Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A quasi-historical cohort study method was used to collect the data of male stomach and liver cancer death and the data of exposure to relevant risk factors from 1984 to 1988 in male tap-water- and raw-water-drinking cohorts (> or = 30 years old) at both the upper and lower reaches of the Huangpu River. Total person-years observed are 172,448. The Odds Ratios of drinking water from the lower reaches for male stomach cancer and liver cancer death are 2.021 (p < 0.01) and 1.851 (p < 0.01), respectively, in unconditional logistic regression analysis after controlling possible confounding factors. The result shows that drinking water from the lower reaches of the Huangpu River is one of the important risk factors for male stomach and liver cancer death in local areas.
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PMID:Effects of drinking water from the lower reaches of the Huangpu River on the risk of male stomach and liver cancer death. 184 71

Protein from hog which is recognized by human monoclonal antibody (HB4C5), generated from a patient with large cell lung carcinoma, was identified as carboxypeptidase A by comparison of the protein with carboxypeptidase A in enzymatic activity, immunologic reactivity, and amino acid sequence. Carboxypeptidase A activity was also found in human cancer tissue, and purified antigen from cancer tissue recognized by the antibody HB4C5 was reacted with rabbit anti-carboxypeptidase A serum, indicating that carboxypeptidase A is an antigen of HB4C5. Since large amounts of carboxypeptidase A can be obtained from porcine sources, a simple method for its purification was established. The fraction which was most reactive with HB4C5 was obtained from acetone powder of porcine pancreas by successive applications of water extraction, ammonium sulfate precipitation, trypsin treatment, and Mono Q column chromatography. Its apparent molecular weight was 40,000, according to SDS polyacrylamide gel electrophoresis. When the reactivity of IgG in sera with the purified carboxypeptidase A was measured, the detection rates for lung, ovary, larynx, uterus, and liver cancer were more than 50%, while the rates for stomach and breast cancer were around 30%, and pancreatic cancer, benign diseases, and normal controls were minimally detected.
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PMID:Serodiagnosis of cancer using porcine carboxypeptidase A as an animal antigen recognized by human monoclonal antibody HB4C5. 187 99

Four thousand eighty inbred rats were maintained from weaning on various different concentrations of N-nitrosodiethylamine (NDEA) or N-nitrosodimethylamine (NDMA). The principal aim was to characterize the dose-response relationship for the effects of these agents on esophageal cancer (NDEA) or on various types of liver cancer (NDEA and NDMA), although NDEA also caused a few tumors of the nasopharynx and NDMA also caused a few tumors of the lung. The numbers of tumors of mesenchymal and Kupffer cells in the liver were too few to allow easy characterization of the dose-response relationships, and although NDMA induced large numbers of bile duct neoplasms, NDEA did not. Thus, the four principal dose-response relationships studied were of NDEA on esophageal or liver cells and of NDMA on bile duct or liver cells. At doses sufficiently high for the median time to death from the disease of interest to be estimated, relationships were observed of the general form (Dose rate) x (median)n = constant where n was about 2.3 for the first three relationships and about 1 for the last one (NDMA on liver cell tumors). By contrast, at doses sufficiently low for longevity to be nearly normal (median survival about 2.5 years), there remained no material dependence on the dose rate of the age distribution of the induced neoplasms. At these low dose rates, the number of liver (but not of esophageal) neoplasms induced by treatment was simply proportional to the dose rate. This finding is not surprising, since the background incidence of liver (but not of esophageal) neoplasms was appreciable. The linear relationship observed at low dose rates (below 1 ppm) suggests that under these experimental conditions, among rats allowed to liver their natural life span, a dose of 1 ppm of NDEA or NDMA in the drinking water will cause about 25% to develop a liver neoplasm, a dose of 0.1 ppm will cause about 2.5% to do so, and a dose of 0.01 ppm will cause about 0.25% to do so, etc., with no indication of any "threshold." (At these low dose rates, the incidence of liver neoplasms appears likely to exceed greatly that of esophageal neoplasms.) In addition, even quite low dose rates of the test agents caused a variety of nonneoplastic liver abnormalities (e.g., hyperplastic nodules, or shrinkage of hepatocytes) at a frequency roughly proportional to the dose rate.
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PMID:Effects on 4080 rats of chronic ingestion of N-nitrosodiethylamine or N-nitrosodimethylamine: a detailed dose-response study. 825 18

