Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1864663 (HCC)
 2,985 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prognostically relevant factors and treatment were analysed in 103 patients suffering from primary epithelial liver tumors (88 HCC, 15 CCC). Ninety of them underwent operations: 14 liver transplantations, 32 resections, 44 explorative laparotomies. The resection rate was 38%, the 30-day mortality in transplantation 14%, in resection 22%. The 5-year survival after resection was about 25%. Liver transplantation resulted in 50% 1-year and 40% 2-year survival. Long-term prognosis was positively influenced by cirrhosis and formation of a tumor capsule. Indications for operative management depend only on extension of tumor growth and concomiting liver cirrhosis as biology of epithelial liver tumors is poorly understood.
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PMID:[Prognosis and therapy of primary epithelial liver tumors. Evaluating a personal patient sample]. 217 93

Primary liver cancer, particularly HCC, is increasing in certain countries, notably Japan. Although hepatitis B virus has been etiologically linked to hepatocarcinogenesis and integration of its DNA into hepatocyte chromosomal DNA has been emphasized, other etiologic factors seem to have an interplay with virus infection. Histopathology of HCC has geographic variations. An expanding encapsulated HCC is most common in Japan, whereas it is nearly nonexistent in the West; such regional differences can only be explained by differences in the major etiologic factors. Early detection of HCC is now possible with ultrasound examination combined with AFP measurement, and this strategy has been executed with success in the Far East where HCC is endemic among cirrhotics. The speed of tumor growth can be measured with accuracy by ultrasound examination. Preneoplastic or early lesions of HCC in a cirrhotic liver seem to be adenomatous hyperplastic nodules or foci, and the conventional histological criteria for malignant liver cells do not seem applicable to such lesions. Although advanced cirrhosis is a real deterrent for hepatic surgery, hepatic resection affords a better survival compared with any nonsurgical therapeutic modality. Transcatheter arterial embolization is one of the current preferences of the hepatologist for inoperable patients. Lastly, a new staging scheme has been proposed for the assessment of prognosis and for comparison of efficacy of various therapeutic modalities.
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PMID:Primary liver cancer. Quadrennial review lecture. 301 22

Twenty-five cases of small hepatocellular carcinoma (HCC; diameter < or = 30 mm) were evaluated for overall morphologic features and growth patterns. The tumors often showed a well-differentiated, normotrabecular histologic pattern and insidious interstitial invasion, which resembled benign hepatocytes scattered in connective tissues. As the tumor grew, a less-differentiated tumor area became predominant. Portal tracts included in small HCC nodules were quantitatively assessed, revealing that they progressively reduced in number with tumor growth. The tumor margin was often reported to be unclear. The present results indicate that the histologic grade of tumor differentiation, capsular formation, existence of liver cirrhosis and patterns of interstitial invasion are important factors for determining the nature of the margin. The score of argyrophilic nuclear organizer regions (AgNOR) was examined in 5 cases showing typical interstitial invasion with the insidious type. In each case, the AgNOR score of the invading tumor cells was lower than that of tumor cells within the HCC nodules, but higher than benign hepatocytes in cirrhotic parenchyma. It clarified that the growth activity of well-differentiated HCC was rather suppressed upon their interstitial invasion.
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PMID:Growth patterns and interstitial invasion of small hepatocellular carcinoma. 764 31

We studied a selective enhancement of the mitomycin C (MMC)-induced antitumor effect focusing on the intracellular metabolism by NAD(P)H:quinone oxidoreductase (DT-diaphorase, DTD). The level of cellular DTD activity related well to the degree of MMC-induced DNA total cross links and cell growth inhibition in human cancer cell lines, KB, PH101, SH101 and K562. A DTD inhibitor, dicoumarol (DIC) or flavin adenine dinucleotide (FAD), inhibited the MMC-induced DNA damage and cytotoxicity at a non-toxic concentration. The DTD-mediated MMC activation was pH-dependent, and highest at pH 6 and lowest at pH 8. Although an inverse relationship appeared to exist between DTD activity and MMC efficacy in human xenografts implanted into nude mice and 9 fresh human tumor specimens, the investigation in 3 culture cells, HEC-46, HCC-48 and HCC-50, established from those xenografts, showed that DTD activated MMC in a pH-dependent manner as well as the other cell lines. Significant tumor pH reduction from 7.1 to 6.7 by continuous glucose infusion also increased the MMC-induced tumor growth inhibition in the human tumor xenografts. Thus, we conclude that bioreductive activation by DTD in a pH-dependent manner may be of key importance in the MMC-induced antitumor effect and that an increased MMC efficacy at a reduced pH caused by hyperglycemia may be applied to clinical use as a new manipulation for a biochemical modulation of MMC.
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PMID:DT-diaphorase as a target enzyme for biochemical modulation of mitomycin C. 856 14

