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)

Although hepatocellular carcinoma is probably caused by one or more environmental carcinogens, a genetically determined susceptibility to the development of the tumor has not been excluded. In looking for such a predisposition, we have compared the histocompatibility antigens (HLA) of 102 southern African blacks with histologically proved HCC with those of 208 healthy blacks. The standard two-stage lymphocyte microcytotoxicity method was used to test for 40 antigens: 17 in the A locus, 20 in the B locus, and 3 in the C locus. None of the HLA antigens had a frequency that was significantly different in the patients and the controls. A close association undoubtedly exists between chronic hepatitis B virus infection and hepatocellular carcinoma. If this virus is proved to be oncogenic with respect to hepatocellular carcinoma, a genetic predisposition to the hepatitis B virus carrier state may have an indirect bearing on the etiology of the tumor. Sera from the hepatocellular carcinoma patients were therefore tested for hepatitis B virus markers (HBV surface antigen and antibody against HBV core antigen), and these were related to the patients' histocompatibility antigens. None of the HLA antigen frequencies was significantly different in the surface antigen-positive and the surface antigen-negative patients. As 88% of the patients were anticore positive, no meaningful correlation could be carried out with this marker. Analysis of histocompatibility antigens thus failed to show evidence of a genetic predisposition either to hepatocellular carcinoma or to chronic hepatitis B surface antigenemia in patients with this tumor.
Gastroenterology 1979 Sep
PMID:Histocompatibility antigens in patients with hepatocellular carcinoma and their relationship to chronic hepatitis B virus infection in these patients. 22 45

The value of the leucocyte adherence inhibition (LAI) test in the diagnosis of hepatocellular carcinoma (HCG) was investigated in 36 patients with this tumour. The sensitivity and specificity of the tube LAI test was assessed in 21 patients with HCC, 15 apparently healthy individuals, 9 patients with various forms of benign liver disease and 5 patients with non-hepatic neoplasms. In only 42% of the HCC patients tested was leucocyte adherence to glass reduced to a greater extent than in the healthy controls and in the patients with non-hepatic neoplasms, and the differences were not statistically significant. Moreover, positive results were obtained in 6/9 patients with benign hepatic disease. A further 15 patients were tested against extracts of HCC tissue using the haemacytometer LAI method. Of these, 53% gave positive results. In all, only 17/36 patients (47%) gave positive LAI responses. The test is thus of limited value in the diagnosis of HCC. The high false-negative result rate may be due either to abrogation of the immune response in HCC patients with large tumour burdens or to antigenic heterogeneity in HCC.
Br J Cancer 1979 Sep
PMID:Evaluation of leucocyte adherence inhibition in hepatocellular carcinoma. 22 91

In male Wistar rats, 1 alpha-HCC and 1 alpha, 25-DHCC induced diuretic effects in doses of 2.5 and 25 micrograms/kg p.o., while no such effects of 1 alpha-HCC were seen with a dose of 0.25 microgram/kg p.o. Effect of 1 alpha-HCC appeared later than that of 1 alpha, 25-DHCC, but at 24 hr, the difference disappeared. Similar results were obtained with urinary concentrations of calcium (increase) and phosphorus (decrease). Glomerular filtration rate (GFR) and tubular reabsorption of phosphate (TRP) were remarkably elevated by 1 alpha, 25-DHCC, and effects of 1 alpha-HCC were rather weak and apparently not dose dependent. In light of these results and the finding that there was no difference between the effects of 1 alpha-HCC and 1 alpha, 25-DHCC on serum calcium and phosphorus at 24 hr, the mechanism of action of these sterols on the renal function seems to differ. In male Beagle dogs, 0.25 microgram/kg/day p.o. of 1 alpha-HCC or 1 alpha, 25-DHCC induced a severe hypercalcemia and GFR was decreased in the 1 alpha, 25-DHCC treated group. A gradual recovery occurred with cessation of the administration. Thus decrease in GFR was considered to be due to calcification of the kidney.
Nihon Yakurigaku Zasshi 1979 Sep
PMID:[Studies on biopharmacological actitivy of active vitamin D3 analogues (VII) Effect of 1 alpha-hydroxycholecalciferol on renal function in rats and Beagle dogs (author's transl]. 54 Aug 87