The tumor growth of Walker-256 implanted sc. on dorsum side of hindpaw of Wistar rat were suppressed by warmed (43 degrees C) water immersion. Antitumor effects of hyperthermia were increased by injection (a.i.) of saline mixed with noradrenaline (5 mcg). Although tumors in advanced stage group (D-8) are larger in size and more tumor vascularity than in early stage group (D-4), hyperthermic cytotoxicity were observed in D-8 but not observed in D-4. The hyperthermic energy injured the tumor vessels, which failed to flow the blood to the tumor cells and resulted in sever cytotoxic damage of Walker-256. Therefore, cytotoxic damage could be enhanced by injecting warmed water (43 degrees C) into tumor vessels after chemotherapy (MMC; 0.5 mg/kg) in D-8. Metastatic liver cancer was treated with thermochemotherapy. 5% of glucose warmed (43 degrees C) mixed with 0.1 mg of noradrenaline and heparin was administered into hepatic artery after chemotherapy (2 to 6 mg of MMC a.i.).
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PMID:[Enhancing hyperthermic cytotoxicity in Walker-256 by intraarterial injection of warmed saline]. 210 8

A high performance liquid chromatographic (HPLC) method for the analysis of aflatoxin M1 (AFM1) in urine is described. Urine samples were treated with saturated lead acetate and AFM1 was extracted with chloroform. After washing with water to remove impurities the compound was derivatized with trifluoroacetic acid and the AFM1 derivative was analyzed quantitatively by HPLC. The sample pretreatment is simple and more selective. A good line correlation between AFM1 peak height and its concentration was obtained when AFM1 content was in the range of 50-400 pg. The ratio of recovery was 87.42%. Sensitivity is 0.01 ppb. The method is applicable to trace analysis. Results in urine of residents who live in the high/low liver cancer incidence area in Fushui county were the same as that of previous epidemiological investigation.
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PMID:A new method for the quantitation of aflatoxin M1 in urine by high performance liquid chromatography and its application to the etiologic study of hepatoma. 216 90

In case of an arterial infusion chemoembolization therapy for primary or metastatic liver cancer, gradual release of the anti-cancer drug from lipiodol is a very important factor for a higher drug concentration in the tumor and for longer contact. We studied basic points about what kind of drug form has a gradual drug release. We prepared 3 forms of drugs. (1) Powder form: Powder of ADM, MMC and CDDP was suspended in lipiodol with ultrasonic suspender. (2) URO form: ADM and MMC were dissolved with Urografin and mixed with lipiodol. (3) Surfactant form: ADM and MMC were dissolved with water and then mixed with lipiodol using surfactant. We put lipiodol suspension into physiological saline and then stirred water at 100 rpm with the paddle method, measuring drug release from the suspension or emulsion. Powder form had a lowest drug release. In clinical trials, we administered intra-arterially (1) ADM, MMC dissolved with physiological saline water as usually used (physiological saline water form) (2) Powder form; (3) URO from; (1) CDDP solution as usually used was administered; (2) Powder form. Then we studied the changes of serum concentration of ADM, MMC and CDDP. The results indicated that powder form had the lowest drug release. Thus, the water-soluble anti-cancer drugs ADM, MMC and CDDP should be used in powder form.
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PMID:[Studies on drug release from anti-cancer drug suspended Lipiodol]. 255 Dec 42

A long-term study, using male Wistar rats, was initiated to determine whether the effects of dietary constituents on AFB1-induced liver cancer could be associated with altered microsomal enzyme activity. They were maintained on mice pellets mixed with specific dietary constituents for 7 days and then given a single carcinogenic dose of AFB1 (500 micrograms/rat). After three months, the dietary constituents were discontinued and the animals were left on mice pellets and drinking water only for a period of about 20 months. At the end of the trial period, it was observed that dietary mixtures containing small quantities of either beta-carotene, ascorbic acid, GSH, vitamin E, selenium salt, or uric acid, effectively inhibited the development of AFB1-induced liver cancer and induced increased microsomal enzyme activity. Whereas beta-carotene and uric acid were the most effective inhibitors, vitamin E was the least, yet a significant inhibitor of liver cancer. Hepatic levels of cytochrome P-450, aniline hydroxylase and chlorpromazine demethylase were significantly induced in rats fed fortified food followed by AFB1 treatment than in control animals. The inhibition of liver cancer by dietary factors was probably due to their ability to induce the activity of hepatic microsomal enzymes. Increased enzyme activity could lead to rapid activation of AFB1 metabolism, resulting in loss of activated AFB1 metabolites that attack cell components. Inhibition of liver cancer is therefore associated with induction of increased microsomal enzyme activity.
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PMID:Inhibition of AFB1-induced liver cancer and induction of increased microsomal enzyme activity by dietary constituents. 261 10

