Prevention of liver cancer

Current Opinion in Oncology

Volumn 9, Issue 5, 1997, Pages 492-496

  Guyton, Kathryn Z ^a   Kensler, Thomas W ^b  

^a CCS Associates   (United States)

^b JOHNS HOPKINS BLOOMBERG SCHOOL OF PUBLIC HEALTH   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

HEPATITIS VACCINE;

CANCER MORTALITY; DIETARY INTAKE; DRUG EFFICACY; HEPATITIS B; HUMAN; INCIDENCE; LIVER CANCER; LIVER CARCINOGENESIS; LIVER CIRRHOSIS; NONHUMAN; PREVALENCE; PRIORITY JOURNAL; PROGNOSIS; SCREENING TEST; SHORT SURVEY; VACCINATION;

EID: 0030820314     PISSN: 10408746     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001622-199709050-00016     Document Type: Short Survey

References (24)

1. Skolnick AA: Armed with epidemiologic research, China launches programs to prevent liver cancer. JAMA 1996, 276:1458-1459.
2. Gust ID: Immunisation against hepatitis B in Taiwan. Gut 1996, 38 (Suppl 2):S67-S68.
3. Ahn YO: Strategy for vaccination against hepatitis B in areas with high endemicity: focus on Korea. Gut 1996, 38 (Suppl 2):S63-S66.
4. Yao JL: Perinatal transmission of hepatitis B virus infection and vaccination in China. Gut 1996, 38 (Suppl 2):S37-S38.
5. Ueno Y, Nagata S, Tsutsumi T, Hasegawa A, Watanabe MF, Park HD, Chen GC, Chen G, Yu SZ: Detection of microcystins, a blue-green algal hepatotoxin, in drinking water sampled in Haimen and Fusui, endemic areas of primary liver cancer in China, by highly sensitive immunoassay. Carcinogenesis 1996, 17:1317-1321. This study utilized an enzyme-linked immunosorbent assay with a detection limit of 50 pg/mL to monitor microcystin contamination of over 1000 drinking water samples. An advisory level of below 0.01 μg/L of microcystin in drinking water was proposed.
6. Chen CJ, Wang LY, Lu SN, Wu MH, You SL, Zhang YJ, Wang LW, Santella RM: Elevated aflatoxin exposure and increased risk of hepatocellular carcinoma. Hepatology 1996, 24:38-42.
7. Wang LY, Hatch M, Chen CJ, Levin B, You SL, Lu SN, Wu MH, Wu WP, Wang LW, Wang Q, Huang GT, Yang PM, Lee HS, Santella RM: Aflatoxin exposure and risk of hepatocellular carcinoma in Taiwan. Int J Cancer 1996, 67:620-625. This study supports the view that aflatoxin exposure enhances the hepatic carcinogenic potential of hepatitis B virus.
8. Wang JS, Qian GS, Zarba A, He X, Zhu YR, Zhang BC, Jacobson L, Gange SJ, Munoz A, Kensler TW: Temporal patterns of aflatoxin-albumin adducts in hepatitis 6 surface antigen-positive and antigen-negative residents of Daxin, Qidong County, People's Republic of China. Cancer Epidemiol Biomarkers Prev 1996, 5:253-261.
9. Hollstein M, Soussi T, Thomas G, von Brevern MC, Bartsch 2nd: P53 gene alterations in human tumors: perspectives for cancer control. Recent Results Cancer Res 1997, 143:369-389.
10. Soini Y, Chia SC, Bennett WP, Groopman JD, Wang JS, DeBenedetti VM, Cawley H, Welsh JA, Hansen C, Bergasa NV, Jones EA, DiBisceglie AM, Trivers GE, Sandoval CA, Calderon IE, Munoz Espinosa LE, Harris CC: An aflatoxin-associated mutational hotspot at codon 249 in the p53 tumor suppressor gene occurs in hepatocellular carcinomas from Mexico. Carcinogenesis 1996, 17:1007-1012.
11. Zoli M, Magalotti D, Bianchi G, Gueli C, Marchesini G, Pisi E: Efficacy of a surveillance program for early detection of hepatocellular carcinoma. Cancer 1996, 78:977-985. The surveillance program described in this report involved 164 consecutive patients in Emilia Romagna, Italy, with liver cirrhosis of both viral and alcoholic etiology. Thirty-four patients developed HCC, and 76% of HCC cases were detected by ultrasonography when the cancer was still single and small (< 4 cm). However, effective removal of the lesion was achieved in only two patients.
12. Muto Y, Moriwaki H, Ninomiya M, Adachi S, Saito A, Takasaki KT, Tanaka T, Tsurumi K, Okuno M, Tomita E, Nakamura T, Kojima T: Prevention of second primary tumors by an acyclic retinoid, polyprenoic acid, in patients with hepatocellular carcinoma: hepatoma Prevention Study Group [see comments]. N Engl J Med 1996, 334:1561-1567. This study describes a clinical chemoprevention trial of polyprenoic acid in a Japanese cohort. Hepatitis C virus infection was the primary cause of hepatoma in more than 70% of patients in the study population. Minimal side effects were reported for 600 mg/d polyprenoic acid; a treatment that significantly prevented second primary tumor.
13. Jacobson LP, Zhang B-C, Zhu Y-R, Wang J-B, Wu Y, Zhang Q-N, Yu Y-L, Qian G-S, Kuang S-Y, Li Y-F, et al.: Oltipraz chemoprevention trial in Qidong, People's Republic of China: study design and clinical outcomes. Cancer Epidemiol Biomarkers Prev 1997, 6:257-265.
