Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A screening colonoscopic examination in a 70-year-old man revealed a nonpolypoid type superficial depressed early carcinoma, about 2cm in diameter, in the transverse colon. The lesion was not resected and was observed because of coexisting nonresectable hepatocellular carcinoma (HCC). Fifteen months later, follow-up examinations revealed a polypoid type protuberant advanced carcinoma, about 6 cm in diameter, at the same site. Because complete response of the HCC had been induced by transarterial embolization, the colon carcinoma was operatively resected. There is an indefinite concept that colorectal carcinomas develop without substantial morphological changes, and no superficial depressed carcinoma that developed into a protuberant type advanced carcinoma has been reported. The case reported here provides evidence that some polypoid carcinomas arise from superficial depressed precursors. There is some intermingling between the two postulated colorectal carcinogenic pathways, the conventional polypoid pathway named the "adenoma-carcinoma sequence", and the nonpolypoid pathway, including so-called "de-novo" carcinogenesis.
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PMID:Superficial depressed early carcinoma that developed into protuberant advanced carcinoma in the transverse colon. 1121 Dec 11

It has been proposed that tumor cells frequently associated with partial or total loss of HLA class Ia expression may abnormally express HLA-G class Ib antigen. Such peculiar HLA class I expression would allow tumor cells to escape not only from CD8+T but also from NK-cell cytotoxicity. We studied the cell surface expression of HLA-G using flow cytometry with two HLA-G specific monoclonal antibodies (87G, 01G). The JEG-3 choriocarcinoma cell line, which constitutively expresses HLA-G antigens was used as a positive control. We did not detect the cell-surface HLA-G antigens in the following 75 tumor cell lines: melanoma (22), neuroblastoma (7), retinoblastoma (1), glioma (2), breast carcinoma (3), ovarian carcinoma (3), cervical carcinoma (1), colon carcinoma (3), bladder carcinoma (2), hepatocarcinoma (1), sarcoma (2) and leukemia cell lines: T-lymphocytes (6), B-lymphocytes (13) and myelo-monocytes (9). We found that some myelomonocytic cell lines express on their surface high affinity FcgammaRI (CD64) that may result in the binding of HLA-G specific mabs to their cell surface even in the absence of HLA-G molecules. Our panel of HLA-G negative tumor cell lines accommodated 62 cell lines for which similar analysis have not been reported and also contained 13 cell lines with total or partial loss of HLA class Ia molecules. Our observation imply that under normal culture conditions the cell surface HLA-G reactive with 87G and 01G mabs is absent in most tumor cell lines of different origin.
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PMID:Expression of the non-classical HLA-G antigen in tumor cell lines is extremely restricted. 1126 57

The mRNA for the alpha1-acid glycoprotein (AAG) was expressed not only in hepatoma cells, but also in non-hepatic cancer cells. The expression of the AAG mRNA in HT-29 human colon carcinoma cells is induced by cytokines, IL-6, IL-1, and TNF-alpha, in a manner characteristic of the acute phase response, and the expression of AAG mRNA was up-regulated in differentiated HT-29 cells.
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PMID:Induction of alpha1-acid glycoprotein mRNA by cytokines and differentiation in human colon carcinoma cell. 1135 96

Four new C(19) homolignans with a 5,4'-butano-2,4-cyclohexadienone-6-spiro-3'-(2',3'-dihydrobenzo[b]furan) skeleton, schiarisanrin A, schiarisanrin B, schiarisanrin D, and cytotoxic schiarisanrin C, were isolated from Schizandra arisanensis. Their structure and stereochemistry have been established by spectral and single-crystal X-ray analysis. Schiarisanrin C has cytotoxic activity with ED(50) values of 0.36, 7.1, 4.9, and 5.7 &mgr;g/mL, respectively, against KB epidermoid carcinoma of nasopharynx, COLO-205 colon carcinoma, HEPA hepatoma, and HELA cervix tumor cells.
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PMID:Four New C19 Homolignans, Schiarisanrins A, B, and D and Cytotoxic Schiarisanrin C, from Schizandra arisanensis. 1167 10

Efficacy of chemotherapy in advanced stages of colorectal tumours is limited. The quinolone antibiotic ciprofloxacin was recently shown to inhibit growth and to induce apoptosis in human bladder carcinomas cells. We investigated the effect of ciprofloxacin on colon carcinoma lines in vitro. CC-531, SW-403 and HT-29 colon carcinoma and HepG2 hepatoma cells (control cells) were exposed to ciprofloxacin. Proliferation was assessed by bromodeoxyuridine-incorporation into DNA and apoptosis was measured by flow cytometry after propidium iodide or JC-1 staining. Expression of anti-apoptotic Bcl-2 and pro-apoptotic Bax was analyzed by semiquantitative Western blot analysis and activity of caspases 3, 8 and 9 by substrate-cleavage assays. Ciprofloxacin suppressed DNA synthesis of all colon carcinoma cells time- and dose-dependently, whereas the hepatoma cells remained unaffected. Apoptosis reached its maximum between 200 and 500 microg ml(-1). This was accompanied by an upregulation of Bax and of the activity of caspases 3, 8 and 9, and paralleled by a decrease of the mitochondrial membrane potential. Ciprofloxacin decreases proliferation and induces apoptosis of colon carcinoma cells, possibly in part by blocking mitochondrial DNA synthesis. Therefore, qualification of ciprofloxacin as adjunctive agent for colorectal cancer should be evaluated.
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PMID:Ciprofloxacin induces apoptosis and inhibits proliferation of human colorectal carcinoma cells. 1187 13