The effects of cycloprodigiosin hydrochloride (cPrG-HCl), a new H(+)/Cl(-) symporter, were examined in liver cancer cell lines in vitro and in vivo. In the in vitro MTT assay, cPrG-HCl inhibited the growth of 6 liver cancer cell lines (Huh-7, HCC-M, HCC-T, dRLh-84, and H-35, hepatocellular carcinoma; HepG2, hepatoblastoma) in a dose- and time-dependent manner. The 50% inhibitory concentrations (IC(50)) at 72 hours' treatment for liver cancer cell lines were 276 to 592 nmol/L, while that for isolated normal rat hepatocyte was 8.4 micromol/L. The cPrG-HCl treatment of Huh-7 cells induced apoptosis as confirmed by the appearance of a subG(1) population, intranucleosomal DNA fragmentation, and chromatin condensation. cPrG-HCl raised the pH of acidic organelles and lowered pHi (below pH 6.8). In addition, the apoptosis in Huh-7 cells induced by cPrG-HCl was strongly suppressed when the cells were cultured with imidazole, a cell-permeable base. In the in vivo assay, nude mice bearing subcutaneous xenografted Huh-7 cells received 2 weeks of treatment with cPrG-HCl (1 or 10 mg/kg/d) subcutaneously. This treatment significantly inhibited tumor growth compared with the control after 8 days. The control mice were treated with 1% dimethylsulfoxide (DMSO) in saline (vehicle). A histopathological examination using the terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL) method showed apoptosis in the treated tumor cells. No pathological changes were observed in any organs, and the serum alanine transaminase levels remained within normal limits. These results suggest that cPrG-HCl may be useful for the treatment of hepatocellular carcinoma.
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PMID:Cycloprodigiosin hydrochloride, a new H(+)/Cl(-) symporter, induces apoptosis in human and rat hepatocellular cancer cell lines in vitro and inhibits the growth of hepatocellular carcinoma xenografts in nude mice. 1049 40

Early diagnosis of HCC is possible because certain risk factors for this tumor are known and because sensitive and relatively inexpensive diagnostic tools are available. Early diagnosis of HCC is also possible because of the long phase of asymptomatic tumor growth and the tumor's tendency to grow as a solitary mass in many patients. In two consensus development conferences held in Anchorage, Alaska and in Milan, Italy, chronic carriers of HBsAg, patients with cirrhosis, patients with rare metabolic liver diseases, and individuals with family histories of HCC were identified as patients at high risk for HCC and therefore as candidates for periodic screening. At the Anchorage conference, it was recommended that healthy carriers have at least yearly determinations of serum AFP and that carriers with additional risk factors (e.g., cirrhosis) be screened every 6 months by abdominal US scans and determination of serum AFP levels. No specific recommendations were released for HBsAg-negative patients with chronic liver disease. At the Milan conference, it was recommend that patients with cirrhosis or with certain congenital metabolic conditions known to be at risk for HCC should be screened by AFP determination and US scan twice a year. It was also recommended that HBsAg carriers older than 35 years or with family histories of HCC should be screened for HCC by determinations of serum AFP levels and aminotransferase levels once a year.
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PMID:Screening for cancer in viral hepatitis. 1121 10

Previous studies have shown that there is a high frequency of loss of heterozygosity (LOH) on chromosome 17p13.3 in hepatocellular carcinoma [HCC (M. Fujimori et al., Cancer Res., 51: 89-93, 1991; H. Nagai et al., Oncogene, 14: 2927-2933, 1997; V. Boige et al., Cancer Res., 57: 1986-1990, 1997; Z. Piao et al., Int. J. Cancer, 75: 29-33, 1998; and B. Charroux et al., J. Cell Biol., 148: 1177-1186, 2000)]. The minimum region of LOH on chromosome 17p13.3 in HCC has been defined within the region between D17S643 and D17S1574. Moreover, D17S926 in the minimum region of LOH has the highest frequency of LOH, and its sequencing analysis has been accomplished. In this region, 6 of 13 novel genes have been characterized (X. Zhao, D. Wan, M. He, Yu. Ye, Yi. He, L. Han, M. Guo, Y. Huang, W. Qin, M-W. Wang, W. Chong, J. Chen, L. Zhang, N. Yang, B. Xu, M. Wu, L. Zuo, and J. Gu. A high frequency LOH region on chromosome 17p13.3 in human HCC with densely clustered genes identified, submitted for publication). Here we describe the cloning and characterization of one of these novel genes, designated HCC suppressor 1 (HCCS1), located at this region. HCCS1 had 18 exons, and its full-length cDNA was 2.0 kb. The protein expression product of HCCS1 was located in mitochondria. HCCS1 had a high frequency of mutations in HCC samples, whereas no alteration has been found in matched noncancerous liver tissues. Immunohistochemistry revealed a significantly higher expression of HCCS1 in the noncancerous liver tissues (33 of 35 samples) than in the HCC samples (2 of 35 samples). Transfection of HCCS1 cDNA into the HCC cell line remarkably reduced the efficiency of its colony formation and inhibited tumor growth in nude mice. Taken together, these findings strongly suggest a potential role of HCCS1 as a HCC putative suppressor gene.
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PMID:A novel growth suppressor gene on chromosome 17p13.3 with a high frequency of mutation in human hepatocellular carcinoma. 1160 66

