Experimental models of gene-environment interaction for cancer chemoprevention studies

Current Opinion in Oncology

Volumn 9, Issue 5, 1997, Pages 487-491

  Hursting, Stephen D ^a  

^a UNIVERSITY OF TEXAS   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANTINEOPLASTIC AGENT; CYCLOOXYGENASE 2; NONSTEROID ANTIINFLAMMATORY AGENT; PROTEIN P53; UNINDEXED DRUG;

CANCER; CANCER GENETICS; CANCER PREVENTION; CHEMOPROPHYLAXIS; COLON CARCINOGENESIS; COLON POLYPOSIS; ENVIRONMENTAL FACTOR; GENE EXPRESSION; GENE MUTATION; GENETIC ANALYSIS; GENETIC SUSCEPTIBILITY; NONHUMAN; PRIORITY JOURNAL; SHORT SURVEY; TRANSGENE; TUMOR SUPPRESSOR GENE;

EID: 0030817698     PISSN: 10408746     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001622-199709050-00015     Document Type: Short Survey

References (31)

1. Greenwald P, Nixon DW, Malone WF, Kelloff GJ, Stern HR, Witkin KM: Concepts in cancer chemoprevention research. Cancer 1990, 65:1483-1490.
2. Wattenberg LW: Chemoprevention of cancer by naturally occurring and synthetic compounds. In Cancer Chemoprevention. Edited by Wattenberg L, Lipkin M, Boone CW, Kelloff GJ. Boca Raton: CRC Press; 1992:19-39.
3. Boone CW, Steele VE, Kelloff GJ: Screening for cancer chemopreventive (anticarcinogenic) compounds in rodents. Mutat Res 1992, 267:251-255.
4. Greenwald P, Malone WF, Cerny ME, Stern HR: Cancer prevention research trials. Adv Cancer Res 1993, 61:1-23.
5. Dove WF, Gould KA, Luongo C, Moser AR, Shoemaker AR: Emergent issues in the genetics of intestinal neoplasia. Cancer Surv 1995, 25:335-355.
6. Moser AR, Pitot HC, Dove WF: A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse. Science 1990, 247:322-324.
7. Sandler RS: Aspirin and other non-steroidal anti-inflammatory agents in the prevention of colorectal cancer. Imp Adv Oncol 1996, 96:123-137.
8. Tsujii M, DuBois RN: Alterations in cellular adhesion and apoptosis in epithelial cells overexpressing prostaglandin endoperoxide synthase-2. Cell 1995, 83:493-501.
9. Jacoby RF, Marshall DJ, Newton MA, Nocakovic K, Tutsch K, Cole CE, Lubet RA, Kelloff GJ, Verma A, Moser AR, Dove WF: Chemoprevention of spontaneous intestinal adenomas in the APC min mouse model by the non-steroidal anti-inflammatory drug piroxicam. Cancer Res 1996, 56:710-714. Min mice heterozygous for a mutation in the APC gene, spontaneously develop scores of grossly detectable adenomas throughout the small intestine (rarely in the colon) in 1-3 months of life. Dietary administration of the NSAID piroxicam decreased tumor multiplicity in a dose-dependent fashion, with the control subjects averaging more than 17 small intestinal adenomas per mouse and the high-dose piroxicam group averaging only two adenomas per mouse.
10. Boolbol SK, Dannenberg AJ, Chadburn A, Martucci C, Guo X, Ramonetti JT, Abreu-Goris M, Newmark HL, Lipkin ML, DeCosse JJ, Bertagnolli MM: Cyclooxygenase-2 overexpression and tumor formation are blocked by sulindac in a murine model of familial adenomatous polyposis. Cancer Res 1996, 56:2556-2560. Min mice administered the NSAID sulindac in the drinking water (0.5 mg/d) averaged 0.1 adenomas per mouse compared to control subjects that averaged nearly 12 adenomas per mouse. In addition, Min mice were found to have increased COX-2 expression and prostaglandin E2 levels in the small bowel, relative to wild-type mice. Min mice, relative to wild-types, also displayed reduced rates of enterocyte apoptosis; a type of programmed cell death critical to the maintenance of cell number homeostasis. Treatment with sulindac modulated COX-2 expression, PGE-2 levels, and enterocyte apoptotic rates to levels observed in wild-type mice.
11. Beazer-Barclay Y, Levy DB, Moser AR, Dove WF, Hamilton SR, Vogelstein B, Kinzler KW: Sulindac suppresses tumorigenesis in the min mouse. Carcinogenesis 1996, 17:1757-1760. The NSAID sulindac was administered in the drinking water or in the diet. Sulindac administered by either route significantly reduced adenoma formation and dysplastic foci in the intestines of Min mice.
12. Fodde R, Edelmann W, Yang K: A targeted chain-termination mutation in the mouse Ape gene results in multiple intestinal tumors. Proc Natl Acad Sci U S A 1994, 91:8969-8973.
