Abstract: Disclosed herein is a recombinant polypeptide comprising 1 to 20 copies of an IL-17RB inactivation site (IRIS) sequence. Also disclosed herein is the use of the recombinant polypeptide in the preparation of a conjugate for the treatment of cancers.

Abstract: The present invention relates to an antagonist of interleukin-17B receptor (IL-17RB) which features interruption of the interaction of IL-17RB and MLK4. The present invention also relates to use of such antagonist for treatment of diseases or disorders associated with IL-17RB activation. Further disclosed is a phosphorylated IL-17RB as a biomarker for predicting prognosis and/or monitoring progression of cancer.

Abstract: Methods and compositions for treatment and therapy of cancer are provided. Specifically, antagonists specific for interleukin-17 receptor B (IL-17RB) and its ligand IL-17B are provided. Potent neutralizing antibodies specific for IL-17RB and methods for their manufacture and use are disclosed. The invention also relates to antisense, RNAi and shRNA compositions for the prevention and treatment of cancer, in particular breast cancer and pancreatic cancer.

Abstract: The present invention includes novel RAD51 inhibitors. The compounds of the invention may be useful in preventing or treating cancer in a subject in need thereof. The present invention also includes methods of preventing or treating cancer in a subject in need thereof by administering to the subject a therapeutically effective amount of a compound of the invention.

Abstract: The present invention includes novel RAD51 inhibitors. The compounds of the invention may be useful in preventing or treating cancer in a subject in need thereof. The present invention also includes methods of preventing or treating cancer in a subject in need thereof by administering to the subject a therapeutically effective amount of a compound of the invention.

Abstract: The present invention includes novel RAD51 inhibitors. The compounds of the invention may be useful in preventing or treating cancer in a subject in need thereof. The present invention also includes methods of preventing or treating cancer in a subject in need thereof by administering to the subject a therapeutically effective amount of a compound of the invention.

Abstract: Methods and compositions for treatment and therapy of cancer are provided. Specifically, antagonists specific for interleukin-17 receptor B (IL-17RB) and its ligand IL-17B are provided. Potent neutralizing antibodies specific for IL-17RB and methods for their manufacture and use are disclosed. The invention also relates to antisense, RNAi and shRNA compositions for the prevention and treatment of cancer, in particular breast cancer and pancreatic cancer.

Abstract: The present invention includes novel RAD51 inhibitors. The compounds of the invention may be useful in preventing or treating cancer in a subject in need thereof. The present invention also includes methods of preventing or treating cancer in a subject in need thereof by administering to the subject a therapeutically effective amount of a compound of the invention.

Abstract: Certain embodiments of the present invention provide selected compounds having a molecular structure according to Formula 1: In Formula 1, Z is —CO—, —SO—, or —SO2—; Ar is phenyl, heteroaryl, or heterocycloalkyl; Het is heteroaryl; R is R?, X, or NR1R2; R? is R3, or OR3; R? is R4, or OR4; R1 and R2 are each independently H, alkyl, or acyl; R3 is H, heteroaryl, or alkyl; R4 is H, heteroaryl, or CnH2n+1 (n>2); and X is F, Br, I, CN, or NO2. In some embodiments, compounds having a molecular structure according to Formula 1 have the property of inhibiting a growth of a cell line selected from HeLa and MB468 with a sub-micromolar IC50.

Abstract: Certain embodiments of the present invention provide selected compounds having a molecular structure according to Formula 1: In Formula 1, Z is —CO—, —SO—, or —SO2—; Ar is phenyl, heteroaryl, or heterocycloalkyl; Het is heteroaryl; R is R?, X, or NR1R2; R? is R3, or OR3; R? is R4, or OR4; R1 and R2 are each independently H, alkyl, or acyl; R3 is H, heteroaryl, or alkyl; R4 is H, heteroaryl, or CnH2n+1 (n>2); and X is F, Br, I, CN, or NO2. In some embodiments, compounds having a molecular structure according to Formula 1 have the property of inhibiting a growth of a cell line selected from HeLa and MB468 with a sub-micromolar IC50.