14. Persson I, Yuen J, Bergkvist L, Schairer C: Cancer incidence and mortality in women receiving estrogen and estrogen-progestin replacement therapy: long-term follow-up of a Swedish cohort. Int J Cancer 1996, 67:327-332.
15. Fox JG, Li X, Yan L, Cahill RJ, Hurley R, Lewis R, Murphy JC: Chronic proliferate hepatitis in A/JCr mice associated with persistent Helicobacter hepaticus infection: a model of helicobacter-induced carcinogenesis. Infect Immun 1996, 64:1548-1558.
16. Moriya K, Matsukura M, Kurokawa K, Koike K: In vivo inhibition of hepatitis B virus gene expression by antisense phosphorothioate oligonucleotides. Biochem Biophys Res Commun 1996, 218:217-223.
17. Martin DC, Ruther U, Sanchez-Sweatman OH, Orr FW, Khokha R: Inhibition of SV40 T antigen-induced hepatocellular carcinoma in TIMP-1 transgenic mice. Oncogene 1996, 13:569-576. TIMPs (tissue inhibitors of metalloproteinases) may function as natural tumor suppressors by blocking degradation of extracellular matrix components. This study utilized a double transgenic strategy to demonstrate that TIMP overexpression can inhibit events associated with both initial and later stages of SV40 T antigen-mediated carcinogenesis. These results were supported by the finding that more rapid tumor initiation and progression resulted in SV40 T antigen/TIMP antisense mice.
18. Santoni-Rugiu E, Preisegger KH, Kiss A, Audolfsson T, Shiota G, Schmidt EV, Thorgeirsson SS: Inhibition of neoplastic development in the liver by hepatocyte growth factor in a transgenic mouse model. Proc Natl Acad Sci U S A 1996, 93:9577-9582.
19. Kolaja KL, Bunting KA, Klaunig JE: Inhibition of tumor promotion and hepatocellular growth by dietary restriction in mice. Carcinogenesis 1996, 17:1657-1664.
20. Kato J, Kobune M, Kohgo Y, Sugawara N, Hisai H, Nakamura T, Sakamaki S, Sawada N, Niitsu Y: Hepatic iron deprivation prevents spontaneous development of fulminant hepatitis and liver cancer in Long-Evans Cinnamon rats. J Clin Invest 1996, 98:923-929. Long-Evans Cinnamon rats developed fulminant hepatitis with a 53% mortality rate, and a 100% incidence of liver cancer at week 65; however, rats fed an iron-deficient diet exhibited a striking reduction in liver pathology and a complete prevention of liver cancer development. These findings highlight the contribution of liver toxicity and hepatitis to liver cancer development, and indicate that prevention of these pathologies can impact HCC incidence.
21. Maxuitenko YY, Curphey TJ, Kensler TW, Roebuck BD: Protection against aflatoxin B1-induced hepatic toxicity as short-term screen of cancer chemopreventive dithiolethiones. Fund Appl Toxicol 1996, 32:250-259. This study demonstrates a strong correlation between the GST-P-positive foci and markers of hepatotoxicity, and indicates that dithiolethiones can protect against the hepatotoxicity of aflatoxin.
22. Gerhauser C, You M, Liu J, Moriarty RM, Hawthorne M, Mehta RG, Moon RC, Pezzuto JM: Cancer chemopreventive potential of sulforamate, a novel analogue of sulforaphane that induces phase 2 drug-metabolizing enzymes. Cancer Res 1997, 57:272-278.
23. Primiano T, Kensler TW, Kuppusamy P, Zweier JL, Sutter TR: Induction of hepatic heme oxygenase-1 and ferritin in rats by cancer chemopreventive dithiolethiones. Carcinogenesis 1996, 17:2291-2296, This study demonstrates that 1,2-dithiole-3-thione can affect the expression of several genes controlling hepatic iron homeostasis, including heme oxygenase and the light and heavy subunits of ferritin. Furthermore, hepatic-free iron content was reduced following 1,2-dithiole-3-thione treatment. These results suggest that increased sequestration of intercellular iron in the liver may function in the chemopreventive effects of 1,2-dithiole-3-thione.
24. Primiano T, Gastel JA, Kensler TW, Sutter TR: Isolation of cDNAs representing dithiolethione-responsive genes. Carcinogenesis 1996, 17:2297-2303. In this study, a battery of genes inducible by 1,2-dithiole-3-thione was identified by differential screening of a cDNA library prepared from the liver of treated rats. These included known 1,2-dithiole-3-thione-inducible genes, as well as several not previously associated with the protective effects of 1,2-dithiole-3-thione against chemically induced hepatocarcinogenesis. Novel genes identified by this approach bear homology to those encoding metabolism and signal transduction proteins, although their sequencing and characterization has not yet been completed.