13. Oshima M, Takahashi M, Oshima H, Tsutsumi M, Yazawa K, Sugimura T, Nishimura S, Wakabayashi K, Taketo MM: Effects of docosahexaenoic acid on intestinal polyp development in APC knockout mice. Carcinogenesis 1995, 16:2605-2607.
14. A716 mice provides the strongest evidence to date that COX-2 plays a key role in APC-related tumorigenesis and suggests that specific COX-2 inhibitors have great potential as colon cancer chemopreventive agents.
15. Hollstein M, Sidransky D, Vogelstein B, Harris CC: p53 mutations in human cancers. Science 1991, 253:49-53.
16. Donehower LA, Harvey M, Slagle BL, McArthur MJ, Montgomery CA, Butel J, Bradley A: Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumors. Nature (London) 1992, 356:215-221.
17. Hursting SD, Perkins SN, Phang JM: Calorie restriction delays spontaneous tumorigenesis in p53-knockout transgenic mice. Proc Natl Acad Sci U S A 1994, 91:7036-7040.
18. Hursting SD, Perkins SN, Ward J, Haines D, Phang JM: Chemoprevention of spontaneous tumorigenesis in p53-knockout mice. Cancer Res 1995, 55:3949-3953.
19. -/- mice provide a rapid, relevant, and responsive model for testing chemoprevention strategies to offset p53-deficiency.
20. +/+ mice.
21. Tennant RW, French JE, Spalding JW: Identifying chemical carcinogens and assessing potential risk in short-term bioassays using transgenic mice. Env Health Persp 1995, 103:942-950.
22. Harvey M, McArthur MJ, Montgomery CA, et al.: Spontaneous and carcinogen-induced tumorigenesis in p53-deficient mice. Nature Gen 1993, 4:225-229.
23. Kemp CJ, Wheldon T, Balmain A: P53-deficient mice are extremely susceptible to radiation-induced tumorigenesis. Nature Gen 1994, 8:66-69.
24. Kemp CJ, Donehower LA, Bradley A, Balmain A: Reduction of p53 gene dosage does not increase initiation or promotion but enhances malignant progression of chemically induced skin tumors. Cell 1993, 74:813-822.
25. Gonzalez FJ: Use of transgenic animals in carcinogenesis studies. Mol Carcinog 1996, 16:63-67.
26. McCormick DL, Johnson WD, Rao KV, Bowman-Green T, Steele V, Lubet RA, Kelloff GJ: Comparative activity of N-(4-hydroxyphenyl)-all trans-retinamide and alpha-difluoromethylornithine as inhibitors of lymphoma induction in PIM-transgenic mice. Carcinogenesis 1996, 17:2513-2517.
27. Clifford AJ, Ebeler SE, Ebeler JD, Bills ND, Hinrichs SH, Teissedre PP, Waterhouse AL: Delayed tumor onset in transgenic mice fed an amino-acid-based diet supplemented with red wine solids. Am J Clin Nutr 1996, 64:748-756.
28. Shibata M, Ward JM, Devor DE, Liu M, Green JE: Progression of prostatic intraepithelial neoplasia to invasive carcinoma in C3(1)/SV40 large T antigen transgenic mice: histopathological and molecular biological alterations. Cancer Res 1996, 56:4894-4903. Transgenic mice with prostatic overexpression of the Simian virus-40 large T antigen (which can bind to and inactivate the p53 tumor-suppressor protein and the retinoblastoma tumor suppressor protein) develop prostatic carcinomas within 1 year of age. Because progress in prostate cancer chemoprevention has been hampered by the lack of relevant animal models of that disease and because this model shows pathologic and molecular characteristics similar to those observed in human prostate tumor progression, these mice should be useful for testing prostate cancer chemoprevention strategies.
29. Gingrich JR, Greenberg NM: A transgenic mouse prostate cancer model. Tox Pathol 1996, 24:502-504.
30. Allemand I, Angulo JF: Transgenic and knockout models for studying DNA repair. Biochimie 1995, 77:826-832.
31. Reitmar AH, Cai J, Bjerknes M, Redston M, Cheng H, Pind M, Hay K, Mitri A, Bapat B, Mak T, Gallinger S: MSH2 deficiency contributes to accelerated Apc-mediated intestinal tumorigenesis. Cancer Res 1996, 56:2922-2926. Min mice crossed with MSH2-knockout mice (which are deficient in a critical mismatch repair gene), displayed a greater number of colonic aberrant crypt foci and reduced survival secondary to a greater number and more rapidly developing colonic and small intestinal adenomas than Min mice with normal MSH2 function. The development of models such as the MSH2-deficient Min mice, with multiple genetic lesions, could prove useful in evaluating critical gene-environment interactions relevant to cancer prevention.