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)

In order to detect a possible relationship between alpha-fetoprotein (AFP) levels, total tumour volume at the moment of the discovery and the tumour volume doubling time, we studied a population of 138 patients, affected by Hepatocellular Carcinoma (HCC) discovered at abdominal ultrasound (US) examination and confirmed by liver biopsy in all cases. In each patient the serum AFP level was determined within a week before or after the US examination. A small therapy-free subgroup of 23 patients, was also serially observed for a mean period of 4 months, so making possible the evaluation of the tumour volume doubling time and its relationship with the initial value of AFP. In 81 patients (58.7%) the serum AFP resulted less than 20 ngr/ml in 21 (15.2%), between 20 and 200 and in 36 (26.1%) greater than 200ngr/ml. No statistical correlation was found between the tumour volume calculated on the basis of the US image at the moment of the discovery and the AFP level, even though very high levels (greater than 3000) were found only in large tumours. Furthermore the tumour doubling time was not correlated with the initial value of AFP.
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PMID:Relationship between alpha-fetoprotein serum levels, tumour volume and growth rate of hepatocellular carcinoma in a western population. 172 58

Hepatocellular carcinoma is not only the leading cause of male cancer death in Taiwan, but also one of the most common cancers in the world. The survival of hepatocellular carcinoma patients is very low, mainly due to the lack of effective treatments. Radiation and chemotherapies in general are not satisfactory: surgery itself is the most effective treatment for hepatocellular carcinoma but only on small resectable tumors. The overall prognosis is still poor. Previously, we have found that the level of glucocorticoid receptor and its mRNA in hepatocellular carcinoma was significantly higher than that of the adjacent liver tissue. This correlated well with the elevated serum alpha-fetoprotein levels in patients with hepatocellular carcinoma. Recently, a female hormone, progesterone, has been found to inhibit the expression of alpha-fetoprotein in hepatoma cells. In addition, progesterone has been used to treat a few hepatocellular carcinoma patients with promising responses. These results together with our hypothesis that the expression of alpha-fetoprotein is regulated by glucocorticoid receptor complex in proliferating hepatocellular carcinoma cells lead to the conclusion that steroid hormones and/or their antagonists may interfere with the function of glucocorticoid receptors in tumors, consequently regulate tumor growth. The potential of hormonal therapy for treatment of hepatocellular carcinoma is worthy of further investigation.
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PMID:Hormonal therapy for hepatocellular carcinoma. 172 85

Hematoxylin and eosin (H-E) stained liver sections of 47 autopsy cases of hepatic malignancies were examined. There were 43 cases of hepatocellular carcinoma (subtypes of 30 trabecular, 7 solid, 5 pseudoglandular, and one scirrhous carcinoma), 3 of cholangiocellular carcinoma and one of mixed carcinoma. After immunohistochemical staining, benign hepatocytes reacted positively with anti-epithelial membrane antigen (EMA). Hepatocellular carcinoma cells reacted more weakly than benign hepatocytes. It was noted that the microtubular structure, which could not be demonstrated even by alcian blue or cationic ferric hydroxide colloid stabilized with cacodylate (Fe-CaC), was clearly detected with anti-EMA. The EMA-positive microtubular structures may indicate terminal cholangiolar differentiation. Based on EMA, seven more cases formerly classified as hepatocellular carcinoma by H-E were reclassified as mixed carcinoma, totaling eight (17.0%). The histologic classification of "mixed carcinoma" has been 1.5 to 2.0% of primary liver cancers in Japan, but we suggest there may be more cases of "mixed carcinoma" identified in the future. In conclusion, we emphasize that EMA staining is useful for more accurate classification of hepatic tumors.
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PMID:Histochemical and immunohistochemical analyses of primary carcinoma of the liver. 172 62

Hepatocellular carcinoma commonly invades the portal vein but is rarely seen in the bile duct. When seen, a minor intraductal component usually accompanies a prominent hepatic involvement. We report a case of hepatocellular carcinoma that entirely involved the common bile duct, the hepatic involvement was undiscernible at operation or ultrasonography. The patient had obstructive jaundice both at first presentation and at recurrence. The liver was normal at both explorations. The elevated AFP levels returned to normal after second resection. The diagnosis was confirmed by electron microscopy.
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PMID:Intraductal hepatocellular carcinoma with normal liver--case report. 172 65

