Abstract: The present disclosure relates to combination therapies containing one or more PARP inhibitors and one or more angiogenesis inhibitor. Also described herein are therapeutic uses of such combination therapies for treating various disorders and conditions. The combination therapies and uses thereof can be useful for preventing tumor cell growth, preventing tumor metastasis, inducing an immune response or enhancing an immune response.

Abstract: A series of bone remodeling regulatory peptides and application thereof are disclosed. Through sequence alignment, structure analysis, physical and chemical properties and function prediction, a series of bone remodeling regulatory peptides are designed and synthesized by solid-phase peptide synthesis method: Core peptide sequence: Gly-Xaa-Pro-Gly-Xaa-Xaa-Gly-Xaa-Xaa, A1-1: Gly-Ala-Pro-Gly-Pro-Gln-Gly-Phe-Gln, A1-2-1: Gly-Ala-Pro-Gly-Ala-Pro-Gly-Ser-Gln, A1-4-1: Gly-Pro-Pro-Gly-Pro-Ala-Gly-Phe-Ala, A1-5-3: Gly-Pro-Pro-Gly-Ala-Thr-Gly-Phe-Pro, and OSCpep: Gly-Ala-Pro-Gly-Pro-Ala-Gly-Phe-Ala. These peptides have the features of short length, simple synthesis, low cost, low cytotoxicity, high biological stability, moderate half-life, good bone targeting. They can regulate the differentiation and function of osteoclasts and osteoblasts by adjusting the concentration, thereby achieving the orderly regulation of bone resorption and bone formation, and have wide potential application prospects.

Abstract: The present invention provides methods of treatment of cancer patients having deficiency in at least one non-BRCA1/2 gene involved in the homologous recombination repair (HRR) pathway with a poly(ADP-ribose) polymerase (PARP) inhibitor such as niraparib. In particular, cancer patients having a deficiency in at least one gene selected from the group consisting of BRCA1, BRCA2, ATM, ATR, BAP1, BARD1, BLM, BRIP1, MRE11A, NBN, PALB2, RAD51, RAD51B, RAD51C, RAD51D, RAD52, RAD54L, XRCC2, TP53, or RBI can benefit from treatment with niraparib.

Abstract: The present disclosure relates to combination therapies containing one or more PARP inhibitors and one or more angiogenesis inhibitor. Also described herein are therapeutic uses of such combination therapies for treating various disorders and conditions. The combination therapies and uses thereof can be useful for preventing tumor cell growth, preventing tumor metastasis, inducing an immune response or enhancing an immune response.

Abstract: A polypropylene composition, a preparation method thereof, and a film or a sheet prepared from the polypropylene composition and use thereof. The composition includes 45 parts to 75 parts of a polypropylene, 10 parts to 35 parts of an elastomer, 5 parts to 20 parts of a polyethylene, 0.1 parts to 0.5 parts of an antioxidant, and 0.1 parts to 0.5 parts of a lubricant. A half peak width of a crystallization peak of the polypropylene is 5° C. to 10° C., and a peak temperature of the crystallization peak of the polypropylene is 105° C. to 115° C. The polypropylene composition has a good tenacity, especially a?30° C. low-temperature impact performance. The film or the sheet prepared from the composition and applied to automotive interior parts, can enable the external accessories not only to be less likely to generate sharp fragments while being strongly impacted, but also to have a matte characteristic.

Abstract: A polypropylene composition, a preparation method thereof, and a film or a sheet prepared from the polypropylene composition and use thereof. The composition includes 45 parts to 75 parts of a polypropylene, 10 parts to 35 parts of an elastomer, 5 parts to 20 parts of a polyethylene, 0.1 parts to 0.5 parts of an antioxidant, and 0.1 parts to 0.5 parts of a lubricant. A half peak width of a crystallization peak of the polypropylene is 5° C. to 10° C., and a peak temperature of the crystallization peak of the polypropylene is 105° C. to 115° C. The polypropylene composition has a good tenacity, especially a ?30° C. low-temperature impact performance. The film or the sheet prepared from the composition and applied to automotive interior parts, can enable the external accessories not only to be less likely to generate sharp fragments while being strongly impacted, to guarantee the safety of people, but also to have a matte characteristic.

Abstract: Methods of administering immunoconjugates that bind to FOLR1 are provided. The methods comprise administering an anti-FOLR1 immunoconjugate to a person in need thereof, for example, a cancer patient, at a therapeutically effective dosing regimen that results in minimal adverse effects.

Abstract: Chimeric nonhuman mammals useful as inducible spontaneous cancer models are disclosed. The nonhuman mammals are obtained by introducing one or more genetically modified embryonic stem (ES) cells into an early stage embryo, and then implanting the manipulated embryo into a surrogate mother. The ES cells contain a recombinant oncogene, and also may contain a genetic mutation that deletes or inactivates a tumor suppressor gene. Models of different types of cancer are produced by introducing different combinations of genetic mutations into the ES cells that are introduced into the early stage embryo.

Abstract: A method of producing a tumorigenic mouse cell, the tumorigenicity of which depends on a recombinant gene of interest is disclosed. The method involves: (a) providing a conditionally tumorigenic mouse cell containing a recombinant oncogene operably linked to an inducible promoter, wherein (i) expression of the recombinant oncogene is necessary and sufficient for the tumorigenicity of the tumorigenic mouse cell, and (ii) the inducible promoter is in the uninduced state; and (b) introducing into the cell a recombinant gene of interest that functionally complements the oncogene, thereby restoring tumorigenicity without expression of the inducible recombinant oncogene. Also disclosed is a method of testing a compound for anti-tumor effects.

Abstract: The invention provides an improved directed complementation method for generating a conditionally tumorigenic mouse cell. In a directed complementation method, the tumorigenicity of a conditionally tumorigenic mouse cell depends on either the expression of an inducible recombinant oncogene or the expression of a recombinant gene of interest that functionally complements an uninduced recombinant oncogene. The invention provides a method of producing a tumorigenic mouse cell containing an uninduced oncogene, a recombinant gene of interest that functionally complements the uninduced oncogene, and a Cre-ER system capable of excising the recombinant gene of interest. When the Cre-ER system is activated, the recombinant gene of interest is excised. From the effect on the mouse cell it is possible to determine whether the recombinant gene of interest is a tumor maintenance gene.

Abstract: Chimeric nonhuman mammals useful as inducible spontaneous cancer models are disclosed. The nonhuman mammals are obtained by introducing one or more genetically modified embryonic stem (ES) cells into an early stage embryo, and then implanting the manipulated embryo into a surrogate mother. The ES cells contain a recombinant oncogene, and also may contain a genetic mutation that deletes or inactivates a tumor suppressor gene. Models of different types of cancer are produced by introducing different combinations of genetic mutations into the ES cells that are introduced into the early stage embryo.

Abstract: A method of producing a tumorigenic mouse cell, the tumorigenicity of which depends on a recombinant gene of interest is disclosed. The method involves: (a) providing a conditionally tumorigenic mouse cell containing a recombinant oncogene operably linked to an inducible promoter, wherein (i) expression of the recombinant oncogene is necessary and sufficient for the tumorigenicity of the tumorigenic mouse cell, and (ii) the inducible promoter is in the uninduced state; and (b) introducing into the cell a recombinant gene of interest that functionally complements the oncogene, thereby restoring tumorigenicity without expression of the inducible recombinant oncogene. Also disclosed is a method of testing a compound for anti-tumor effects.