108 results about "Immunodeficient Mouse" patented technology

A small percentage of cells within an established solid tumor have the properties of stem cells. These solid tumor stem cells give rise both to more tumor stem cells and to the majority of cells in the tumor that have lost the capacity for extensive proliferation and the ability to give rise to new tumors. Thus, solid tumor heterogeneity reflects the presence of tumor cell progeny arising from a solid tumor stem cell. We have developed a xenograft model in which we have been able to establish tumors from primary tumors via injection of tumor cells in the mammary gland of severely immunodeficient mice. These xenograft assay have allowed us to do biological and molecular assays to characterize clonogenic solid tumor stem cells. We have also developed evidence that strongly implicates the Notch pathway, especially Notch 4, as playing a central pathway in carcinogenesis.

The present invention provides an immunodeficient mouse (NOG mouse) suitable for engraftment, differentiation and proliferation of heterologous cells, and a method of producing such a mouse. This mouse is obtained by backcrossing a C.B-17-scid mouse with an NOD / Shi mouse, and further backcrossing an interleukin 2-receptor γ-chain gene-knockout mouse with the thus backcrossed mouse. It is usable for producing a human antibody and establishing a stem cell assay system, a tumor model and a virus-infection model.

A small percentage of cells within an established solid tumor have the properties of stem cells. These solid tumor stem cells give rise to both more tumor stem cells and to the majority of cells in the tumor that have lost the capacity for extensive proliferation and the ability to give rise to new tumors. Thus, solid tumor heterogeneity reflects the presence of tumor cell progeny arising from a solid tumor stem cell.We have developed a xenograft model in which we have been able to establish tumors from primary tumors via injection of tumors in the mammary gland of severely immunodeficient mice. These xenograft assay have allowed us to do biological and molecular assays to characterize clonogenic solid tumor stem cells.We have also developed evidence that strongly implicates the Notch pathway, especially Notch 4, as playing a central pathway in carcinogenesis.

A small percentage of cells within an established solid tumor have the properties of stem cells. These solid tumor stem cells give rise both to more tumor stem cells and to the majority of cells in the tumor that have lost the capacity for extensive proliferation and the ability to give rise to new tumors. Thus, solid tumor heterogeneity reflects the presence of tumor cell progeny arising from a solid tumor stem cell.We have developed a xenograft model in which we have been able to establish tumors from primary tumors via injection of tumors in the mammary gland of severely immunodeficient mice. These xenograft assay have allowed us to do biological and molecular assays to characterize clonogenic solid tumor stem cells.We have also developed evidence that strongly implicates the Notch pathway, especially Notch 4, as playing a central pathway in carcinogenesis.

The present invention provides an immunodeficient mouse (NOG mouse) suitable for engraftment, differentiation and proliferation of heterologous cells, and a method of producing such a mouse. This mouse is obtained by backcrossing a C.B-17-scid mouse with an NOD / Shi mouse, and further backcrossing an interleukin 2-receptor γ-chain gene-knockout mouse with the thus backcrossed mouse. It is usable for producing a human antibody and establishing a stem cell assay system, a tumor model and a virus-infection model.

Described herein is a method of expanding human hepatocytes in vivo using an immunodeficient mouse which is further deficient in fumarylacetoacetate hydrolase (Fah). The method comprises transplanting human hepatocytes into the immunodeficient and Fan-deficient mice, administering an IL-IR antagonist to the mouse and allowing the hepatocytes to expand. Alternatively, the method includes transplanting human hepatocytes into the immunodeficient and Fah-deficient mice, wherein the mouse is further deficient for IL-IR and allowing the hepatocytes to expand. The method also allows serial transplantation of the human hepatocytes into secondary, tertiary, quaternary or additional mice.

