Tumor treatment with gliotoxin derivatives

Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Heterocyclic carbon compounds containing a hetero ring...

Reexamination Certificate

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C514S222800

Reexamination Certificate

active

07981878

ABSTRACT:
The present invention describes the use of Notch2 inhibitors for producing a medicament for the treatment of tumours, which tumours are characterized by ligand-independent Notch2 fragments.

REFERENCES:
patent: 2004/0101847 (2004-05-01), Freier et al.
patent: 2004/1001847 (2004-05-01), Freier et al.
patent: 2004/0137569 (2004-07-01), Chan et al.
patent: 0 163 475 (1985-12-01), None
patent: 0 926 242 (1999-06-01), None
patent: 61-277617 (1986-12-01), None
patent: 6220065 (1994-08-01), None
patent: 7227293 (1995-08-01), None
patent: WO 92/10198 (1992-06-01), None
patent: WO 2004/019921 (2004-03-01), None
Tompsett et al. Tuberculostatic activity of blood and urine from animals given gliotoxin. Cornell Medical Center, New York. Feb. 6, 1950.
Karon & Klyce. Effect of inhibition of inflammatory mediators on trauma-induced stromal edema. Investigative Ophthalmology & Visual Science, Jun. 2003, vol. 4, No. 6, pp. 2507-2510.
Vigushin et al. Gliotoxin is a dual inhibitor of farnesyltransferase and geranylgeranyltransferase I with antitumor activity against breast cancer in vivo. Medical Oncology, vol. 21, No. 1, 21-30, 2004.
Tiwari et al. Among circulating hematopoietic cells, B-CLL uniquely expresses functional EPAC1, but EPAC1-mediated Rap1 activation does not account for PDE4 inhibitor-induced apoptosis. Blood, 2004, 103: 2661-2667.
Marzo et al. Farnesyltransferase inhibitor BMS-214662 induces apoptosis in B-cell chronic lymphocytic leukemia cells. Leukemia, 2004, 18, 1599-1604.
Sutton et al. Evidence that gliotoxin enhances lymphocyte activation and induces apoptosis by effects on cyclic AMP levels. Biochemical Pharmacology, vol. 50, No. 12, pp. 2009-2014,1995.
Gaiger et al. Novel molecular diagnostic and therapeutic targets in chronic lymphocytic leukaemia. European Journal of Clinical Investigation, 34 (Suppl. 2), 25-30, 2004.
Cuevas et al., “Meningioma transcript profiles reveal deregulated Notch signaling pathway,”Cancer Res., 65:5070-5075, 2005.
Fan et al., “Notchl and notch2 have opposite effects on embryonal brain tumor growth,”Cancer Res., 64:7787-7793, 2004.
Gardiner et al., “The epipolythiodioxopiperazine (ETP) class of fungal toxins: distribution, mode of action, functions and biosynthesis,”Microbiology, 151:1021-1032, 2005.
Garnis et al., “Involvement of multiple developmental genes on chromosome 1p in lung tumorigenesis,”Hum. Mol. Gen., 14:475-82, 2004.
Hoek et al., “Expression profiling reveals novel pathways in the transformation of melanocytes to melanomas,”Cancer Res., 64:5270-82, 2004.
Hubmann et al., “Involvement of PKC-delta in the regulation of Notch2 ni B-CLL,”Blood, 106(11):Abstract 4990, 2005.
Hubmann et al., “Notch2 is involved in the overexpression of CD23 in B-cell chronic lymphocytic leukemia,”Blood, 99:3742-7, 2002.
Hurne et al., “Inactivation of rabbit muscle creatine kinase by reversible formation of an internal disulfide bond induced by the fungal toxin gliotoxin,”JBC, 275:25202-6, 2000.
Jansen et al., “bcl-2 antisense therapy chemosensitizes human melanoma in SCID mice,”Nat. Med., 4:232-234, 1998.
Jehn et al., “Cutting edge: protective effects of notch-1 on TCR-induced apoptosis,”JI, 162:635-8, 1999.
Jundt et al., “Novel gamma-secretase inhibitor DAPT blocks activated notch signaling and controls tumor cell growth in Hodgkin and anaplastic large cell lymphoma,”Blood, 100(11):Abstract 594, 2002.
