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)

Using 109 hepatocellular carcinomas (HCG), 34 cholangiocellular carcinomas (CCC), 4 mixed hepatocellular-cholangiocellular carcinomas (MHC) and 24 metastatic adenocarcinomas in the liver (MA), an immunohistochemical study on primary carcinoma of the liver was performed by means of the ABC method for carcinoembryonic antigen (CEA), epithelial membrane antigen (EMA), tissue polypeptide antigen (TPA) and keratin. The material consisted of surgical specimens of Kosin Medical College including 50 HCC, 17 CCC and 1 MHC, surgical specimens of 20 HCC from the University of Occupational and Environmental Health, Japan (UOEH) and autopsied specimens from UOEH that included 39 HCC, 17 CCC, 3 MHC and 24 MA. All the specimens were fixed with 10-15% formalin and embedded in paraplast manually at Kosin Medical College and by utilizing an automatic embedding machine with a decompressing procedure at UOEH. The antigenicity of TPA and keratin was preserved better in the specimens of Kosin Medical College than in those from UOEH. It is therefore assumed that manually embedded specimens are superior to specimens embedded by using an embedding machine with regard to the preservation of some antigenicities. The immunoreactivity of the 4 antigens in CCC cells was significantly higher than that in HCC cells, and the intracellular localization of antigens generally showed several characteristics in HCC and CCC. However, as the same localization of antigens is also seen in both HCC cells and CCC cells, it is considered that the immunohistochemical examination using plural antibodies is not always useful for a differential diagnosis between HCC and CCC, which is difficult in conventional sections. That TPA in HCC may be an oncodevelopmental antigen is suggested by the facts that the higher the grade of HCC, the higher the immunoreactivity of HCC cells, that hepatocytes with possible higher activity sometimes showed a positive reaction in the present study and that TPA is expressed in fetal hepatocytes in a fetus up to 20 weeks in the literature.
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PMID:[An immunohistochemical study on primary carcinoma of the liver]. 248 71

The question whether expression of drug metabolizing enzymes in human liver is altered by liver neoplasm remains controversial; however, the ability or unability of tumour cells to metabolize certain drugs may be important for developing therapeutic strategies. We therefore investigated the abundance and localization of two classes of drug metabolizing enzymes [cytochrome P4503A (CYP3A) and pi-type glutathione-S-transferase] by means of immunohistochemistry (standard ABC technique) in patients with hepatocellular carcinoma (HCC, n = 16) and with liver metastasis from adenocarcinoma (n = 53) in comparison to normal controls (n = 5). The distribution of CYP3A in normal liver samples showed a characteristic pattern of four to five layers of stained hepatocytes surrounding the central vein. Eleven out of 16 cases of HCC showed expression of CYP3A; staining was less intense than in normal liver and zonation was completely lost. In contrast, only 5 out of 53 samples of metastasis stained positively for CYP3A. The difference between primary and secondary neoplasm was statistically significant (chi-square, P < 0.0001). Pi-type glutathione-S-transferase (GST) stained positively in 9 out of 16 HCC and in 48 out of 53 cases of liver metastasis (chi-square, P < 0.01) indicating a higher percentage of immunostaining in liver metastasis. In summary, we observed differences in the abundance and distribution pattern of CYP3A and GST between primary and secondary neoplasma of human liver and in comparison to normal controls. In combination with established methods these data may contribute to the establishment of reliable test systems for distinguishing primary from secondary liver tumours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential expression of drug metabolizing enzymes in primary and secondary liver neoplasm: immunohistochemical characterization of cytochrome P4503A and glutathione-S-transferase. 840 68

Immunohistochemistry (ABC method) and in situ hybridization (DNA-RNA) were used to detect c-myc and p53 gene expression in tissues of human HCC and nearby non-tumorous liver (NT) from 23 patients. The results showed that the positive rates of P62c-myc were 87% (20/23) in HCC and 91% (21/23) in NT. The positive rates of P53 protein were 39% (9/23) in HCC as well as in NT. The positive rates of c-myc and p53 mRNA were 70% (16/23) and 56% (13/23) in HCC and NT respectively. The expression of c-myc and p53 at protein level was significantly correlated with that at mRNA level. These observations suggest a close association of c-myc and p53 gene overexpression with hepatocarcinogenesis. Immunohistochemistry (ABC method) on section of paraffin embedded tissue is a reliable method for detecting c-myc and p53 gene expression in HCC.
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PMID:[Overexpression of c-myc and p53 gene in human hepato-cellular carcinoma--a study with immunohistochemistry and in situ hybridization]. 869 90