In experimental studies, bovine lactoferrin (bLF) has been found to significantly inhibit colon, esophagus, lung, and bladder carcinogenesis in rats when administered orally in the post-initiation stage. Furthermore, concomitant administration with carcinogens resulted in inhibition of colon carcinogenesis, possibly by suppression of phase I enzymes, such as cytochrome P450 1A2 (CYP1A2), which is preferentially induced by carcinogenic heterocyclic amines. Enhancement of the activities of their phase II counterparts, such as glutathione S-transferase might have also played a critical role in post-initiation suppression in a study of tongue carcinogenesis. Anti-metastatic effects were moreover detected when bLF was given intragastrically to mice bearing highly metastatic colon carcinoma 26 cells (Co 26Lu), with apparent enhancing influence on local and systemic immunity. Marked increase in the number of cytotoxic T and NK cells in the mucosal layer of the small intestine and peripheral blood cells was thus found, this in turn enhancing the production of Interleukin 18 (IL-18) and caspase-1 in the epithelial cells of the small intestine, with possible consequent induction of interferon (IFN)-gamma positive cells. Furthermore, bLF has been found to exert anti-hepatitis C virus (HCV) activity in a preliminary clinical trial in patients with chronic active hepatitis due to this virus, a main causative factor in hepatocellular carcinoma development in Japanese. More extensive clinical trials are now underway in the National Cancer Center Hospital and other institutes to further explore the preventive potential against colon carcinogenesis.
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PMID:Cancer prevention by bovine lactoferrin and underlying mechanisms--a review of experimental and clinical studies. 1190 37

Nitropolycyclic aromatic hydrocarbons (NPAHs) are found in diesel exhaust and ambient air. NPAHs as well as polycyclic aromatic hydrocarbons (PAHs) are known to have mutagenicity, carcinogenicity, and endocrine-disruptive effects. In the present study, the inducibility of the human cytochrome P450-1 (CYP1) family by NPAHs was compared with those produced by their parent PAHs and some reductive metabolites, amino-PAHs. Furthermore, to investigate the differences in the inducibility of the CYP1 family in human tissues, various human tissue-derived cell lines, namely HepG2 (hepatocellular carcinoma), ACHN (renal carcinoma), A549 (lung carcinoma), MCF-7 (breast carcinoma), LS-180 (colon carcinoma), HT-1197 (bladder carcinoma), HeLa (cervix of uterus adenocarcinoma), OMC-3 (ovarian carcinoma), and NEC14 (testis embryonal carcinoma), were treated with NPAHs, PAHs, or amino-PAHs. The mRNA levels of CYP1A1, CYP1A2, and CYP1B1 were determined with reverse transcription-polymerase chain reaction (RT-PCR). The cell lines were classified into two groups: CYP1 inducible cell lines, comprising HepG2, MCF-7, LS-180, and OMC-3 cells, and CYP1 non-inducible cell lines, comprising ACHN, A549, HT-1197, HeLa, and NEC14 cells. In inducible cell lines, the induction profile of chemical specificity was similar for CYP1A1, CYP1A2, and CYP1B1, although the extent of induction differed among the cell lines and for the CYP isoforms. Pyrene, 1-nitropyrene, 1-aminopyrene, 1,3-, 1,6-, and 1,8-dinitropyrenes slightly induced CYP1 mRNAs, but 1,3-dinitropyrene produced a 6-fold induction of CYP1A1 mRNA in MCF-7 cells. 2-Nitrofluoranthene and 3-nitrofluoranthene exhibited stronger inducibility than fluoranthene in the inducible cell lines. 6-Nitrochrysene induced CYP1 mRNAs to the same extent or more potently than chrysene. The induction potencies of 6-nitrobenzo[ a]pyrene and 7-nitrobenz[ a]anthracene were weaker than those of their parents benzo[ a]pyrene and benz[ a]anthracene, respectively. This study demonstrated that NPAHs as well as PAHs induced human CYP1A1, CYP1A2, and CYP1B1 in a chemical-, CYP isoform-, and cell-specific manner. Furthermore, the cell-specific induction of the CYP1 family was not related to the expression levels of aryl hydrocarbon receptor, aryl hydrocarbon nuclear translocator, or estrogen receptors alpha and beta.
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PMID:Induction of CYP1A1, CYP1A2, and CYP1B1 mRNAs by nitropolycyclic aromatic hydrocarbons in various human tissue-derived cells: chemical-, cytochrome P450 isoform-, and cell-specific differences. 1210 46

