Chemistry: natural resins or derivatives; peptides or proteins; – Peptides of 3 to 100 amino acid residues
Reexamination Certificate
2007-01-23
2007-01-23
Helms, Larry R. (Department: 1643)
Chemistry: natural resins or derivatives; peptides or proteins;
Peptides of 3 to 100 amino acid residues
C530S350000, C514S002600
Reexamination Certificate
active
10324993
ABSTRACT:
Saposin C was shown to be a trophic factor for a variety of cancer cells, e.g., prostate, lung, breast, and colon cancer cells. These cells expressed saposin C and responded to saposin C by increased levels of cell proliferation, cell migration, and cell invasion. Such activities typify and promote the neoplastic process. For prostate cancer, the androgen-insensitive prostate cancer cells responded to saposin C by higher levels of cell proliferation, cell migration and cell invasion than did the androgen-sensitive prostate cells. Stromal cells (from the prostate) were also responsive to saposin C-mediated signals in a manner typical of growth promoting compounds. The androgen-insensitive prostate cells were stimulated by saposin C to express higher levels of the urokinase plasminogen activator (uPA) and its receptor (uPAR), two proteins known to be involved in cell invasion. A conjugate of a peptide of the active region of saposin C (TX14A) and a toxin (saporin) was made and was shown to decrease the survival of prostate cancer cells, and the other cancer cells that were found to express saposin C (including cancers cells of the breast, colon, and lung). This conjugate or a compound of analogous action that inhibits cellular growth acting via a saposin-C binding receptor can be used to decrease tumor growth and/or treat disorders of stromal proliferation (e.g., benign prostatic hyperplasia, atherosclerosis, and vascular restenosis).
REFERENCES:
patent: 5191067 (1993-03-01), Lappi et al.
patent: 5478804 (1995-12-01), Calabresi et al.
patent: 5576288 (1996-11-01), Lappi et al.
patent: 5679637 (1997-10-01), Lappi et al.
patent: 5696080 (1997-12-01), O'Brien et al.
patent: 5700909 (1997-12-01), O'Brien
patent: 5714459 (1998-02-01), O'Brien et al.
patent: 6268347 (2001-07-01), O'Brien
patent: 6326467 (2001-12-01), Net et al.
patent: 6348194 (2002-02-01), Huse et al.
patent: 6420126 (2002-07-01), Huse et al.
Jain, “Barriers to drug delivery in solid tumors”, Sci Am. 171(1): 58-65, 1994.
Freshney, Culture of Animal Cells, A Manual of Basic Technique, Alan R. Liss, Inc., 1983, New York, pp. 3-4.
Dermer, Bio/Technology, 1994, 12:320.
Andreasen, P. et al., “The urokinase-type plasminogen activator system in cancer metastasis,” Int. J. Cancer, vol. 72, pp. 1-22 (1997).
Andreasen, P.A. et al., “Plasminogen activator inhibitors: hormonally regulated serpins,” Mol. and Cell. Endocrinol., vol. 68, pp. 1-19 (1990).
Blasi et al., “Urokinase-type plasminogen activator: proenzyme, receptor and inhibitors,” J Cell Biol., vol. 104, pp. 801-804 (1987).
Brunner, N. et al., “The urokinase plasminogen activator receptor in blood from healthy individuals and patients with cancer,” APMIS, vol. 107, pp. 160-167 (1999).
Byrne, R.L. et al., “Peptide growth factors in the prostate as mediators of stromal epithelial interaction,” Br. J. Urol., vol. 77, pp. 627-633 (1996).
Campana, W. et al., “Prosaptide activates the MAPK pathway by a G-protein-dependent mechanism essential for enhanced sulfatide synthesis by Schwann cells,” FASEB J., vol. 3, pp. 307-314 (1998).
Chang, M.H.Y. et al., “Saposins A, B, C, and lysosomal storage disorders,”Clin. Chem , vol. 46, pp. 167-174 (2000).
Cherry, J.P. et al., “Analysis of cathepsin D forms and their clinical implications in prostate cancer,” J. Urol., vol. 160. pp. 2223-2228 (1998).
Chiarodo, A., “National Cancer Institute roundtable on prostate cancer: future research directions,” Cancer Res., vol. 51, pp. 2498-2505 (1991).
Chung, L.W., “The role of stromal-epithelial interaction in normal and malignant growth,” Cancer Surveys, vol. 23, pp. 33-42 (1995).
Chung, L.W.K. et al., “Prostate epithelial differentiation is dictated by its surrounding stroma,” Mol. Biol. Reports, vol. 23, pp. 13-19 (1996).
