Provided is a method for producing an animal model of osteoblastic bone metastasis. A non-human animal in which an osteoblastic lesion is formed in a wide range has been successfully produced with a probability of 100% by: administering a calcineurin inhibitor to a non-human animal; and injecting a tumor cell into an artery or a vein of the non-human animal, wherein the non-human animal and the tumor cell are in an allogeneic or xenogeneic relation.

The presently disclosed subject matter provides hydrogel precursor compositions (e.g., solutions) for forming three-dimensional hydrogels that support growth of physiologically relevant tissue when at least one cell is cultured in the three-dimensional hydrogel, kits comprising the hydrogel precursor composition, three-dimensional hydrogels, methods of forming the three-dimensional hydrogels, methods of growing the physiologically relevant tissue using the three-dimensional hydrogels, physiologically relevant tissue grown in the three-dimensional hydrogels, methods of producing hormone-responsive tissue (e.g., milk-producing mammary tissue and related methods of producing milk), methods of screening for candidate agents useful for modulating hormonal responses (e.g., modulating milk production), method of screening for candidate therapeutic agents using the physiologically relevant tissue grown in the three-dimensional hydrogels (e.g., personalized cancer treatments), and related methods of treatment (e.g., administering agents identified using the methods herein, transplanting physiologically relevant tissue produced using the methods, etc.).

Provided are expression vector constructs encoding IL-12 p35 and IL-12 p40 proteins where each protein or component thereof can be expressed utilizing appropriate promoters and/or translation modifiers. Also provided are methods of use for the expression vectors.

Animal models that are permissive for human polyomaviruses and their uses for the screening of candidate agents are described.

Provided herein is a model, in particular a mouse model, for assessing or evaluating toxicity to an immunotherapy, for example a therapeutic cell therapy, such as a cell therapy containing engineered cells, such as T cells, expressing a recombinant receptor, e.g. a chimeric antigen receptor (CAR). Also provided is a method for generating the mouse model. Also provided herein are methods of use for the mouse models of toxicity, such as to evaluate modified or alternative immunotherapies, and/or to evaluate test agents, including agents to assess as potential interventions to reduce, prevent, or ameliorate toxicity to immunotherapy in human subjects and/or for use in combination with an immunotherapy, e.g. CAR−T cell therapy.

An object of the present invention is to provide a method of treating thoracic cancer using a checkpoint inhibitor in combination with Ad-REIC/Dkk-3. The present invention is a pharmaceutical composition for treating thoracic cancer comprising REIC/Dkk-3 in combination with a check point inhibitor and a method for treating thoracic cancer by administering Ad-REIC/Dkk-3 and a check point inhibitor to a thoracic cancer patient.

The present disclosure relates to a DNA construct, and a strain into which a recombinant vector comprising the DNA construct has been introduced. The DNA construct according to the present disclosure allows the expression levels of genes, operably linked downstream of first and second promoters, in a host strain or cell, to be balanced, so that cancer diagnosis and treatment may be performed simultaneously. In addition, the DNA construct of the present disclosure completely does not allow the anticancer protein and the reporter protein to be expressed at all in the absence of doxycycline, and thus it allows the anticancer protein to be expressed at an appropriate dose for cancer treatment by controlling whether or not treatment with doxycycline is performed, and at the same time, enables the size of the cancer to be monitored in real time depending on the expression level of the reporter protein.

Provided herein are compositions and methods for studying cancer therapeutics and etiology, for example, mouse cancer models, cancer cell lines, and uses thereof. Human p53 knock-in (Hupki) mice with a Y220 (e.g., Y220C, Y220H, or Y220S) mutation in p53 are provided. These Hupki-Y220 mice can be used, for example, to examine tumorigenesis in different tissues, investigate mechanisms of gain of function, develop mouse models of cancer, generate cancer cell lines that can be implanted into recipient mice, and test potential therapeutics.

There is disclosed patient derived xenograft (PDXs) cells/systems/models and/or derivatives, parental (unlabelled) and/or labelled, expressing a fluorescent protein or a luciferase, or a combination thereof; for evaluating therapies comprising nasopharyngeal carcinoma (EBV positive and/or EBV negative). In another embodiment, there is disclosed a method of evaluating the efficacy of an agent used to treat nasopharyngeal carcinoma (NPC) comprising: preparing a non-human model; whereby the non-human model carries cells from NPC xenograft; labelling the cells from the NPC xenograft with gfp-luc2 marker using a lentiviral vector system; and growing the cells in short term in vitro culture; including adaptation of said culture into multi-well plates for use in further screening and/or evaluation assays; wherein the NPC xenograft is PDX.

The current disclosure provides methods and compositions useful in preparing transformed and immortalized zebra and quagga mussel cells that function as disseminated neoplastic (DN) cells, as well as the cells produced thereby. Also provided are methods for using such mussel DNCs in cell culture, in vitro, and within live mussels in the lab or in the wild, to control mussel populations such as invasive zebra mussel or quagga mussel populations.