The level of sulfo-Lea (SO3-3Gal beta 1-3(Fuc alpha 1-4)GlcNAc) epitope recognized by monoclonal antibody (mAb) 91.9H in hepatic metastasis of colon carcinoma is known to be lower than at the primary sites. We examined 19 human colon carcinoma cell lines for their production of this epitope. Sixteen cell lines were found to produce high M(r) components that metabolically incorporated [35S]sulfate and were resistant to heparitinase I and chondroitinase ABC, and 8 of them were reactive with mAb 91.9H as shown by western blotting analysis. These were all of the 4 cell lines derived from well differentiated primary tumors (HCCP-2998, LS174T, GEO, and CBS), 2 of 10 cell lines (DLD-1 and HCT116) from moderately to poorly differentiated primary tumors, and 2 of 5 cell lines (SW480 and HCC-M1544) from metastases. Incubation of LS174T cells with benzyl-N-acetyl-alpha-D-galactosaminide abrogated the incorporation of [35S]sulfate and the reactivity of mAb 91.9H with high M(r) components in the cell lysates. Sodium chlorate, which inhibits the formation of 3'-phosphoadenosine 5'-phosphosulfate, also inhibited the [35S]sulfate incorporation and reactivity with mAb 91.9H. These treatments did not change the incorporation of [14C]threonine into high M(r) components. These results indicated that sulfo-Lea epitopes were expressed on O-linked carbohydrate chains in sulfomucins. Immunohistochemical studies of tumor tissues in nude mice indicated that sulfo-Lea was expressed at the site of orthotopic transplantation in the cecum. The expression appeared to be suppressed in liver metastatic foci in nude mice.
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PMID:Expression of mucin-associated sulfo-Lea carbohydrate epitopes on human colon carcinoma cells. 1008 87

AIM:To study hepatocarcinogenesis of hepatitis C virus (HCV).METHODS: Expression of HCV antigens (CP10, NS3 and NS5) and several cancer-associated gene products (ras p21, c-myc, c-erbB-2, mutated p53 and p16 protein) in the tissues of hepatocellular carcinoma (HCC, n = 46) and its surrounding liver tissue were studied by the ABC(avidin-biotin complex) immunohistochemical method. The effect of HCV infection on expression of those gene products in HCC was analyzed by comparing HCV antigen positive group with HCV antigen negative group.RESULTS:Positive immunostaining with one, two or three HCV antigens was found in 20 (43.5%) cases,with either of two or three HCV antigens in 16 (34.8%) cases, and with three HCV antigens in 9 (19.6%) cases.Deletion rate of p16 protein expression in HCC with positive HCV antigen (80%, 16/20)was significantly higher than that in HCC with negative HCV antigen. Whereas no significant difference of the other gene product expression was observed between the two groups.CONCLUSION:HCV appears related to about one third of cases of HCC in Chongqing, the southwest of China, and it may be involved in hepatocarcinogenesis by inhibi ting the function of p16 gene, which acts as a negative regulator of cell cycle.
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PMID:Effect of HCV infection on expression of several cancer-associated gene products in HCC. 1181 78

Our purpose was to summarize current knowledge on "multidrug resistance", or MDR, an intrinsic or acquired cross resistance to a variety of structurally and functionally unrelated drugs, still representing one of the major problems in the therapy of cancer and other diseases. MDR depends on various mechanisms, the best known being the activity of ABC transport proteins, mainly Pgp, MDR1 gene product,and MRPs; but also other transporters can cause resistance, for example TAP, a peptide transporter, CFTR, cystic fibrosis transmembrane regulator, ABCG2, or breast cancer resistance protein (BCRP) and LRP, lung resistance protein. MDR has been detected in nearly all types of cancer, because it affects many organs and can occur against a wide number of drugs; it is frequent even in other diseases, such as epilepsy and HIV. We focused on MDR phenomenon in HCC, one of the commonest tumors in the world, and one of the most resistant to pharmacological treatment. This characteristic might be partly determined by a link between MDR and angiogenic phenotypes. The relationship between MDR in hepatocellular carcinoma and the effectiveness of therapeutic treatments has been particularly examined. Finally, the importance to overcome the strong chemoresistance of hepatocellular carcinoma with methods alternative to drugs, namely gene therapy, which makes use of antisense oligonucleotides and anti-MDR1 ribozymes, has been pointed out.
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PMID:[MDR (multidrug resistance) in hepatocarcinoma clinical-therapeutic implications]. 1499 22

