Treatment for glioblastoma
Abstract
The present invention includes a composition and method for treating a glioblastoma in a human or animal subject comprising the steps of: identifying the human or animal subject in need of treatment of a glioblastoma, wherein the human or animal is no longer responsive to at least one of chemotherapy, surgery, or radiation therapy; and administering to the human or animal subject a therapeutically effective amount of a composition comprising: an amount of a curcumin or curcuminoids in one or more liposomes, or curcumin or curcuminoids and empty liposomes and administered prior to, concomitantly, or after administration of the curcumin or curcuminoids, that is effective for treating the glioblastoma, wherein the liposomal curcumin or curcuminoids, or empty liposomes, eliminate the QT prolongation caused by the curcumin or curcuminoids; and at least one chemotherapeutic agent that is synergistic with curcumin to treat the glioblastoma.
Claims
exact text as granted — not AI-modifiedWhat is claimed is:
1 . A method for treating a glioblastoma in a human or animal subject comprising the steps of:
identifying the human or animal subject in need of treatment of a glioblastoma, wherein the human or animal is no longer responsive to at least one of chemotherapy, surgery, or radiation therapy; and administering to the human or animal subject a therapeutically effective amount of a composition comprising: an amount of a curcumin or curcuminoids in one or more liposomes, or curcumin or curcuminoids and empty liposomes and administered prior to, concomitantly, or after administration of the curcumin or curcuminoids, that is effective for treating the glioblastoma, wherein the liposomal curcumin or curcuminoids, or empty liposomes, eliminate the QT prolongation caused by the curcumin or curcuminoids; and at least one chemotherapeutic agent that is synergistic with curcumin to treat the glioblastoma.
2 . The method of claim 1 , wherein the chemotherapeutic agent is selected from at least one of temozolomide, etoposide, doxorubicin, cisplatin, paclitaxel, carmustine, lomustine, ceramide and phosphorylcholine.
3 . The method of claim 1 , wherein the QT prolongation is LQTS.
4 . The method of claim 3 , wherein the liposomal curcumin or curcuminoids, or empty liposomes are provided intravenously.
5 . The method of claim 1 , wherein the composition increases ceramide production of the glioblastoma cell.
6 . The method of claim 1 , wherein the composition increases phosphorylcholine production of the glioblastoma cell.
7 . The method of claim 1 , wherein the glioblastoma cells are sensitized to an agent to which they have become refractory as a result of increased ceramide production in the glioblastoma cell.
8 . The method of claim 1 , wherein the glioblastoma cells are sensitized to an agent to which they have become refractory as a result of increased phosphorylcholine production in the glioblastoma cell.
9 . A method for treating a glioblastoma in a human or animal subject comprising the steps of:
identifying the human or animal subject in need of treatment of a glioblastoma, wherein the human or animal is no longer responsive to at least one of chemotherapy, surgery, or radiation therapy; and administering to the human or animal subject a therapeutically effective amount of a composition comprising: an amount of a curcumin or curcuminoids in one or more liposomes, or curcumin or curcuminoids and empty liposomes and administered prior to, concomitantly, or after administration of the curcumin or curcuminoids, that is effective for treating the glioblastoma, wherein the liposomal curcumin or curcuminoids, or empty liposomes, eliminate the QT prolongation caused by the curcumin or curcuminoids; and at least one chemotherapeutic agent that is synergistic with curcumin to treat the glioblastoma, selected from at least one of temozolomide, etoposide, doxorubicin, cisplatin, paclitaxel, carmustine, lomustine, ceramide and phosphorylcholine.
10 . The method of claim 9 , wherein the QT prolongation is LQTS.
11 . The method of claim 9 , wherein the liposomal curcumin or curcuminoids, or empty liposomes are provided intravenously.
12 . The method of claim 9 , wherein the composition increases ceramide production of the glioblastoma cell.
13 . The method of claim 9 , wherein the composition increases phosphorylcholine production of the glioblastoma cell.
14 . The method of claim 9 , wherein the glioblastoma cells are sensitized to an agent to which they have become refractory as a result of increased ceramide production in the glioblastoma cell.
15 . The method of claim 9 , wherein the glioblastoma cells are sensitized to an agent to which they have become refractory as a result of increased phosphorylcholine production in the glioblastoma cell.
16 . A method of determining the effectiveness of a candidate drug that is a chemotherapeutic agent that sensitizes or synergizes with curcumin to treat the glioblastoma, the method comprising:
measuring the effect of a candidate agent on a glioblastoma cell; administering the candidate drug to a first subset of glioblastoma cells, and a combination of the candidate drug with curcumin to a second subset of glioblastoma cells; and determining if the curcumin sensitizes or synergizes the glioblastoma cells to the candidate agent in the first versus the second subset of glioblastoma cells.
17 . The method of claim 16 , wherein the method further comprises the step of determining if the candidate drug increases ceramide production of the glioblastoma cell.
18 . The method of claim 16 , wherein the method further comprises the step of determining if the candidate drug increases phosphorylcholine production of the glioblastoma cell.
19 . The method of claim 16 , wherein the method further comprises the step of determining if the glioblastoma cells are sensitized to an agent to which they have become refractory as a result of increased ceramide production in the glioblastoma cell.
20 . The method of claim 16 , wherein the method further comprises the step of determining if the glioblastoma cells are sensitized to an agent to which they have become refractory as a result of increased phosphorylcholine production in the glioblastoma cell.Cited by (0)
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