Abstract: Certain embodiments of the present invention provide selected compounds having a molecular structure according to Formula 1: In Formula 1, Z is —CO—, —SO—, or —SO2—; Ar is phenyl, heteroaryl, or heterocycloalkyl; Het is heteroaryl; R is R?, X, or NR1R2; R? is R3, or OR3; R? is R4, or OR4; R1 and R2 are each independently H, alkyl, or acyl; R3 is H, heteroaryl, or alkyl; R4 is H, heteroaryl, or CnH2n+1 (n>2); and X is F, Br, I, CN, or NO2. In some embodiments, compounds having a molecular structure according to Formula 1 have the property of inhibiting a growth of a cell line selected from HeLa and MB468 with a sub-micromolar IC50.

Abstract: A massage tool includes a main body; and an active member coupled to the main body. The active member includes an active material capable of being heated for transferring heat to the main body so as to activate or reactivate the massage tool. If necessary, more than one active material may be included in the active member. Heat can be transferred from the active material to the main body by way of conduction of the active material or convection of an active vapor released from the active material. The active vapor, for example, can be steam for providing heat and/or vaporized essential oil for aromatic treatment. The active material, for example, can be heated by an external heating source or an internal heating source.

Abstract: Chronic myelogenous leukemia (CML), and in particular imatinib resistant CML is treated using compositions and methods in which a Rad51-inhibitor and a kinase inhibitor are administered. Most preferably, the Rad51 inhibitor comprises an indolyl isoquinoline structure and the kinase inhibitor is a BCR-ABL inhibitor.

Abstract: Certain embodiments of the present invention provide selected compounds having a molecular structure according to Formula 1: In Formula 1, Z is —CO—, —SO—, or —SO2—; Ar is phenyl, heteroaryl, or heterocycloalkyl; Het is heteroaryl; R is R?, X, or NR1R2; R? is R3, or OR3; R? is R4, or OR4; R1 and R2 are each independently H, alkyl, or acyl; R3 is H, heteroaryl, or alkyl; R4 is H, heteroaryl, or CnH2n+1 (n>2); and X is F, Br, I, CN, or NO2. In some embodiments, compounds having a molecular structure according to Formula 1 have the property of inhibiting a growth of a cell line selected from HeLa and MB468 with a sub-micromolar IC50.

Abstract: The present invention provides methods, kits, and compositions for treating cancer with cytotoxic agents. Preferably, the cytotoxic agents are selected from: IL-25, BMP1O, FGF1 1, VDBP, ATIII and IL1-F7, and any combination thereof. In other preferred embodiments, the cancer is breast cancer. These agents can be supplied, for example, as proteins or as part of nucleic acid expression vector.

Abstract: Contemplated compounds disrupt interaction between BRCA2 and RAD51, likely by binding to RAD51. Based on the crucial role of the BRCA2-RAD51 complex formation in DNA repair and the role of RAD51 in the control of entry into S-phase from G1, numerous compositions and methods are presented. Among other advantageous uses, contemplated compounds may be employed as protective agents for non-neoplastic cells in chemotherapy before exposure of the cells to a chemotherapeutic drug, and/or as DNA-damage sensitizer for neoplastic cells.

Abstract: The present invention provides methods and compounds for inhibiting HEC1 activity for the treatment of diseases involving cell hyperproliferation, e.g. cancer. The present invention also provides methods of identifying compounds for inhibiting HEC1 activity.

Abstract: Chronic myelogenous leukemia (CML), and in particular imatinib resistant CML is treated using compositions and methods in which a Rad51-inhibitor and a kinase inhibitor are administered. Most preferably, the Rad51 inhibitor comprises an indolyl isoquinoline structure and the kinase inhibitor is a BCR-ABL inhibitor.

Abstract: Contemplated compounds disrupt interaction between BRCA2 and RAD51, likely by binding to RAD51. Based on the crucial role of the BRCA2-RAD51 complex formation in DNA repair and the role of RAD51 in the control of entry into S-phase from G1, numerous compositions and methods are presented. Among other advantageous uses, contemplated compounds may be employed as protective agents for non-neoplastic cells in chemotherapy before exposure of the cells to a chemotherapeutic drug, and/or as DNA-damage sensitizer for neoplastic cells.

Abstract: Disclosed are methods of controlling cell cycle progression by introducing into a cell to be controlled a composition selected from the group consisting of p56RB protein, a fragment of the p56RB protein, and the gene encoding p56RB protein to alter the cell cycle progression while maintaining the viability of the cell. The p56RB protein has been found to have the unexpected and surprising characteristic of being soluble in low concentrations of glycerol, thereby enhancing its value in pharmaceutical applications and the gene encoding p56RB when delivered to the hyperproliferating cell inhibits cellular proliferation.