; later, they decrease in attenuation and sometimes develop a pseudocapsule.
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PMID:Imaging of nontraumatic hemorrhagic hepatic lesions. 1071 37

We describe the case of a male patient with biopsy-proven non-resectable liver adenoma at age 32 who presented 17 years later with hepatocellular carcinoma and nephrotic syndrome. Autopsy demonstrated systemic amyloidosis A. Review of the medical literature disclosed only three previous published cases of liver tumors associated with systemic amyloidosis. The association of non-hematologic neoplasias with systemic amyloidosis is rare and our literature review revealed only three cases of systemic amyloidosis in patients with liver tumors. We present here the case of a patient with apparent transition of liver adenoma to hepatocellular carcinoma with associated systemic amyloidosis.
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PMID:Systemic amyloidosis associated with hepatocellular carcinoma. Case report and literature review. 1128 49

Advances in imaging technology and development of liver-specific contrast agents have significantly increased the role of radiology in the detection and characterization of processes diffusely involving the liver. Tailored magnetic resonance imaging (MRI) sequences allow an accurate detection of many storage and metabolic diseases, such as iron overload disorders and steatosis (fatty liver). Faster scanning techniques available with both computed tomography (CT) and MRI provide, by assessing contrast dynamics, sufficient information for the characterization of diffuse neoplastic and vascular disorders. Characteristic changes in attenuation on CT, signal intensity on MRI, and enhancing features can be used to diagnose specific diffuse diseases such as candidiasis, diffuse/multifocal hepatocellular carcinoma, and schistosomiasis. Although an overlap in imaging findings still exists, familiarity with the imaging features of uncommon disorders such as Wilson's disease, amyloidosis, and sarcoidosis may be diagnostic in the proper clinical setting. This review focuses on the current role of imaging in the detection and characterization of diffuse liver disorders. Recent developments that have amplified the role of noninvasive diagnostic evaluation of these conditions are especially highlighted.
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PMID:Imaging of diffuse liver disease. 1143 72


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