It has been well recognized that results of treatment in hepatocellular carcinoma with main portal vein tumor thrombus (Vp 3 HCC) are very poor. But we tried aggressive transcatheter treatment (one shot or continuous hepatic arterial infusion, TAE) and hepatectomy with postoperative TAE in 52 cases by Vp3 HCC in recent 10 years. Analysis of the results disclosed that PR or CR cases were observed only in the series of continuous hepatic arterial infusion therapy. And cumulative survival rate was the best in the series of hepatectomy (50% survival interval is 18 months). We concluded that hepatectomy and resection of the tumor thrombus with postoperative TAE is the best treatment in Vp3 HCC.
Nihon Geka Gakkai Zasshi 1992 Sep
PMID:[Clinical evaluation of operative and non-operative treatment in hepatocellular carcinoma with main portal vein tumor thrombus]. 133 17

Over a 30 month period from 1987 to 1990, selective hepatic cannulation under fluoroscopic control was performed in 57 consecutive patients with primary and secondary malignancies of the liver. Fifty-three patients were subsequently treated using intra-arterial Lipiodol emulsified with epirubicin. The tumours treated were hepatocellular carcinoma (n = 35), metastatic adenocarcinoma (n = 14), intrahepatic cholangiocarcinoma (n = 3) and leiomyosarcoma (n = 1). For hepatocellular carcinoma the cumulative survival was 38% at one year; the median survival was 12.2 months for Stage I, 6.3 months for Stage II and 0.9 months for Stage III tumours. In metastatic disease the cumulative survival was 63% at one year. These data suggest that targeted intra-arterial chemotherapy with Lipiodol-epirubicin is a useful palliative therapy for patients with Stage I and II HCC, and that a controlled trial of this treatment should be undertaken.
HPB Surg 1991 Sep
PMID:Selective regional chemotherapy of unresectable hepatic tumours using lipiodol. 165 18

A retrospective analysis of 35 stage IV HCC (26 IV-A case and 9 IV-B cases) which underwent reduction surgery from 1983 suggested a possibility to extend their survival period by decrease in their tumor-mass and subsequent immunochemotherapy for improvement of their depressed immunity. Their operability depended on the clinical stage of accompanying liver cirrhosis and extent of distant organ metastasis. It is of first importance for reduction surgery to select intrahepatic multiple tumors, slow-growing and not rapidly to induce distant organ metastases, among them. Intrahepatic tumors arising from multicentric origins were found in 42% in IV-A cases but 0% in IV-B. DNA ploidy analysis of the multicentric tumors in 8 cases did not show any clear indication of resectable tumors according to DNA index. The present immunochemotherapy is composed of a continuous infusion of IL2 and intermittent one-shot injections of 10mg ADR to the remnant liver by using subcutaneously implanted pump. In patients who could enhance peripheral NK and LAK activities by the immunotherapy, decreases in intra- and extra- hepatic tumors were observed. The 2 year-survival rate was 49% in IV-A, but only one case who is receiving the immunotherapy is surviving over 2 years in IV-B.
Nihon Geka Gakkai Zasshi 1991 Sep
PMID:[Significance of reduction surgery for stage IV hepatocellular carcinoma (HCC) and postoperative immunochemotherapy for extension of survival period]. 165 92

Dependence on T1 contrast can be reduced by changing the excitation flip angle. Low flip-angle spin-echo imaging can reduce imaging time because repetition time (TR) is reduced. The authors assessed the efficacy of low flip-angle spin-echo images in phantoms and in liver. MR phantoms made from polyvinyl alcohol gel to model the properties of normal liver, HCC, and hemangioma were scanned with various flip angles at TR 2400 and 1200 msec. Measured signal intensities fitted well with theoretical values. The T1 contrast of signal intensity decreased as the flip angle was reduced, accompanied by a decrease in signal-to-noise ratio (S/N). Thirty patients with hepatic space-occupying lesions (23 with HCC, three with metastases and four with hemangioma) were studied by conventional SE (CSE) at 2400/60/2 (TR/TE/NEX [number of excitations]) (10 min 46 sec imaging time) and low flip-angle SE (LFSE) at 1200/60/30 degrees/2 (TR/TE/FA/NEX) (5:20) and/or 1200/60/30 degrees/4 (10:18). The sensitivity of CSE in detecting lesions was 93% (44/47). It was 92% (35/38) for LFSE with two NEX and 94% (34/36) for LFSE with four NEX pulse sequences. The contrast-to-noise ratio (C/N) for images (HCC/liver, hemangioma/liver) obtained by LFSE with four NEX was significantly higher than that for those obtained by CSE (4.8 vs 3.5, p less than 0.01; 13.4 vs 9.7, p less than 0.01, respectively). Although the C/N (lesion/liver) for LFSE with two NEX sequences was lower than that of CSE for any type of lesion (3.0 vs 3.5 for HCC; 5.1 vs 6.3 for metastases; 8.3 vs 9.7 for hemangioma), the difference was not significant. Although reducing the flip angle from 90 degrees to 30 degrees with two NEX resulted in a decrease in S/N (10.7 to 8.9 for HCC; 15.3 to 11.9 for metastases; 20.0 to 18.1 for hemangioma; 7.4 to 6.3 for normal liver; 10.7 to 10.1 for spleen), the difference was not significant. For hepatic space-occupying lesions, low flip-angle spin-echo imaging is useful to obtain T2-weighted images in a shorter imaging time without sacrificing lesion detectability.
Nihon Igaku Hoshasen Gakkai Zasshi 1991 Sep 25
PMID:[Low flip-angle spin-echo imaging of the liver. Basic study and its application to hepatic space-occupying lesions]. 165 32