Recent fundamental research has disclosed the presence of multiple genetic alterations including activation of oncogenes and inactivation of tumor suppressor genes in various human cancers. These multiple genetic alterations are thought to be correlated with multiple stages of carcinogenesis and further progression. Hepatocellular carcinoma (HCC) is a typical example. The majority of HCCs are associated with infection by hepatitis virus B or C. In the damaged liver, small nodular lesions develop due to clonal expansion of hepatocytes. Some of these nodules are diagnosed as early HCC of the well differentiated type and correspond to in situ or microinvasive carcinoma. Within these nodules, moderately or poorly differentiated HCCs often emerge as nodule-in-nodule lesions when the diameter of the nodules exceeds 1.5 cm. Ordinary HCCs formed by progression show highly increased cell proliferation, neovascularization, production of high-molecular-mass forms of basic fibroblast growth factor and aneuploidy in some tumors. Corresponding to this stage of malignant progression, HCCs show loss of heterozygosity for multiple chromosomes including chromosomes 4, 16q and 17p. Tumor suppressor gene p53, located on 17p, is frequently mutated in high-grade, but not in early, HCCs. Thus, it is strongly suggested that inactivation of multiple tumor suppressor genes plays an important role in progression, and probably directly or indirectly causes chromosome instability, enhanced cell proliferation and neovascularization.
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PMID:Pathology and molecular mechanisms of multistage human hepatocarcinogenesis. 172 34

Hepatocellular carcinoma is one of the five leading human cancers causing at least 250,000 deaths each year. One of the major risk factors for this disease is exposure to dietary aflatoxins, and the development of appropriate molecular dosimetry biomarkers would facilitate the identification of individuals at risk. This study was undertaken to explore the relationship between dietary intake of aflatoxins and the excretion of the major aflatoxin-DNA adduct and other metabolites into the urine of chronically exposed people. The following protocol was developed for this investigation in Guangxi Autonomous Region, People's Republic of China, where the diets of 30 males and 12 females (ages, 25-64 years) were monitored for 1 week and aflatoxin intake levels determined each day. Starting on the fourth day, total urine volumes were obtained in consecutive 12-h fractions for 3 or 4 days. High performance liquid chromatography and competitive radioimmunoassay analyses were done on each of the urine samples, and the relationships between excretion of total aflatoxin metabolites, aflatoxin-N7-guanine, aflatoxin M1, aflatoxin P1, and aflatoxin B1, and aflatoxin B1 intake values were determined. The average intake of aflatoxin B1 by men was 48.4 micrograms/day, giving a total mean exposure during the study period of 276.8 micrograms. The average daily intake by women was 77.4 micrograms/day, resulting in a total average exposure during the 7-day period of 542.6 micrograms aflatoxin B1. Initial efforts to characterize aflatoxin metabolites in urine samples were with an analysis by competitive radioimmunoassay. The analysis by linear regression of the association between aflatoxin B1 intake/day and total aflatoxin metabolite excretion/day showed a correlation coefficient of only 0.26. These findings stimulated the immunoaffinity/analytical high performance liquid chromatography analysis for individual metabolites. When the data were analyzed by linear regression analysis, the aflatoxin N7-guanine excretion and aflatoxin B1 intake from the previous day showed a correlation coefficient of 0.65 and P less than 0.000001. Similar analysis for aflatoxin M1 resulted in a correlation coefficient of 0.55 and P less than 0.00001, whereas there was no positive statistical association between exposure in the diet and aflatoxin P1 excretion, despite aflatoxin P1 being quantitatively a major metabolite. Analysis of the total aflatoxin-N7-guanine excretion in the urine during the complete collection period plotted against the total aflatoxin B1 exposure in the diet for each of the individuals, smoothing the day to day variations, revealed a correlation coefficient of 0.80 and P less than 0.0000001.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Molecular dosimetry of urinary aflatoxin-DNA adducts in people living in Guangxi Autonomous Region, People's Republic of China. 172 85