Introduction: Leukodystrophies constitute heterogenous group of rare heritable disorders primarily affecting the white matter of central nervous system. These conditions are often under-appreciated among physicians. The first clinical manifestations of leukodystrophies are often nonspecific and can occur in different ages from neonatal to late adulthood periods. The diagnosis is, therefore, challenging in most cases.Area covered: Herein, the authors discuss different aspects of leukodystrophies. The authors used MEDLINE, EMBASE, and GOOGLE SCHOLAR to provide an extensive update about epidemiology, classifications, pathology, clinical findings, diagnostic tools, and treatments of leukodystrophies. Comprehensive evaluation of clinical findings, brain magnetic resonance imaging, and genetic studies play the key roles in the early diagnosis of individuals with leukodystrophies. No cure is available for most heritable white matter disorders but symptomatic treatments can significantly decrease the burden of events. New genetic methods and stem cell transplantation are also under investigation to further increase the quality and duration of life in affected population.Expert opinion: The improvements in molecular diagnostic tools allow us to identify the meticulous underlying etiology of leukodystrophies and result in higher diagnostic rates, new classifications of leukodystrophies based on genetic information, and replacement of symptomatic managements with more specific targeted therapies.Abbreviations: 4H: Hypomyelination, hypogonadotropic hypogonadism and hypodontia; AAV: Adeno-associated virus; AD: autosomal dominant; AGS: Aicardi-Goutieres syndrome; ALSP: Axonal spheroids and pigmented glia; APGBD: Adult polyglucosan body disease; AR: autosomal recessive; ASO: Antisense oligonucleotide therapy; AxD: Alexander disease; BAEP: Brainstem auditory evoked potentials; CAA: Cerebral amyloid angiopathy; CADASIL: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy; CARASAL: Cathepsin A-related arteriopathy with strokes and leukoencephalopathy; CARASIL: Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy; CGH: Comparative genomic hybridization; ClC2: Chloride Ion Channel 2; CMTX: Charcot-Marie-Tooth disease, X-linked; CMV: Cytomegalovirus; CNS: central nervous system; CRISP/Cas9: Clustered regularly interspaced short palindromic repeat/CRISPR-associated 9; gRNA: Guide RNA; CTX: Cerebrotendinous xanthomatosis; DNA: Deoxyribonucleic acid; DSB: Double strand breaks; DTI: Diffusion tensor imaging; FLAIR: Fluid attenuated inversion recovery; GAN: Giant axonal neuropathy; H-ABC: Hypomyelination with atrophy of basal ganglia and cerebellum; HBSL: Hypomyelination with brainstem and spinal cord involvement and leg spasticity; HCC: Hypomyelination with congenital cataracts; HEMS: Hypomyelination of early myelinated structures; HMG CoA: Hydroxy methylglutaryl CoA; HSCT: Hematopoietic stem cell transplant; iPSC: Induced pluripotent stem cells; KSS: Kearns-Sayre syndrome; L-2-HGA: L-2-hydroxy glutaric aciduria; LBSL: Leukoencephalopathy with brainstem and spinal cord involvement and elevated lactate; LCC: Leukoencephalopathy with calcifications and cysts; LTBL: Leukoencephalopathy with thalamus and brainstem involvement and high lactate; MELAS: Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke; MERRF: Myoclonic epilepsy with ragged red fibers; MLC: Megalencephalic leukoencephalopathy with subcortical cysts; MLD: metachromatic leukodystrophy; MRI: magnetic resonance imaging; NCL: Neuronal ceroid lipofuscinosis; NGS: Next generation sequencing; ODDD: Oculodentodigital dysplasia; PCWH: Peripheral demyelinating neuropathy-central-dysmyelinating leukodystrophy-Waardenburg syndrome-Hirschprung disease; PMD: Pelizaeus-Merzbacher disease; PMDL: Pelizaeus-Merzbacher-like disease; RNA: Ribonucleic acid; TW: T-weighted; VWM: Vanishing white matter; WES: whole exome sequencing; WGS: whole genome sequencing; X-ALD: X-linked adrenoleukodystrophy; XLD: X-linked dominant; XLR: X-linked recessive.
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PMID:An update on clinical, pathological, diagnostic, and therapeutic perspectives of childhood leukodystrophies. 3182 48