Changes of nucleotide sequences and expressions of cellular oncogenes in human hepatoma cell lines, PLC/PRF/5, HCC-M and HCC-T cells, were examined by Southern and Northern blot analyses. The probes used are DNA fragment of myc, N-, H-, K-ras, fos, fms, raf, erb-A, erb-B, and erb-B2 genes and synthetic oligonucleotides corresponding to the part of N-, H-, K-ras genes. The results are as follows. DNA amplification and rearrangement were not detected in these three human hepatoma cell lines. Point mutations at codons 12, 13, and 61 in N- and K-ras genes were not demonstrated in these cell lines. N-, H-, K-ras and myc transcripts were detected in these three cell lines. However, fos gene transcript was detected only in PLC/PRF/5 and HCC-M cells which were derived from hepatitis B related hepatocellular carcinoma and having integrated hepatitis B virus (HBV) DNA. These data showed that there are no specific proto-oncogene expression into RNA except for myc and ras genes, nor DNA rearrangement in these 3 human hepatoma cell lines with regards to at least 10 different oncogenes examined and suggest the relationship between fos gene expression and integration of HBV DNA in host cell DNA.
Keio J Med 1991 Sep
PMID:Proto-oncogene expression in three human hepatoma cell lines, HCC-M, HCC-T and PLC/PRF/5. 166 47

Through analyses of HBV DNA integratns in human cellular DNA, we identified three different integrant types, each of which may reflect the process of primary integrant formation by the viral DNA. The first type, which we call "simple type" consists of integrants found in some hepatocellular carcinomas (HCC's). The structure of the viral genome is simple, and part of it is deleted. The viral cohesive end sequence appears at one of the viral-cellular DNA junctions, and integration has elicited a microdeletion in the target cellular DNA sequence. This structure suggests viral DNA replication intermediates as substrates for integration. Judging from its frequency in HCC, this type may represent the most preferred one, if not all, among the primary integration products. The second type, which we call "complex type" is essentially the same as the first type, except tht the viral genome structure is complex. We considered the possibility that they may have been produced via the same process, using preformed complex viral genomes such as "novel form DNA's" (Rogler and Summers, 1982) as substrates. In cultured fetal hepatocytes, integration of HBV DNA can occur only a few days after infection. Among such integrants, we found a third type integrant, having a simple viral genome, but having a larger cellular DNA deletion. We propose that different forms of viral DNA may be used as substrates in the integration process, and the process is characterized by its eliciting of deletions of different size in the target cellular DNA. The most preferred substrate may be the one producing the simple type integrants, and the most frequently occurring deletion in the target DNA may be the microdeletion.(ABSTRACT TRUNCATED AT 250 WORDS)
Gastroenterol Jpn 1990 Sep
PMID:Different type of hepatitis B virus (HBV) DNA integrants that may reflect the integration process. 217 69

Cellular DNAs of chronically hepatitis B virus (HBV)-infected human livers were analysed by Southern blot hybridization for the presence of integrated HBV DNA. In 15 out of 16 tissue samples, random HBV DNA integration was evident. By molecular cloning and structural analyses of 19 integrants from 3 chronic hepatitis tissues, rearrangement of HBV DNA with inverted duplication or translocation of cellular flanking DNA at the virus-cell junction was noted. Thus, the rearrangement of HBV DNA or cellular flanking DNA not to be a specific incident of HCC formation. Analyses of various integrants bearing HBV DNA rearrangement and their cellular counterpart DNAs failed to indicate any gross structural alteration in cellular DNA except for a small deletion at the integration sites, indicating HBV DNA rearrangement with inverted duplication to possibly occur prior to integration. Based on nucleotide sequencing analyses of virus-virus junctions, a mechanism of this inverted duplication of HBV DNA is proposed, in which an illegitimate recombination may take place by means of a patchy homology on one side of adjoining viral sequences.
Gastroenterol Jpn 1990 Sep
PMID:Integrated structures of HBV DNA in chronic hepatitis and hepatoma tissues. 217 70


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