Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Carbohydrate doai
Reexamination Certificate
2000-02-23
2003-04-08
Nguyen, Dave T. (Department: 1633)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Carbohydrate doai
C424S093200, C435S320100, C435S455000, C435S458000
Reexamination Certificate
active
06544955
ABSTRACT:
BACKGROUND OF THE INVENTION
1. Field of the Invention
This invention relates generally to the fields of molecular biology and more specifically to the effect of adenovirus E1A on tumor cells.
2. Background Information
Both radiation and chemotherapy have significantly contributed to the treatment of cancer. However, impediments to successful therapy by either form of treatment still remain. For example, some tumor types fail to respond to either radiation or chemotherapy. In other instances, originally responsive malignant cells may experience a relapse and become resistant to treatment.
There is evidence that the expression of certain proteins, such as various oncogenes, can increase the susceptibility of cells to apoptosis, also known as programmed cell death. Further, there is evidence that some of these proteins may also confer susceptibility to apoptosis induced by anticancer agents. However, relatively few studies have been done to observe these effects on human tumor cells and there have been no reports on the effect of adenovirus E1A on the sensitivity of human tumor cells and the response of these E1A-expressing cells to chemotherapeutic agents or irradiation.
Given the shortcomings of current chemotherapy and irradiation, namely lack of response and resistance or tolerance to chemotherapy agents, there is a need for developing additional forms of treatment which can enhance a response to chemotherapy or irradiation.
The present invention satisfies these needs and provides related advantages as well. The present invention provides novel methods for treating a tumor cell and enhancing a patient's response to irradiation and chemotherapy.
SUMMARY OF THE INVENTION
The present invention is directed to methods of sensitizing a human tumor cell with adenovirus E1A. The methods involve treating a human tumor cell by, first, introducing into the tumor cell nucleic acid encoding a polypeptide having adenovirus E1A activity, expressing the E1A active polypeptide in the cell, and then either contacting the E1A expressing tumor cell with a chemotherapeutic agent or irradiating the E1A-expressing tumor cell.
The invention also provides methods of enhancing a subject's response to chemotherapy or irradiation by introducing into a subject's tumor cells nucleic acid encoding a polypeptide having adenovirus E1A activity, expressing the E1A active polypeptide in the cells and finally, administering either a chemotherapeutic agent or irradiation. This invention also provides a method of treating cancer.
REFERENCES:
patent: 5516631 (1996-05-01), Frisch
patent: 5651964 (1997-07-01), Hung et al.
patent: 5747964 (1998-05-01), Roth et al.
patent: 5776743 (1998-07-01), Frisch
patent: WO 94/09160 (1994-04-01), None
patent: WO 94/18992 (1994-09-01), None
Blaese et al., “Vectors in cancer therapy: how will they deliver?”Cancer Gene Therapy, 2:291-297 (1995).
Brown, D.,The Washington Post, Dec. 8, 1995, pp. A1 & A22.
Canman and Kastan, “Induction of apoptosis by tumor suppressor genes and oncogenes”Cancer Biol., 6:17-25 (1995).
Chen et al., “Induction by E1A oncogene expression of cellular susceptibility to lysis by TNF”Nature, 330:581-583 (1987).
Coghlan et al.,New Scientist, 148:14-15 (1995).
Cook et al., “E1A oncogene expression level in sarcoma cells: an independent determinant of cytolytic susceptibility and tumor rejection”Oncogene, 8:625-635 (1993).
Cook et al., “Expression of the adenovirus E1A onogene during cell transformation is sufficient to induce susceptibility to lysis by hose inflammatory cells”Proc. Natl. Acad. Sci. USA, 83:6965-6969 (1986).
Cook et al., “Adenovirus E1A gene induction of susceptibility to lysis by natural killer cells and activated macrophages in infected rodent cells”J. Virology, 61:3510-3520 (1987).
Cook et al., “Differential induction of cytolytic susceptibility by E1A, myc, and ras oncogenes in immortilized cells”J. of Virology. 63:3408-3415 (1989).