Acyclic retinoid (ACR), a novel synthetic retinoid, can prevent the recurrence of human hepatoma after surgical resection of primary tumors, but the molecular mechanisms by which ACR exerts antitumor effects are not known. In this study, we found that ACR inhibited the growth of three human hepatoma cell lines. In HepG2 cells, this inhibition was associated with an arrest of the cell cycle in G(0)-G(1), increased cellular levels of p21(CIP1), decreased levels of the hyperphosphorylated form of the retinoblastoma protein, and decreased levels of cyclin D1, but no significant changes were seen in the levels of the p16(INK4a), p27(KIP1), cyclin-dependent kinase 4, cyclin-dependent kinase 6, glycogen synthase kinase 3beta, or beta-catenin proteins. ACR also caused a decrease in the level of cyclin D1 mRNA. Cotreatment of HepG2 human hepatoma cells with the proteasome inhibitor N-acetyl-Leu-Leu-norleu-al did not prevent the ACR-induced decrease in cyclin D1 protein, in contrast to the protective effect of N-acetyl-Leu-Leu-norleu-al on the cyclin D1 protein in cells treated with all-trans-retinoic acid. In transient transfection reporter assays, ACR, but not all-trans-retinoic acid, inhibited transcription from the cyclin D1 promoter. As reported previously in colon carcinoma cells, we found that in hepatoma cells, cyclin D1 promoter activity is markedly stimulated by the beta-catenin/T-cell factor pathway. Nevertheless, even in the presence of excess beta-catenin, ACR markedly inhibited the transcriptional activity of the cyclin D1 promoter. This is the first systematic study of the inhibitory effects of ACR, or any other retinoid compound, on beta-catenin/T-cell factor-stimulated cyclin D1 promoter activity in human tumor cells. These novel effects of ACR provide further evidence that ACR may be a valuable agent in the chemoprevention and therapy of hepatoma and possibly other human malignancies.
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PMID:Growth inhibition of human hepatoma cells by acyclic retinoid is associated with induction of p21(CIP1) and inhibition of expression of cyclin D1. 1212 33

Ten different samples of five Hypericum sp. were tested on brine shrimps, human colon carcinoma and human hepatoma cell lines for their cytotoxic activities. H. triquetrifolium Turra. (Rafina) showed the highest activity (LC50 = 22 mg/mL) on brine shrimps, while the extracts of the other nine samples showed significant to moderate activities (LC50 from 37 to 107 mg/mL). H. empetrifolium Wild. (Parnon) showed the highest activity in human colon carcinoma and human hepatoma cell lines, with LC50 values 29 and 25.1 mg/mL, respectively, while the LC50 values of the other samples were more than 45 mg/mL. It is very interesting to observe that most Hypericum samples showed good antioxidant activity in vitro.
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PMID:Antioxidant and cytotoxic activities of Hypericum sp. on brine shrimps and human cancer cell lines. 1245 72

Aryl hydrocarbon receptor repressor (AhRR) has been recently identified as a negative factor that suppresses aryl hydrocarbon receptor (AhR)-mediated transcriptional gene expression. In the present study, the expression level of AhRR in normal human tissues was determined. AhRR mRNA was detected in liver, breast, colon, kidney, lung, bladder, uterus, testis, ovary, and adrenal gland. The expression level in the testis was prominently high. AhRR mRNA was also detected in various human tissue-derived cell lines, HepG2 (hepatocellular carcinoma), MCF-7 (breast carcinoma), LS-180 (colon carcinoma), ACHN (renal carcinoma), A549 (lung carcinoma), HT-1197 (bladder carcinoma), HeLa (cervix of uterus adenocarcinoma), NEC14 (testis embryonal carcinoma), and OMC-3 (ovarian carcinoma). Since the expression level of AhRR mRNA was prominently high in HeLa cells, it is suggested that the high expression level of AhRR might work as a negative factor for the low inducibility of the CYP1 family in HeLa cells. The expression of AhRR mRNA was induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 3-methylchoranthrene (3-MC) in HepG2, MCF-7, LS-180, and OMC-3 cells, but not in ACHN, A549, HT-1197, HeLa, and NEC14 cells. The responsiveness was similar to the cell-specific inducibility of the CYP1 family. The inducibility of AhRR mRNA by nitropolycyclic aromatic hydrocarbons (NPAHs) as well as their parent PAHs was compared in HepG2 and OMC-3 cells. The chemical-specific inducibility of AhRR was also similar to that of the CYP1 family determined in our previous study. These results indicated that AhRR is also induced in chemical- and cell-specific manners.
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PMID:Expression of aryl hydrocarbon receptor repressor in normal human tissues and inducibility by polycyclic aromatic hydrocarbons in human tumor-derived cell lines. 1265 30


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