Abstract: The present invention provides a compositions and methods for the treatment of cancer, including pancreatic cancer, breast cancer and melanoma, in a human patient. The methods and compositions of the present invention employ curcumin or a curcumin analogue encapsulated in a colloidal drug delivery system, preferably a liposomal drug delivery system. Suitable colloidal drug delivery systems also include nanoparticles, nanocapsules, microparticles or block copolymer micelles. The colloidal drug delivery system encapsulating curcumin or a curcumin analogue is administered parenterally in a pharmaceutically acceptable carrier.

Abstract: The present invention provides cell permeable NF-?B inhibitors consist of a polypeptide derived from the p65 subunit of NF-?B and a protein transduction domain derived from antennapedia third helix sequence. The inhibitor suppressed NF-?B activation induced by TNF, LPS, IL-1, okadaic acid, PMA, H2O2 and cigarette smoke condensate. NF-?B-regulated reporter gene expression induced by TNF, TNFR1, TRADD, TRAF2, NIK, IKK and p65 was suppressed by the inhibitor. The inhibitor enhanced TNF- and chemotherapeutic agent-induced apoptosis. Overall these results demonstrate a NF-?B inhibitor that can selectively inhibit NF-?B activation induced by various inflammatory stimuli, down-regulate NF-?B mediated gene expression and upregulate apoptosis.

Abstract: The present invention provides a method of reducing or inhibiting osteoclast development induced by the receptor for activation of nuclear factor kappa B ligand (RANKL), comprising the step of contacting said osteoclast, or a precursor of the osteoclast, with a pharmacologically effective dose of compounds such as diferuloylmethane, guggulsterone, 1?-Acetoxychavicol or analogues thereof.

Abstract: The present invention provides cell permeable NF-?B inhibitors consist of a polypeptide derived from the p65 subunit of NF-?B and a protein transduction domain derived from antennapedia third helix sequence. The inhibitor suppressed NF-?B activation induced by TNF, LPS, IL-1, okadaic acid, PMA, H2O2 and cigarette smoke condensate. NF-?B-regulated reporter gene expression induced by TNF, TNFR1, TRADD, TRAF2, NIK, IKK and p65 was suppressed by the inhibitor. The inhibitor enhanced TNF- and chemotherapeutic agent-induced apoptosis. Overall these results demonstrate a NF-?B inhibitor that can selectively inhibit NF-?B activation induced by various inflammatory stimuli, downregulate NF-?B mediated gene expression and upregulate apoptosis.

Abstract: The present invention is directed to the applications of a novel cytokine, named THANK, for TNF homologue that activates apoptosis, NF-?B and c-jun N-terminal kinase. Such applications include using THANK inhibitors to inhibit the activation of NF-?B and to treat a pathological condition caused by the activation of NF-?B. Also provided is a method of inhibiting growth of a wide variety of tumor cells by administering THANK protein.

Abstract: The present invention provides a RANK (receptor activator of NF-&kgr;B) inhibitor consisted of a TRAF-6 (TNF receptor-associated factor-6) binding domain attached to a leader sequence. The decoy peptide inhibits RANKL (RANK ligand)-mediated osteoclast differentiation, thus indicating that targeted disruption of interaction between RANK and TRAF6 may prove useful as a therapeutic for metabolic bone disorders, leukemia, arthritis, and metastatic cancer of the bone.

Abstract: A cytotoxic protein designated tumor necrosis factor is identified in nature. It is recovered in substantially homogeneous form by treatment with hydrophobic substances and ion exchange resins. The protein is conclusively identified by its amino acid sequences. Therapeutic compositions are provided.

Abstract: The present invention is directed to the applications of a novel cytokine, named THANK, for TNF homologue that activates apoptosis, NF-&kgr;B and c-jun N-terminal kinase. Such applications include using THANK inhibitors to inhibit the activation of NF-&kgr;B and to treat a pathological condition caused by the activation of NF-&kgr;B. Also provided is a method of inhibiting growth of a wide variety of tumor cells by administering THANK protein.

Abstract: The present invention provides methods for the therapeutic application of TRANK, a novel cytokine. TRANK is secreted by cells and activates NF-&kgr;B, c-Jun N-terminal kinase (JNK) and downstream gene products. Provided is a method of inhibiting NF-&kgr;B activation in an individual in need of such treatment, comprising the step of administering an effective dose of an anti-TRANK antibody to said individual.

Abstract: The present invention is directed to the applications of a novel cytokine, named THANK, for TNF homologue that activates apoptosis, NF-&kgr;B and c-jun N-terminal kinase. Such applications include using THANK inhibitors to inhibit the activation of NF-&kgr;B and to treat a pathological condition caused by the activation of NF-&kgr;B. Also provided is a method of inhibiting growth of a wide variety of tumor cells by administering THANK protein.