Cook et al., “Role of tumor necrosis factor-&agr; in E1A oncogene-induced susceptibility of neoplastic cells to lysis by natural killer cells and activated macrophages”J. of Immunology, 142:4527-4534 (1989).
Crystal, Ronald G., “Transfer of genes to humans; early lessons and obstacles to success”Science, 270:404-410 (1995).
Culver et al., “Gene therapy for cancer”Trends in Genes, 10:174-178 (1994).
Duerksen-Hughes et al., “Adenovirus E1A renders infected cells sensitive to cytolysis by tumor necrosis factor”J. of Immunology, 143:4193-4200 (1989).
Evan et al., “Induction of apoptosis in fibroblasts by c-myc protein”Cell, 69:119-128 (1992).
Fanidi et al., “Cooperative interaction between c-myc and bcl-2 proto-oncogenes”Nature, 359:554-556 (1992).
Frisch, Steven M., “Antioncogenic effect of adenovirus E1A in human tumor cells”Proc. Natl. Acad. Sci. USA, 888:9077-9081 (1991).
Frisch and Francis, “Disruption of epithelial cell-matrix interactions induces apoptosis”J. Cell Biol., 124:619-626 (1994).
Fujiwara et al., “Induction of chemosensitivity in human lung cancer cells in vivo by adenovirus-mediated transfer of the wild-type p53 gene”Cancer Research, 54:2287-2291 (1994).
Gruber and Greil, “Apoptosis and therapy of malignant diseases of the hematopoietic system”Int. Arch. Allergy Immunol., 105:368-373 (1994).
Lowe et al., “p53-Dependent apoptosis modulates the cytotoxicity of anticancer agents”Cell, 74:957-967 (1993).
Marshall, E., “Gene therapy's growing pains”Science, 269:1050-1055 (1995).
Martin and Green, “Apoptosis as a goal of cancer therapy”Current Opinion in Oncology, 6:616-621 (1994).
Mastrangelo et al. “Gene therapy for human cancer: An essay for clinicians”Seminars in Oncology, 23:4-21 (1996).
Matsuzaki et al., “Mechanism of selective killing by dilinoleoylglycerol of cells transformed by the E1A gene of adenovirus type 12”Cancer Research, 49:5702-5707 (1989).
Miller et al., “Improved retroviral vectors for gene transfer and expression”Biotechniques, 7:980-990 (1989).
Rao et al., “The adenovirus E1A proteins induce apoptosis, which is inhibited by the E1B 19-kDa and Bcl-2 proteins”Proc. Natl. Acad. Sci. USA, 89:7742-7746 (1992).
Sanchez-Prieto et al., “Modulation of cellular chemoresistance in keratinocytes by activation of different oncogenes”Int. J. Cancer, 60:235-243 (1995).
Sanchez-Prieto et al., “Carcinoma cell lines become sensitive to DNA-damaging agents by the expression of the adenovirus E1A gene”Oncogene, 13:1083-1092 (1996).
Sinkovics and Horvath, “Apoptosi by genetic engineering”Leukemia, 8:S98-S102 (1994).
Stein, J. (in: Internal Medicine, 4thEd., Mosby Year Book, pp. 699-715 1993.
Walker et al., “E1A oncogene induction of cytolytic susceptibility eliminates sarcoma cell tumorigenicity”Proc. Natl. Acad. Sci. USA, 88:6491-6495 (1991).
Yu et al., “Adenovirus type E1A gene products act as transformation suppressors of the neu oncogene”Mol. Cell. Biol., 11:1745-1750 (1991).
Yu et al., “Reexpression of neu-encoded oncoprotein counteracts the tumor-suppressing but not the metastasis-suppressing function of E1A”Cancer Research, 53:5784-5790 (1993).
Campbell & Flores LLP
Nguyen Dave T.
The Burnham Institute
LandOfFree
Method of sensitizing tumor cells with adenovirus E1A does not yet have a rating. At this time, there are no reviews or comments for this patent.
If you have personal experience with Method of sensitizing tumor cells with adenovirus E1A, we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Method of sensitizing tumor cells with adenovirus E1A will most certainly appreciate the feedback.
Profile ID: LFUS-PAI-O-3104077