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Neoplasia, liver

Taylor GN, Lloyd RD, Mays CW, et al. 1992. Promotion of radiation-induced liver neoplasia by ethanol. Health Phys 62(2) 178-182. [Pg.264]

Baumann, P.C. and J.C. Harshbarger. 1985. Frequencies of liver neoplasia in a feral fish population and associated carcinogens. Mar. Environ. Res. 17 324-327. [Pg.1396]

Risk Assessment. The Reitz model is based on the assumption that cytotoxicity and reparative hyperplasia are responsible for liver neoplasia. Dose-surrogates, a more sophisticated and more accurate measure of target tissue dose derived from measuring a pharmacodynamic effect, were used. [Pg.133]

Lipshutz GS, Brennan TV, Warren RS. Thorotrast-induced liver neoplasia a collective review. J Am Coll Surg 2002 195(5) 713-18. [Pg.3402]

Promoters appear to have a relatively high tissue specificity. Thus, phenobarbital functions as a promoter for rodent liver neoplasia but not urinary bladder neoplasia. Saccharin, on the other hand, promotes urinary bladder neoplasia but not liver neoplasia in the rat. Similarly, 12-o-tetradecano-ylphorbol-13-acetate (phorbol ester) is a potent skin and forestomach neoplasm promoter in the laboratory rodent but has no appreciable activity in the liver. Other agents, such as the antioxidants 3-t-butyl-4-methoxyphenol and 2,6-di-t-butyl-4-met-hoxyphenol, may act as promoters in one organ and antipromoters in another and have no effect in a third organ. Thus, the practical definition of a promoter must include the designation of the susceptible tissue. [Pg.459]

Liver disease is the most important cause of increased transaminase activity in serum. In most types of liver disease, ALT activity is higher than that of AST exceptions may be seen in alcoholic hepatitis, hepatic cirrhosis, and liver neoplasia. In viral hepatitis and other forms of liver disease associated with acute hepatic necrosis, serum AST and ALT... [Pg.604]

C) often show sinusoidal CD34 this is especially helpful on needle aspirates or biopsies to identify primary liver neoplasia. [Pg.224]

Two devices are commercially available. Thera-Sphere (glass microsphere MDS Nordion, Kana-ta, Canada) was approved in 1999 by the Food and Drug Administration (FDA) under a Humanitarian Device Exemption (HDE) for the treatment of unresectable hepatocellular carcinoma (HCC) in patients who can have appropriately positioned hepatic arterial catheters with or without portal vein thrombosis [1]. SIR-Spheres (resin microsphere Sirtex Medical, Lane Cove, Australia) were granted full pre-marketing approval in 2002 by the FDA for the treatment of colorectal metastases in conjunction with intra-hepatic FUDR [2]. Both devices have European approval for liver neoplasia and approvals in various Asian countries. [Pg.148]

No signs of liver, kidney, or testicular damage was observed in mice administered 5000ppm 4 hours/day, 5 days/week for 12 weeks. Chronic administration of enflurane at 3000ppm for up to 78 weeks did not lead to an increased incidence of neoplasia in Swiss/ICR mice. Similarly, no carcinogenic effect was observed in another study in which treatment started in utero. ... [Pg.293]

Chemical injuries to the liver depend on the type of toxic agent, the severity of intoxication, and the type of exposure, whether acute or chronic. The six basic types of liver damage are fatty liver, necrois, hepatobiliary dysfuntions, viral-hke hepatitis, and (on chronic exposure) cirrhosis and neoplasia. A number of organic chemicals and drugs induce fatty liver and hver necrosis. [Pg.203]

As with many enzymes the role of AMP aminohydrolase in the hierarchy of metabolic catalysts is not clearly understood. Enzymic activity in muscle is markedly reduced in the dystrophic mouse (161, 162), in humans suffering from Duchanne type muscular dystrophy (163), in hypokaliemic periodic paralysis (164), and upon denervation of normal and dystrophic mouse gastronemii (165). Activity is reported to increase in both transplanted and primary hepatomas (151) and in precancerous livers prior to the onset of neoplasia induced by feeding or by intraabdominal injections of the potent carcinogen 3 -methyl-4-dimethyl-aminoazobenzene (166). The weak carcinogen, 4 -methyl-4-dimethyl-aminoazobenzene was not effective (166). Increases in enzyme activity concomitant with altered nuclear-nucleolar morphology, nuclear RNA content, and nuclear RNA biosynthesis were also observed after injections of thioacetamide, a hepatocarcinogen (167, 168). [Pg.71]

World Health Organization. Combined oral contraceptives and liver cancer. The WHO Collaborative Study of Neoplasia and Steroid Contraceptives. Int J Cancer 1989 43(2) 254-9. [Pg.195]


See other pages where Neoplasia, liver is mentioned: [Pg.1382]    [Pg.1389]    [Pg.1395]    [Pg.1382]    [Pg.1389]    [Pg.1395]    [Pg.585]    [Pg.609]    [Pg.113]    [Pg.673]    [Pg.675]    [Pg.1382]    [Pg.1389]    [Pg.1395]    [Pg.1382]    [Pg.1389]    [Pg.1395]    [Pg.585]    [Pg.609]    [Pg.113]    [Pg.673]    [Pg.675]    [Pg.747]    [Pg.67]    [Pg.1352]    [Pg.1382]    [Pg.1616]    [Pg.101]    [Pg.122]    [Pg.90]    [Pg.257]    [Pg.165]    [Pg.81]    [Pg.532]    [Pg.214]    [Pg.1959]    [Pg.36]    [Pg.98]    [Pg.1352]    [Pg.1382]    [Pg.1662]    [Pg.321]    [Pg.294]    [Pg.235]    [Pg.245]    [Pg.1320]    [Pg.209]    [Pg.214]   
See also in sourсe #XX -- [ Pg.676 , Pg.677 ]




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Neoplasia

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