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 analog 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 analog is administered parenterally in a pharmaceutically acceptable carrier.

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 inventive subject matter relates to methods for modulating an eicosanoid metabolic process in cells of an animal in need thereof, which comprises administering to the animal an amount of the inventive compositions effective for regulating the activity of an eicosanoid oxygenase. In particular, the inventive subject matter relates to methods for modulating arachidonic acid metabolism by administering an amount of the inventive compositions effective for regulating the activity of lipoxygenases and cyclooxygenases.

Abstract: The inventive subject matter relates to methods for modulating an eicosanoid metabolic process in cells of an animal in need thereof, which comprises administering to the animal an amount of the inventive compositions effective for regulating the activity of an eicosanoid oxygenase. In particular, the inventive subject matter relates to methods for modulating arachadonic acid metabolism by administering an amount of the inventive compositions effective for regulating the activity of lipoxygenases and cyclooxygenases.

Abstract: The inventive subject matter relates to methods for modulating an eicosanoid metabolic process in cells of an animal in need thereof, which comprises administering to the animal an amount of the inventive compositions effective for regulating the activity of an eicosanoid oxygenase. In particular, the inventive subject matter relates to methods for modulating arachadonic acid metabolism by administering an amount of the inventive compositions effective for regulating the activity of lipoxygenases and cyclooxygenases.

Abstract: The inventive subject matter relates to methods for modulating an eicosanoid metabolic process in cells of an animal in need thereof, which comprises administering to the animal an amount of the inventive compositions effective for regulating the activity of an eicosanoid oxygenase. In particular, the inventive subject matter relates to methods for modulating arachadonic acid metabolism by administering an amount of the inventive compositions effective for regulating the activity of lipoxygenases and cyclooxygenases.

Abstract: The inventive subject matter relates to methods for modulating an eicosanoid metabolic process in cells of an animal in need thereof, which comprises administering to the animal an amount of the inventive compositions effective for regulating the activity of an eicosanoid oxygenase. In particular, the inventive subject matter relates to methods for modulating arachadonic acid metabolism by administering an amount of the inventive compositions effective for regulating the activity of lipoxygenases and cyclooxygenases.

Abstract: The present invention provides a compositions and methods for the treatment of Neurofibromatosis Type 1 and 2, 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 to target Merlin and proteins of the Merlin pathway. 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: All multiple myeloma cell lines examined showed constitutively active I?B kinase (IKK), I?B? phosphorylation and constitutively active NF-?B. Curcumin, a chemopreventive agent, suppressed constitutive I?B? phosphorylation through inhibition of IKK activity and downregulated NF-?B. Curcumin also downregulated expression of NF-?B-regulated gene products such as I?B?, Bcl-2, Bcl-xL, cyclin D1 and interleukin-6. Consequently, curcumin suppressed multiple myeloma cell proliferation and arrested cells at the G1/S phase of the cell cycle. Curcumin also induced apoptosis and chemosensitivity to vincristine. Overall, results presented herein provide a molecular basis for the treatment of multiple myeloma patients with this pharmacologically safe agent.

Abstract: The inventive subject matter relates to methods for modulating an eicosanoid metabolic process in cells of an animal in need thereof, which comprises administering to the animal an amount of the inventive compositions effective for regulating the activity of an eicosanoid oxygenase. In particular, the inventive subject matter relates to methods for modulating arachadonic acid metabolism by administering an amount of the inventive compositions effective for regulating the activity of lipoxygenases and cyclooxygenases.

Abstract: All multiple myeloma cell lines examined showed constitutively active I?B kinase (IKK), I?B? phosphorylation and constitutively active NF-?B. Curcumin, a chemopreventive agent, suppressed constitutive I?B? phosphorylation through inhibition of IKK activity and downregulated NF-?B. Curcumin also downregulated expression of NF-?B-regulated gene products such as I?B?, Bcl-2, Bcl-xL, cyclin D1 and interleukin-6. Consequently, curcumin suppressed multiple myeloma cell proliferation and arrested cells at the G1/S phase of the cell cycle. Curcumin also induced apoptosis and chemosensitivity to vincristine. Overall, results presented herein provide a molecular basis for the treatment of multiple myeloma patients with this pharmacologically safe agent.

Abstract: The present invention provides methods of inhibiting metastasis of a tumor and methods of treating a tumor using a combination of an inhibitor of the activation of nuclear factor NF-?B and a cancer chemotherapeutic agent. In one embodiment of the present invention, combination of curcumin and paclitaxel (taxol) can be used to treat and inhibit metastasis of breast tumor.

Abstract: The present invention provides methods of inhibiting metastasis of a tumor and methods of treating a tumor using a combination of an inhibitor of the activation of nuclear factor NF-?B and a cancer chemotherapeutic agent. In one embodiment of the present invention, combination of curcumin and paclitaxel (taxol) can be used to treat and inhibit metastasis of breast tumor.

Abstract: The present invention provides a RANK (receptor activator of NF-?B) inhibitor consisted of a TRAF-6 (TNF receptor-associated factor-6) binding domain attached to a leader sequence. The peptide inhibitor 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: The present invention provides an inhibitor of NF-?B, guggulsterone and its analogs. Guggulsterone suppresses NF-?B activation induced by TNF, phorbol ester, okadaic acid, cigarette smoke, H2O2 and IL-1?, as well as constitutive NF-?B activation expressed in most tumor cells. One mechanism by which guggulsterone inhibits activation of NF-?B is through suppression of I?B? phosphorylation and I?B? degradation. NF-?B-dependent gene transcription is modulated by guggulsterone and its analogs. In particular, induction by TNF, TNFR1, TRADD, TRAF2, NIK and IKK, is modulated by guggulsterone and its analogs. In addition, guggulsterone decreased the expression of genes involved in anti-apoptosis (IAP1, XIAP, Bfl-1/A1, bcl-2, cFLIP, survivin), proliferation (cyclin D1, c-myc) and metastasis (MMP-9, COX2 and VEGF).

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: Pharmaceutical compositions suitable for aerosol delivery to a subject that include curcumin dispersed in a lipid vehicle, wherein the lipid has a transition temperature of less than about 15° C., are disclosed. In addition, methods of treating a pathological condition in a subject that include providing one of the claimed pharmaceutical compositions and administering the composition to the subject are disclosed. For example, the pathological condition can be a hyperproliferative disease, such as cancer, an inflammatory disease, or a pulmonary disease.

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 a method of treating a cancerous or pre-cancerous state in an individual in need of such treatment, comprising the step of administering a pharmacologically effective dose of a curcuminoid to the individual.

Abstract: All multiple myeloma cell lines examined showed constitutively active I&kgr;B kinase (IKK), I&kgr;B&agr; phosphorylation and constitutively active NF-&kgr;B. Curcumin, a chemopreventive agent, suppressed constitutive I&kgr;B&agr; phosphorylation through inhibition of IKK activity and downregulated NF-&kgr;B. Curcumin also downregulated expression of NF-&kgr;B-regulated gene products such as I&kgr;B&agr;, Bcl-2, Bcl-xL, cyclin D1 and interleukin-6. Consequently, curcumin suppressed multiple myeloma cell proliferation and arrested cells at the G1/S phase of the cell cycle. Curcumin also induced apoptosis and chemosensitivity to vincristine. Overall, results presented herein provide a molecular basis for the treatment of multiple myeloma patients with this pharmacologically safe agent.