B6C3F1 mice and Sprague-Dawley rats were provided drinking water containing 6-31 mM (1-5 g/liter) trichloroacetic acid (TCA), 8-39 mM (1-5 g/liter) dichloroacetic acid (DCA), or 11-32 mM (1-3 g/liter) monochloroacetic acid (MCA) for 14 days. TCA and DCA, but not MCA, increased the mouse relative liver weight in a dose-dependent manner. Rat liver weights were not altered by TCA or DCA treatment, but were depressed by MCA. Hepatic peroxisome proliferation was demonstrated by (1) increased palmitoyl-CoA oxidase and carnitine acetyl transferase activities, (2) appearance of a peroxisome proliferation-associated protein, and (3) morphometric analysis of electron micrographs. Mouse peroxisome proliferation was enhanced in a dose-dependent manner by both TCA and DCA, but only the high DCA concentration (39 mM) increased rat liver peroxisome proliferation. MCA was ineffective in both species. Three other mouse strains (Swiss-Webster, C3H, and C57BL/6) and two strains of rat (F344 and Osborne-Mendel) were examined for sensitivity to TCA. TCA (12 and 31 mM) effectively enhanced peroxisome proliferation in all mouse strains, especially the C57BL/6. A more modest enhancement in the Osborne-Mendel (288%) and F344 rat (167%) was seen. Dosing F344 rats with 200 mg/kg TCA in water or corn oil for 10 days increased peroxisome proliferation 179 and 278%, respectively, above the vehicle controls. These studies demonstrate that the mouse is more sensitive than the rat with respect to the enhancement of liver peroxisome proliferation by TCA and DCA and suggest that if peroxisome proliferation is critical for the induction of hepatic cancer by TCA and DCA, then the rat should be less sensitive or refractory to tumor induction.
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PMID:Species and strain sensitivity to the induction of peroxisome proliferation by chloroacetic acids. 281 84

Combined administration of 0.1% nitrite and 0.1% aminopyrine in the drinking water for eight to ten weeks resulted in subsequent development of both hepatocellular nodules and cholangiofibrotic lesions/cholangiocellular carcinomas in Syrian golden hamsters. Additional prior dosing with Opisthorchis viverrini metacercariae (100/animal) induced inflammatory and proliferative changes in the livers of infected hamsters and was associated with a significant increase in yields of hepatocellular and cholangiocellular preneoplastic and neoplastic lesions. Thus, environmental factors thought to be casually related to the high levels of human liver cancer observed in the Northeastern provinces of Thailand were sufficient to bring about development of equivalent tumors in experimental animals. The results indicate that parasite associated liver injury and non-specific compensatory regeneration may play an important role in generation of both hepatocellular and cholangiocellular carcinomas in man.
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PMID:Generation of high yields of Syrian hamster cholangiocellular carcinomas and hepatocellular nodules by combined nitrite and aminopyrine administration and Opisthorchis viverrini infection. 284 84

Although primary hepatoma is not very frequent in alcoholics, the incidence of hepatoma in cases of hepatitis B infection combined with heavy alcohol drinking is high. In the present study, the effects of chronic alcohol administration on the development of chemical-induced hepatic cancer in rats were analyzed. In 70% hepatectomized Wistar strain male rats, a single dose (1 mg per 100 gm body weight) of diethylnitrosamine was injected intraperitoneally. Eight weeks after the injection, 20% alcohol-10% sucrose solution (diethylnitrosamine-alcohol group), 0.1% sodium phenobarbital solution (diethylnitrosamine-phenobarbital group), 10% sucrose solution (diethylnitrosamine-sucrose group) or tap water (diethylnitrosamine-alone group) was given as drinking water for 32 weeks. The numbers of visible nodules per liver were significantly greater in the diethylnitrosamine-alcohol and diethylnitrosamine-phenobarbital groups compared to the diethylnitrosamine-alone and diethylnitrosamine-sucrose groups. The numbers of enzyme-altered foci which were positive to gamma-glutamyl transpeptidase staining per square centimeter of liver section were also greater in the diethylnitrosamine-alcohol and diethylnitrosamine-phenobarbital groups than in the diethylnitrosamine-alone and diethylnitrosamine-sucrose groups, although the numbers of nodules and enzyme-altered foci were significantly larger in the diethylnitrosamine-phenobarbital group than in the diethylnitrosamine-alcohol group. The enzyme-altered foci areas calculated by gamma-glutamyl transpeptidase staining were significantly larger in the diethylnitrosamine-alcohol and diethylnitrosamine-phenobarbital groups than in the diethylnitrosamine-alone and diethylnitrosamine-sucrose groups. Histologically, visible nodules observed in diethylnitrosamine-phenobarbital and diethylnitrosamine-alcohol groups showed characteristic features of neoplastic nodules. These results indicate that alcohol has a promoter action on the development of chemically induced hepatic cancer like phenobarbital.
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PMID:Effects of ethanol on experimental hepatocarcinogenesis. 286 66


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