Hepatocellular carcinoma has one of the poorest 5 year survival rates of any human cancer. Preventive measures offer the best possibility of ameliorating this disease and chemoprotective agents are being developed for this purpose. The dithiolethiones, including oltipraz and the unsubstituted molecule 1,2-dithiole-3-thione, have been shown to be potent inhibitors of aflatoxin-induced hepatic tumorigenesis in rats. However, subsequent evaluation of dithiolethiones or other chemoprotective agents in human clinical trials will require the development of intermediate, non-invasive biomarkers to evaluate the efficacy of these interventions. In this study, levels of molecular dosimetry biomarkers for determining genotoxic damage caused by aflatoxin B1 have been measured in a chronic exposure model with male F344 rats wherein half the animals were fed a diet supplemented with 0.03% 1,2-dithiole-3-thione to lower their risk for tumors and the other half were fed unsupplemented AIN-76A diet and were at high risk for tumor development. Levels of hepatic aflatoxin-DNA adducts, serum aflatoxin-albumin adducts and excreted aflatoxin-N7-guanine adducts in urine were determined following multiple administrations of 250 micrograms aflatoxin B1/kg body wt on days 0-4 and 7-11 to assess the use of the serum and urinary biomarkers as indices of chemoprotective efficacy. In the rats fed 1,2-dithiole-3-thione, the overall diminutions in the levels of hepatic DNA adducts, urinary aflatoxin-N7-guanine and serum aflatoxin-albumin adducts over the 2 week exposure period were 76, 62 and 66% respectively. This parallelism in reductions of levels of biomarkers relative to target organ DNA adduct burden suggests that these biomarkers are predictive short-term, non-invasive measures for assessing the efficacy of chemoprotective interventions in experimental studies and can be applied to human clinical trials directed at populations at high risk for aflatoxin exposure and primary hepatocellular carcinoma.
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PMID:Molecular dosimetry of urinary aflatoxin-N7-guanine and serum aflatoxin-albumin adducts predicts chemoprotection by 1,2-dithiole-3-thione in rats. 173 61

Tyrosinaemia type I is a recessively inherited disorder caused by a deficiency of fumarylacetoacetase (FAH), the last enzyme in tyrosine degradation. The presumed toxic agents are fumaryl- and maleylacetoacetate which are converted to succinylacetone (SA), a metabolite found in increased amounts in urine and plasma of the patients. The major clinical features are progressive liver damage and renal tubular defects with hypophosphataemic rickets. Renal tubular dysfunctions with secondary rickets may be lacking altogether, even in chronic patients. Hepatocellular carcinoma is a major cause of death in the chronic form. Diagnosis of the disorder is made by assay of SA in urine and serum and by determination of FAH in lymphocytes or fibroblasts. Prenatal diagnosis is performed by SA assay in amniotic fluid supernatant and FAH analysis in cultured amniotic fluid cells or chorionic villus material. Presence of a 'pseudodeficiency' gene for FAH prevents prenatal diagnosis by enzyme analysis in some families, and this gene also precludes identification of heterozygotes outside tyrosinaemia families. Immunoblot analyses show that acute patients and some chronic patients lack immunoreactive FAH protein. cDNA probes for FAH have been developed and several polymorphisms related to the FAH gene have been reported, which may allow prenatal diagnosis in families with complex genotypes. The gene for FAH has been mapped to chromosome 15 q23-q25. Liver transplantation is the ultimate treatment; most patients continue to excrete SA in urine after liver transplantation and therefore there is a possibility of kidney disease after transplantation.
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PMID:Tyrosinaemia type I--an update. 174 21

Hepatocellular carcinoma in woodchuck were characterized for woodchuck hepatitis virus integration nea c-myc oncogene. In one tumor, viral integration resulted in overexpression of a c-myc viral cotranscript. In a second tumor, viral insertion, 600 bp upstream of c-myc exon 1, was associated with increased levels of normal c-myc mRNA. These results demonstrate that integration of woodchuck hepatitis virus near a proto-oncogene can contribute to the genesis of liver tumors. From a comparison of a single hepatitis B virus (HBV) integration site in a human hepatoma with the corresponding unoccupied site have shown HBV DNA insertion in a putative cellular exon. This exon presented striking similarity to the DNA-binding domain of the thyroid/steriod hormones receptors. The corresponding cDNA has been isolated (hap gene) as shown to encode the retinoic acid receptor. It is most probable that consequent to HBV insertion, hap gene became inappropriately expressed as an altered chimaeric gene retinoic acid receptor, thus contributing to the cell transformation. As for woodchuck these results strongly support the possibility that HBV, may play a direct role in liver carcinogenesis by insertional mutagenesis.
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PMID:[Hepatitis B virus and hepatocellular carcinoma]. 177 42

Hepatocellular carcinoma with a tumor thrombus extending into the right atrium has been considered beyond the reach of resection. These patients usually die within a short period because of pulmonary embolism, heart failure, or cancer progression. The only treatment is hepatic resection with removal of the tumor thrombus. A 38-year-old woman underwent left lobectomy with removal of the tumor thrombus with the use of cardiopulmonary bypass. The patient had an uneventful course and is doing well 15 months after surgery, without signs of recurrence. We have proved that hepatic resection with removal of a tumor thrombus extending into the right atrium can be carried out successfully. The next problem is whether the lives of these patients can be prolonged by this operation.
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PMID:Hepatocellular carcinoma with tumor thrombus extending into the right atrium: report of a successful resection with the use of cardiopulmonary bypass. 184 85


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