Knowles et al., “Human hepatocellular carcinoma cell lines secrete the major plasma proteins and hepatitis B surface antigen,”Science, 209:497-499, 1980.
Kweon et al., “Gliotoxin-mediated apoptosis of activated human hepatic stellate cells,”J. Hepato., 39:38-42, 2003.
Lauring and Overbaugh, “Evidence that an IRES within the Notch2 coding region can direct expression of a nuclear form of the protein,”Mol. Cell, 6:939-45, 2000.
Lee et al., “Anti-angiogenic activities of gliotoxin and its methylthioderivative, fungal metabolites,”Arch. Pharm. Res., 24:397-401, 2001.
Lee et al., “Notch 2-positive progenitors with the intrinsic ability to give rise to pancreatic ductal cells,”Lab. Invest., 85:1003-12, 2005.
Lehmann et al., “MUC18, a marker of tumor progression in human melanoma, shows sequence similarity to the neural cell adhesion molecules of the immunoglobulin superfamily,”Proc. Natl. Acad. Sci. USA, 86:9891-9895, 1989.
Leong and Karsan, “Recent insights into the role of Notch signaling in tumorigenesis,”Blood, 107:2223-33, 2006.
Lewis et al., “Detection of gliotoxin in experimental and human aspergillosis,”Infect. and Immun., 73:635-7, 2005.
Lieber et al., “Establishment of a continuous tumor-cell line (panc-1) from a human carcinoma of the exocrine pancreas,”Int. J. Cancer, 15:741-747, 1975.
Lin et al., “Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3,”Cell, 116:527-40, 2004.
Maillard et al., “Mastermind critically regulates Notch-mediated lymphoid cell fate decisions,”Blood, 104:1696-1702, 2004.
Martin et al., “Quantitative proteomic analysis of proteins released by neoplastic prostate epithelium,”Cancer Res., 64:347-55, 2004.
Massi et al., “Evidence for differential expression of Notch receptors and their ligands in melanocytic nevi and cutaneous malignant melanoma,”Modern Pathology, 19:246-254, 2006.
Miele, “Notch signaling,”Clin. Cancer Res., 12:1074-9, 2006.
Müllbacher et al., “Selective resistance of bone marrow-derived hemopoietic progenitor cells to gliotoxin,”PNAS, 84:3822-5, 1987.
Nickoloff et al., “Notch signaling as a therapeutic target in cancer: a new approach to the development of cell fate modifying agents,”Oncogene, 22:6598-6608, 2003.
Orr et al., “Mechanism of action of the antifibrogenic compound gliotoxin in rat liver cells,”Hepatology, 40:232, 2004.
Paris et al., “Inhibition of angiogenesis and tumor growth by βand γ-secretase inhibitors,”European Journal of Pharmacology, 514:1-15, 2005.
Park et al., “Characterization of cell lines established from human hepatocellular carcinoma,”Int. J. Cancer, 62:276-282, 1995.
Parr et al., “The possible correlation of Notch-1 and Notch-2 with clinical outcome and tumour clinicopathological parameters in human breast cancer,”Int. J. Mol. Med., 14:779-786, 2004.
Radtke and Raj, “The role of Notch in tumorigenesis: oncogene or tumour suppressor?,”Nat. Rev. Cancer, 3:756-67, 2003.
Santagata et al., “JAGGED1 expression is associated with prostate cancer metastasis and recurrence,”Cancer Res., 64:6854-6857, 2004.
Schwarzmeier et al., “Regulation of CD23 expression by Notch2 in B-cell chronic lymphocytic leukemia,”Leuk. Lymphoma, 46:157-165, 2005.
Sutton et al., “In vivo immunosuppressive activity of gliotoxin, a metabolite produced by human pathogenic fungi,”Infect. and Immun., 62:1192-8, 1994.
Vigushin et al., “Gliotoxin is a dual inhibitor of farnesyltransferase and geranylgeranyltransferase I with antitumor activity against breast cancer in vivo,”Med. Oncol., 21:21-30, 2004.
Yunis et al., “Human pancreatic carcinoma (MIA PaCa-2) in continuous culture: sensitivity to asparaginase,”Int. J. Cancer, 19:128-135, 1977.
Zhang et al., “Notch signaling pathway contributes to osteosarcoma growth, tumorigenesis and metastasis,”AACR Meeting Abstracts, 2006.

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