A method of treating cancer includes administering a dose of a chemotherapy agent in combination with a dose of a composition consisting essentially of attenuated Salmonella typhimurium. The dose of the chemotherapy agent is lower than a maximum effective dose of the chemotherapy agent. The combination provides a synergistic reduction in tumor burden when compared to the reduction in tumor burden provided by administration of an equivalent dose of the chemotherapy agent without the composition consisting essentially of attenuated Salmonella typhimurium.

The present invention relates to a brain tumor animal model that directly reflects the phenomenon in a human patient and a method of preparing the same, and more specifically, a brain tumor animal model that mutations are introduced into p53, Pten, and EGFR genes, a screening method of a therapeutic agent for a brain tumor using the animal model, and a preparing method thereof.

The ubiquitin ligase, RNF5, regulates the gut microbiota composition and influences the immune checkpoint response to tumors. RNF5 deficient animals exhibit significant inhibition of tumor development as well as an altered gut microbiota composition. Methods of treating cancer by administering to a subject one or more selected bacterial species and/or one or more prebiotics that promote the growth of one or more selected bacterial species are disclosed. Also disclosed are methods of treating cancer by administering to a subject one or more selected bacterial species and/or one or more prebiotics that promote the growth of one or more selected bacterial species in combination with one or more anti-cancer agents.

Methods and compositions capable of modulating activity of TLX (NR2E1), a nuclear receptor essential for neural stem cell self-renewal are provided. The modulation may comprise downregulating TLX expression and/or modulating TET3. In addition, methods of delivering shRNAs using dendrimer nanoparticles into glioblastoma stem cells are provided. The methods and compositions are useful for treating and preventing the progression of brain cancer, e.g., glioblastoma.

The present invention provides genetically modified non-human animals which are deficient in at least one or more types of CD3 genes selected from the group consisting of endogenous CD3ε, CD3δ, and CD3γ in its genome and functionally express at least one or more types of human CD3 genes selected from the group consisting of human CD3ε, CD3δ, and CD3γ. In the genetically modified non-human animals of the present invention, mature T cell differentiation and production can take place, and immunocompetent cells including T cells can exert their functions. The genetically modified non-human animals of the present invention enable efficient evaluation and screening in the development of therapeutic agents and therapeutic methods that use human CD3-mediated targeted drugs.

An objective of the present invention is to provide non-human animal models of cancer pathology, which mimic the hierarchical organization, cancer progression process, or biological property of human cancer tissues, and uses thereof. To achieve the objective described above, first, the present inventors transplanted cells of NOG-established cancer lines into NOG mice and morphologically observed the resulting tissue organization. As a result, the non-human animal models were demonstrated to exhibit pathologies (the hierarchical organization, cancer progression process, or biological properties of the cancer cells) similar to that of human cancer. Specifically, the present inventors succeeded in preparing non-human animal models exhibiting pathologies more similar to a human cancer, and cell culture systems using NOG-established cancer cell lines where the in vitro cell morphology is more similar to that of human cancer.

Compositions and methods of making isolated binding molecules (e.g. an antibodies) or antigen-binding fragment thereof useful as therapeutics for treating and/or preventing diseases associated with cells expressing claudin18.2, including tumor-related diseases such as gastric cancer, esophageal cancer, pancreatic cancer, lung cancer, ovarian cancer, colon cancer, hepatic cancer, head-neck cancer, and cancer of the gallbladder are described. Also, described are pharmaceutical formulations comprising the described compositions for the treatment of diseases either as single agent (e.g., naked antibodies) or as adjuvant therapy with other antigen-binding anticancer agents such as immune checkpoint inhibitors (e.g., anti-CTLA-4 and anti-PD-1/PD-L1 monoclonal antibodies), and/or by combination therapies where the anti-claudin18.2 antibodies are administered before, after, or concurrently with chemotherapy.

The present disclosure describes a method for the treatment of pancreatic cancer includes administering an effective amount of an MK2 inhibiting agent. In other aspects, the method may include administering the effective amount of the MK2 inhibiting agent in combination with a chemotherapy composition. In additional aspects, a composition for the treatment of pancreatic cancer is disclosed that includes an effective amount of an MK2 inhibiting agent and an effective amount of a chemotherapy composition.

The present invention includes compositions and methods for identification of membrane targets for enhancement of T cell activity against a disease, disorder or condition, and/or enhancing T cell anti-tumor activity in a subject in need thereof. In some embodiments, the disease is cancer. In further embodiments, the cancer is glioblastoma (GBM) or breast cancer.

Methods of treating castration-resistant and castration-sensitive prostate cancer using a compound having the following structure (I):

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or a pharmaceutically acceptable salt or zwitterionic form thereof, are provided.