Although neovascularization is regarded as an essential factor for tumor growth, it is unclear whether pancreatic adenocarcinoma is also influenced by this process. Furthermore, the reported microvessel count (MVC) data can not be compared due to the diversity of evaluating methods, and the relation between MVC data and metastatic potentials remains controversial. A total of 24 pancreatic adenocarcinomas and 24 adjacent non-cancerous pancreatic parenchyma were analyzed for MVC using anti-CD31 antibody. In addition, the MVC of 15 hypervascular tumors (10 hepatocellular carcinomas: HCC and 5 islet cell pancreatic tumors: ICT), 30 other types of adenocarcinomas (10 gastric, 10 colon and 10 intraductal papillary mucinous tumors of the pancreas: IPMT), as well as that of non-cancerous areas, were also analyzed. The extent of hepatic and peritoneal spread in 24 pancreatic adenocarcinoma patients was classified and correlations with MVC were evaluated. The mean MVC of 24 pancreatic adenocarcinomas (31.6 +/- 11.1) was actually lower than that of HCCs (91.6) or ICTs (56.4). The diversity is temperate as compared with that of other adenocarcinomas, i.e., 42.9 in gastric carcinomas, 35.6 in colon carcinomas and 32.5 in IPMT. MVC in non-cancerous areas were significantly higher in the pancreas (112.8) than in the stomach (29.6) or colon (26.3). MVC ratios of the cancerous area to the non-cancerous area were significantly lower in the pancreas (0.2818 +/- 0.100) than in the stomach (1.569 +/- 0.526, p<0.001) or the colon (1.423 +/- 0.493, p<0.001). MVC were higher in diffuse hepatic metastasis patients (36.0) than in limited metastasis patients (25.7). In conclusion, MVC in pancreatic adenocarcinoma revealed vascular volume to actually be lower than that of hypervascular tumors. We believe, however, that this hypovascularity is due mainly to contrast with the hyper-vascular non-cancerous pancreas, since MVC in the cancerous area itself was at the same level as in other adenocarcinomas. In addition, we revealed MVC to be of value for predicting the extent of liver metastasis.
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PMID:Neovascularization in pancreatic ductal adenocarcinoma: Microvessel count analysis, comparison with non-cancerous regions and other types of carcinomas. 1183 87

1,25-dihydroxycholecalciferol [1,25-(OH)2 D3] has been shown to have antiproliferative effects in a wide variety of cancer cell lines. In vivo studies, although often limited by the development of hypercalcemia, have also shown the potential usefulness of 1,25-(OH)2 D3 in inhibiting tumor growth. The potential usefulness of the drug has been hampered by the development of hypercalcemia. This pilot clinical study was designed to evaluate the preclinical results that have shown, locoregional administration of 1,25-(OH)2 D3 in lipiodol can prevent the development of hypercalcemia. Eight patients with refractory HCC were given a single intrahepatic arterial dose (50, 75 or 100 microg) of 1,25-(OH)2 D3 dissolved in 5 ml of lipiodol. Following this, for 4 weeks serum calcium, 1,25-(OH)2 D3, alpha-fetoprotein and a range of biochemical indices were monitored. While, in 3 patients the calcium levels exceeded the normal range, even at these extremely high doses, non of the patients developed grade 3 hypercalcemia. 1,25-(OH)2 D3 administration also led to transient stabilization of serum alpha-fetoprotein in these patients. The data obtained support the hypothesis that, in patients with HCC, locoregional delivery of 1,25-(OH)2 D3 in lipiodol can allow administration of supra-pharmacological doses of the drug without the development of hypercalcemia.
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PMID:Hepatic intra-arterial injection of 1,25-dihydroxyvitamin D3 in lipiodol: Pilot study in patients with hepatocellular carcinoma. 1223 33

Most patients with HCC do not qualify for surgical interventions. In carefully selected patients, TACE may improve survival, reduce the rate of tumor growth, and decrease the incidence of portal vein occlusion. Since the introduction of TACE in the 1980s, the technical aspects of the procedure have significantly improved. Sophisticated angiographic equipment and techniques have made superselective arterial catheterization possible for more focused drug delivery. The use of ethiodized oil allows for more effective targeting of HCC and provides dual embolization of the hepatic artery and the portal venules supplying the tumor. Many important technical questions about TACE remain unanswered at this time: there are no reliable, standardized patient selection criteria, ideal cytotoxic agents have not yet been identified, the optimal dose of ethiodized oil has not been confirmed, and the optimal frequency and timing of repeat treatment sessions remain unknown. One major limitation of TACE--the need for repeated treatments, which can result in deterioration of liver function--may be avoided by use of a combination of interventional therapies. The combination of limited TACE with PEI or RFA may lead to improved survival and decreased risk of liver failure. More recently, two excellent randomized clinical trials have demonstrated significant survival benefit for patients treated with TACE when compared with those treated symptomatically.
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PMID:Hepatic artery embolization for hepatocellular carcinoma: technique, patient selection, and outcomes. 1273 33


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