Abstract: Biologically active lymphotoxin polypeptides are synthesized in recombinant cell culture. Novel nucleic acid and vectors incorporating same are provided. The compositions and processes herein enable the economical preparation of compositions containing uniform lymphotoxin polypeptides and variant lymphotoxins having amino acid sequences that differ from those found in nature. The lymphotoxins are purified to a specific activity of 2-10×107 units/mg of protein by purification using a novel immobilized, lymphotoxin-neutralizing monoclonal antibody.

Abstract: The present invention provides a novel human cytokine termed Oncoinhibin. The protein Oncoinhibin is secreted by human erythroblastoid cells, has a molecular weight of approximately 28 kDa and exerts diverse neoplastic activity. The present invention also provides a method for treating neoplastic cells using human Oncoinhibin and a pharmaceutical composition comprised essentially of Oncoinhibin.

Abstract: The present invention is drawn to the inhibition of activation of NF-.kappa.B by caffeic acid phenethyl ester (CAPE) and two analogues of CAPE. Tumor necrosis factor (TNF) activation of NF-.kappa.B is completely blocked by CAPE in a dose- and time-dependent manner, as is activation by phorbol ester, ceramide, hydrogen peroxide, and okadaic acid. Additionally, capsaicin (8-methyl-N-vanillyl-6-noneamide) and resiniferatoxin inhibit the activation of NF-.kappa.B induced by different agents.

Abstract: The present invention provides an isolated and purified protein derived from Bacillus thuringiensis subspecies thuringiensis, having a molecular weight of approximately 20 kDa of SDS-PAGE, said protein having the partial amino acid sequence shown in SEQ ID No. 1, and wherein said protein displays cytotoxic effects against tumor cells. Also provided is a method of treating a neoplastic cell comprising administering a therapeutically effective dose of the composition of the present invention to said cell, and a method of activating macrophages, comprising administering a therapeutically effective dose of the composition of the present invention to said macrophages.

Abstract: The present invention provides a method of inhibiting the activation of the NF.kappa.B transcription factor in an animal in need of such treatment comprising the step of administering to said animal a pharmacologically effective dose of curcumin. Also provided is a method of inhibiting the nuclear translocation of the p65 subunit of the NF.kappa.B transcription factor in a cell or in an animal in need of such treatment comprising the step of administering to said animal a pharmacologically effective dose of curcumin.

Abstract: The present invention provides an isolated and purified protein that associates with the cytoplasmic domain of the p60 form of the tumor necrosis factor receptor, having a molecular weight of about 52-55 kDa on SDS-PAGE, is a phosphoprotein, and does not bind to the p80 form of the tumor necrosis factor receptor. Also provided is an isolated and purified protein kinase that binds to the cytoplasmic domain of the p60 form of the tumor necrosis factor receptor, said kinase phosphorylates the p60 form of the tumor necrosis factor receptor. Also provided are various methods of manipulating this tumor necrosis factor receptor-associated protein and kinase in order to reduce various biological effects of tumor necrosis factor.

Abstract: The present invention provides an isolated and purified protein that associates with the cytoplasmic domain of the p80 form of the tumor necrosis factor receptor, having a molecular weight of 59 kDa on SDS-PAGE, is a phosphoprotein, and does not bind to the p60 form of the tumor necrosis factor receptor. Also provided is an isolated and purified protein kinase that associates with the cytoplasmic domain of the p80 form of the tumor necrosis factor receptor, said kinase phosphorylates both the p80 and p60 forms of the tumor necrosis factor receptor and phosphorylates a 59 kDa molecular weight protein associated with the cytoplasmic domain of the p80 form of the tumor necrosis factor receptor. Also provided are various methods of reducing the biological effects of tumor necrosis factor.

Abstract: The present invention provides an isolated and purified protein derived from Bacillus thuringiensis subspecies thuringiensis, having a molecular weight of approximately 20 kDa of SDS-PAGE, said protein having the partial amino acid sequence shown in SEQ ID No. 1, and wherein said protein displays cytotoxic effects against tumor cells. Also provided is a method of treating a neoplastic cell comprising administering a therapeutically effective dose of the composition of the present invention to said cell.

Abstract: Biologically active lymphotoxin polypeptides are synthesized in recombinant cell culture. Novel nucleic acid and vectors incorporating same are provided. The compositions and processes herein enable the economical preparation of compositions containing uniform lymphotoxin polypeptides and variant lymphotoxins having amino acid sequences that differ from those found in nature. The lymphotoxins are purified to a specific activity of 2-10.times.10.sup.7 units/mg of protein by purification using a novel immobilized, lymphotoxin-neutralizing monoclonal antibody.

Abstract: Tumor necrosis factor antagonists are administered in therapeutically effective doses to suppress inflammatory immune-potentiated events. The antagonists of this invention typically are selected from among several classes but preferably are neutralizing antibodies directed against tumor necrosis factor. The antagonists are useful in suppressing transplantation immunity and in the treatment of autoimmune diseases.