Abstract: Methods for treating tumors comprise contacting tumor cells expressing the vitamin D receptor with a vitamin D receptor ligand that inhibits homologous recombination in the tumor cells, and contacting the tumor cells with an amount of a Poly(ADP) Ribose Polymerase 1 (PARP-1) inhibitor. Inhibiting homologous recombination produces a synergistic therapeutic effect between the vitamin D receptor ligand and PARP-1 inhibitor, and may overcome PARP-1 resistance in killing tumor cells.

Abstract: Methods for treating tumors comprise contacting tumor cells expressing the vitamin D receptor with a vitamin D receptor ligand that inhibits homologous recombination in the tumor cells, and contacting the tumor cells with an amount of a Poly(ADP) Ribose Polymerase 1 (PARP-1) inhibitor. Inhibiting homologous recombination produces a synergistic therapeutic effect between the vitamin D receptor ligand and PARP-1 inhibitor, and may overcome PARP-1 resistance in killing tumor cells.

Abstract: Methods for treating tumors comprise contacting tumor cells expressing the vitamin D receptor with a vitamin D receptor ligand that inhibits homologous recombination in the tumor cells, and contacting the tumor cells with an amount of a Poly(ADP) Ribose Polymerase 1 (PARP-1) inhibitor. Inhibiting homologous recombination produces a synergistic therapeutic effect between the vitamin D receptor ligand and PARP-1 inhibitor, and may overcome PARP-1 resistance in killing tumor cells.

Abstract: Methods for treating tumors comprise contacting tumor cells expressing the vitamin D receptor with a vitamin D receptor ligand that inhibits homologous recombination in the tumor cells, and contacting the tumor cells with an amount of a Poly(ADP) Ribose Polymerase 1 (PARP-1) inhibitor. Inhibiting homologous recombination produces a synergistic therapeutic effect between the vitamin D receptor ligand and PARP-1 inhibitor, and may overcome PARP-1 resistance in killing tumor cells.

Abstract: Methods for treating tumors comprising cells expressing the vitamin D receptor are provided, and comprise inhibiting the expression or the biologic activity of the vitamin D receptor in the tumor cells, and/or inhibiting the expression or the biologic activity of a constituent of the vitamin D receptor signaling pathway in the tumor cells, and administering to the tumor cells an effective amount of gemcitabine.

Abstract: Systems and methods for diagnosing or characterizing a predisposition to colon cancer are provided. Cell nuclei may be evaluated for the presence or quantity of gamma-H2AX foci. Nucleic acids may be evaluated for the presence, type, or quantity of genomic instability or surrogates of dsDNA breaks such as ataxia telangiectasia mutated (ATM), Rad3-related protein (ATR), and Tumor suppressor p53-binding protein 1 (53BP1) in gamma-H2AX foci. Nucleic acids comprising a germline nucleic acid sequence of the ERCC6, WRN, TERT, and FAAP100 genes may be sequenced or probed to determine if the nucleic acid sequence includes one or more alterations that cause genomic instability, dsDNA breaks, or gamma-H2AX foci or otherwise predispose a subject to develop colon cancer.

Abstract: Systems and methods for diagnosing or characterizing a predisposition to colon cancer are provided. Cell nuclei may be evaluated for the presence or quantity of gamma-H2AX foci or their total gamma-H2AX levels. Nucleic acids may be evaluated for the presence, type, or quantity of genomic instability or surrogates of dsDNA breaks such as ataxia telangiectasia mutated (ATM), Rad3-related protein (ATR), and Tumor suppressor p53-binding protein 1 (53BP1) in gamma-H2AX foci. Nucleic acids comprising a germline nucleic acid sequence of the ERCC6, WRN, TERT, SHPRH, and FAAP100 genes may be sequenced or probed to determine if the nucleic acid sequence includes one or more alterations that cause genomic instability, dsDNA breaks, or gamma-H2AX foci or otherwise predispose a subject to develop colon cancer.

Abstract: Methods for treating tumors comprising cells expressing the vitamin D receptor are provided, and comprise inhibiting the expression or the biologic activity of the vitamin D receptor in the tumor cells, and/or inhibiting the expression or the biologic activity of a constituent of the vitamin D receptor signaling pathway in the tumor cells, and administering to the tumor cells an effective amount of gemcitabine.

Abstract: An isolated nucleic acid is provided which encodes a transiently-expressed kinetochore protein, CENP-F. Also provided are the purified polypeptide encoded by the nucleic acid sequence, and antibodies immunologically specific for the polypeptide. These biological molecules are useful as markers of cellular proliferation, particularly for the identification of cells in the G2 and M phases of the cell cycle. Methods are provided for using the nucleic acid, protein and antibodies for assessing cellular proliferation in biological fluids and tissue samples, and for detecting the presence of autoantibodies to the protein.