Dano, K. et al., “Cancer invasion and tissue remodeling-cooperation of protease systems and cell types,” APMIS, vol. 107, pp. 120-127 (1999).
Davol, P. et al., “Targeting human prostatic carcinoma through basic fibroblast growth factor receptors in an animal model: characterizing and circumventing mechanisms of tumor resistance,” The Prostate, vol. 40, pp. 178-191 (1999).
Davol, P. et al., “The mitotoxin, basic fibroblast growth factor-saporin, effectively targets human prostatic carcinoma in an animal model,” J. Urol., vol. 156, pp. 1174-1179 (1996).
Festuccia, C. et al., “Plasminogen activation system modulates invasive capacity and proliferation in prostatic tumor cells,” Clin. Exp. Metastasis, vol. 16, pp. 513-528 (1998).
Gaylis et al., F., “Plasminogen activators in human prostate cancer cell lines and tumors: correlation with the aggressive phenotype,” J. Urol., vol. 142, pp. 193-198 (1989).
Gnanapragasam, V. et al., “Androgen receptor signaling in the prostate,” Br. J. Urol., vol. 86, pp. 1001-10013 (2000).
Guo, C. et al., “Mitogenic signaling in androgen sensitive and insensitive prostate cancer cells,” J. Urol., vol. 163, pp. 1027-1032 (2000).
Henry, J.A. et al., “Prognostic significance of the estrogen-related protein, cathepsin D, in breast cancer,” Cancer, vol. 65, pp. 265-271 (1990).
Hiraiwa, M. et al., “Cell death prevention, mitogen-activated protein kinase stimulation, and increased sulfatide concentration in Schwann cells and oligodendrocytes by prosaposin and prosaptides,” Proc.Natl.Acad.Sci. USA, vol. 94, pp. 4778-4781 (1997).
Hiraiwa, M. et al. “Lysosomal proteolysis of prosaposin, the precursor of saposins (sphingolipid activator proteins): its mechanisms and inhibition by ganglioside.” Arch Biochem. Biophys., vol. 341, pp. 17-24 (1997).
Hiraiwa, M. et al., “Prosaposin receptor: evidence for a G-protein associated receptor”, Biochem. Biophys. Res. Commun., vol. 240, pp. 415-418 (1997).
Lamharzi, N. et al., “Decreased in the level and mRNA expression of LH-RH and EGF receptors after treatment with LH-RH antagonist Cetrorelix in DU-145 prostate tumor xenografts in nude mice,” Int. J. Oncol., vol. 13, pp. 429-435 (1998).
Lappi, D. et al., “Entering through the doors of perception: characterization of a highly selective substance P receptor-targeted toxin,” Neuropeptides, vol. 34, pp. 323-328 (2000).
Lin, D.-l. et al., “Interleukin-6 induces androgen responsiveness in prostate cancer cells through up-regulation of androgen receptor expression,” Clin. Cancer Res., vol. 7, pp. 1773-1781 (2001).
Liotta, L. et al., “Effect of plasminogen activator (urokinase), plasmin, and thrombin on glycoprotein and collagenous components on basement membrane,” Cancer Res., vol. 41, pp. 4629-4634 (1981).
Makar, R. et al., “Immunohistochemical analysis of cathepsin D in prostate carcinoma,” Modern Pathol., vol. 7, pp. 747-751 (1994).
Mayagarden, S. et al., “Evaluation of cathepsin D and epidermal growth factor receptor in prostate carcinoma,” Modern Pathol., vol. 7, pp. 930-936 (1994).
McConnell, J.D. et al., “Benign prostatic hyperplasia: Diagnosis and Treatment,” Clinical Practice Guideline, No. 8, AHCPR Publication No. 94-0582, Agency for Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human Service, Rockville, Maryland, 166 pages (1994).
Misasi, R. et al., “Prosaposin treatment induces PC12 entry in the S phase of the cell cycle and prevents apoptosis: activation of ERKs and sphingosine kinase,” FASEB. J., vol. 15, pp. 467-474.
Misasi, R. et al., “Prosaposin prosapeptide, a peptide form prosaposin induce an increase in ganglioside content on NS20Y neuroblastoma cells,” Glycoconjugate J., vol. 13, pp. 195-202 (1996).
Mohler, J. et al., “Androgen and glucocorticoid receptors in the stroma and epithelium of prostatic hyperplasia and carcinoma,” Clin. Cancer Res., vol. 2, pp. 889-895 (199
Koochekpour Shahriar
Sartor A. Oliver
Board of Supervisors of Louisiana State University and Agricultu
Davis Bonnie J.
Helms Larry R.
Runnels John H.
Sang Hong
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