Muir-torre-like syndrome in Fhit deficient mice

Multicellular living organisms and unmodified parts thereof and – Nonhuman animal – Transgenic nonhuman animal

Reexamination Certificate

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C800S008000, C800S003000, C800S021000

Reexamination Certificate

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06924414

ABSTRACT:
The invention provides nonhuman transgenic animals with a disrupted FHIT gene. The invention further provides transgenic mice in which one or both Fhit alleles have been inactivated. Preferably, the Fhit-deficient mice develop multiple tumors of both visceral and sebaceous origin, similar to those of Muir-Torre familial cancer syndrome. The present invention further relates to the generation of these transgenic mice and their use as model systems to study the effects of carcinogenic agents in promoting clonal expansion of neoplastic cells in cancers, preferably gastrointestinal cancers of which Muir-Torre syndrome is a subset. The invention further relates to testing therapeutic agents for their efficacy in the prevention and treatment of cancer, preferably gastrointestinal cancer.

REFERENCES:
patent: 5087571 (1992-02-01), Leder et al.
patent: 5698766 (1997-12-01), Julius et al.
patent: 5907079 (1999-05-01), Mak et al.
patent: 5928884 (1999-07-01), Croce et al.
patent: 6025137 (2000-02-01), Shyjan
patent: 6242212 (2001-06-01), Croce et al.
Mullins, 1990, Nature, vol. 344, p. 541-544.
Hammer, 1990, Cell, vol. 63,. p. 1099-1112.
Mullins, 1989, EMBO Journal, vol. 8, p. 4065-4072.
Taurog, 1988, J. Immunol., vol. 141, p. 4020-4023.
Wall, 1996, Theriogenology, vol. 45, p. 57-68.
Ebert, 1988, Mol. Endocrinology, vol. 2, p. 277-283.
Overbeek, 1994, “Factors affecting transgenic animal production,” Transgenic animal technology, pp. 96-98.
Mullins, 1996, J. Clin. Invest., vol. 98, pp. S37-S40.
Capecchi, 1994, Scientific American, vol. 270, p. 34-41.
Pekarsky, 1998, Cancer Res., vol. 58, p. 3409-3414.
Huebner et al. Annu. Rev. Genet. 1998. vol. 32, p. 7-31.
Zanesi, PNAS, 2001, vol. 98, p. 10250-10255.
Fong et al., “Induction of a Muir-Torre-like syndrome in Fhit deficient mice” (Abstract),Proceedings of the American Association for Cancer Research Annual Meeting(Mar. 2000) No. 41:68; 91stAnnual Meeting of the American Association for Cancer Research, San Francisco, California USA (Apr. 1-5, 2000).
Fong and Magee, “Dietary zinc deficiency enhances esophageal cell proliferation and N-nitrosomethylbenzylamine (NMBA)-induced tumor incidence in C57BL/6 mouse”,Cancer Letters143:63-69 (1999).
Fong Louise Y Y et al., “Muir-Torre-like syndrome in Fhit-deficient mice”,Proceedings of the National Academy of Sciences of USA, National Academy of Science(Apr. 25, 2000), pp. 4742-4747.
Dumon Kristoffel R et al., “FHIT gene therapy prevents tumor development in Fhit-deficient mice”,Proceedings of the National Academy of Sciences of USA, National Academy of Science(Mar. 13, 2001), pp. 3346-3351.
Ji Lin et al., “Induction of apoptosis and inhibition of tumorigenicity and tumor growth by adenovirus vector-mediated fragile histidine triad (FHIT) gene overexpression”,Cancer Research, American Association for Cancer Research(Jul. 15, 1999); vol. 59, No. 14, pp. 3333-3339.
Croce C M et al., “Role of Fhit in Human Cancer”,Journal of Clinical Oncology(May 5, 1999); vol. 17, No. 5, pp. 1618-1624.

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