摘要:
Recombinant pox viruses capable of expressing an immunogenic fragment of the MUC1 tumor-associated antigen are disclosed. The recombinant viruses can be used as vaccines to prevent the establishment of or treat tumors or pre-tumorous cells expressing the MUC1 tumor-associated antigen. The vaccines can be provided as an admixture comprising: (1) a recombinant pox virus encoding the immunogenic fragment of the MUC1 tumor-associated antigen, and (2) a recombinant pox virus encoding a T-cell co-stimulatory factor. The vaccine admixture can be used, e.g., to prevent establishment of tumors or pre-tumorous cells expressing the MUC1 tumor-associated antigen. The MUC1 specific cytotoxic T-cells can be isolated and expanded and used in a method for treating a host having a tumor expressing MCU1 positive tumor cells.
摘要:
The present invention provides for chimeric proteins comprising a MUC1 extracellular (MUC1-EC) polypeptide and a carrier polypeptide that function as traps for MUC1 ligands.
摘要:
Methods for improved administration and dosing of DPD inhibitors in combination with 5-FU and/or 5-FU prodrugs are provided, comprising first administering to a patient in need thereof a DPD inhibitor that substantially eliminates activity of the enzyme and thereafter administering 5-FU or a 5-FU prodrug, wherein the level of 5-FU or 5-FU prodrug is in substantial excess of DPD inhibitor in the patient.
摘要:
The invention provides methods of reducing or preventing oxidative stress-induced cell death by contacting a cell with a compound that inhibits the kinase activity and/or the mitochondrial translocation of c-Abl. The methods of the invention can be used to treat individuals individual diagnosed as having or being at risk of contracting a disorder characterized by excessive oxidative stress-induced cell death.
摘要:
The present disclosure demonstrates the successful use of constitutive promoters operatively linked to genes encoding radiosensitizing or radioprotecting factors, administered to cells, tissues, or patients in conjunction with radiation exposure. Also disclosed are pharmacological preparations to be used to increase the levels of radiosensitizing compounds such as TNF-α, or radioprotective compounds such as MnSOD, in specified tissues or tumors of a subject.
摘要:
Disclosed are methods of synergistically inhibiting growth of a glioma cell comprising contacting the cell with temozolomide and TNFα, or with temozolomide, TNFα, and radiation. Also disclosed are methods of synergistically inhibiting growth of a glioma in a human cancer patient comprising administering temozolomide and TNFα, or with temozolomide, TNFα, and radiation. Pharmaceutical combinations and therapeutic combinations suitable for use in the methods of the invention are also disclosed.
摘要:
Immunostimulatory compositions that contain fused cells formed by fusion between dendritic cells and non-dendritic cells, methods of using these compositions, and methods of generating dendritic cell hybrids.
摘要:
Isolated DNA encompassing the DF3 enhancer as well as a sequence encoding a heterologous polypeptide provides epithelial tissue-selective gene expression of the heterologous polypeptide, useful in methods of therapy.
摘要:
The present disclosure provides methods of identifying and making compounds and pharmaceutical compositions thereof that inhibit the interaction between MUC1 and Abl. The invention also provides in vivo, in vitro, and ex vivo methods of inhibiting such an interaction. Also featured are in vitro and in vivo methods of stimulating the Abl-dependent apoptotic pathway in cells expressing MUC1. In such methods, the compounds, compositions, and methods described herein are generally useful in the treatment of various cancers. The disclosure also provides methods for inhibiting Abl, and such methods, and compounds and compositions for use in the methods are generally useful for the treatment of cancers, inflammatory conditions, atherosclerotic lesions, and neurologic disorders.
摘要:
The present invention relates to the signalling pathways connecting DNA damage, such as that induced by ionizing radiation or alkylating agents, and phosphorylation by tyrosine kinases.