The invention belongs to technical field of animal genetic engineering, and specifically relates to immunodeficient mice, a manufacturing method thereof and applications. The manufacturing method comprises using NOD-Scid IL2rg- / - immunodeficient mice (NSI mice), and deleting Foxnl gene or Fah gene. Through deleting the Fah gene on the NSI mice, NSIF mice are obtained. The NSIF mice can be used to efficiently establish a novel humanized mouse model, used for liver physiological and pathological research. Through deleting the Foxnl gene on the NSI mice, the NSIF mice are obtained. The NSIF mice have no body hair, and immune system is further defected. The NSIF mice provide convenience for establishment, monitoring, and measurement of solid tumor.

Targeting metabolic enzymes in human cancer Abstract Lung cancer is a devastating disease and a major therapeutic burden with poor prognosis. The functional heterogeneity of lung cancer (different tumor formation ability in bulk of tumor) is highly related with clinical chemoresistance and relapse. Here we find that, glycine dehydrogenase (GLDC), one of the metabolic enzyme involved in glycine metabolism, is overexpressed in various subtypes of human lung cancer and possibly several other types of cancers. GLDC was found to be highly expressed in tumor-initiating subpopulation of human lung cancer cells compared with non-tumorigenic subpopulation. By array studies we showed that normal lung cells express low levels of GLDC compared to xenograft and primary tumor. Functional studies showed that RNAi inhibition of GLDC inhibits significantly the clonal growth of tumor-initiating cells in vitro and tumor formation in immunodeficient mice. Overexpression of GLDC in non-tumorigenic subpopulation convert the cells to become tumorigenic. Furthermore, over-expression of GLDC in NIH / 3T3 cells and human primary lung fibroblasts can transform these cells, displaying anchorage-independent growth in soft agar and tumor-forming in mice. Not only is GLDC is expressed human lung cancer, it is also up-regulated in other types of cancer, such as colon cancer. RNAi knockdown of GLDC in colon cancer cell line, CACO-2 cells, can also inhibit the tumor formation in mice. Thus GLDC maybe a new metabolic target for treatment of lung cancer, and other cancers.

The invention discloses a human NF2- / - vestibular schwannoma Schwann cell line and an establishment method thereof. The establishment method includes: A, separating Schwan cells in tumors to obtain human NF2- / - primary Schwann cells (human NF2- / - Schwann cells), and carrying out primary culture; B, establishing immunodeficient mouse sciatic nerve human NF2- / - primary Schwann cell transplanted tumor model; C, collecting transplanted tumors greater than 1 cm in diameter from mouse sciatic nerves by screening; D, separating Schwann cells, and carrying out primary cell culture; E, carrying out five successive generations and more of passage culture; F, performing screening to obtain NF2- / - vestibular Schwann cells which are consistent to human NF2- / - primary Schwann cells and transplanted tumor primary cell strains in cellular form and main biological characteristic and which are capable of infinite passage. The NF2- / - vestibular schwannoma Schwann cell line herein has the success rate of95% and above to grow transplanted tumors.

The present invention provides embryonic stem cells obtainable from an embryo of an immunodeficient mouse which is deficient in both Rag2 and Jak3 genes by culture in the presence of a GSK3 inhibitor and an MEK inhibitor, as well as a transgenic mouse, which is created with the use of these embryonic stem cells.

The invention discloses feed applied to immunodeficient mice. The feed is prepared from the following components in parts by mass: 10-20 parts of wheat middlings, 2-10 parts of bran, 35-45 parts of expended maize, 17-25 parts of soybean meal, 5-11 parts of fish meal, 1-4 parts of maize protein powder, 0.5-1.5 parts of beer yeast, 1-4 parts of vegetable oil, 0.3-0.6 part of choline chloride, 0.1-0.5 part of methionine, 0.1-0.5 part of lysine, 3-5 parts of mineral salt premix and 0.1-0.2 part of vitamin premix. Through frequent adjustment of the formula and the process, a formula and a preparation process of the feed which is balanced in nutrition and high in palatability, and is applicable to the immunodeficient mice are determined; through the optimization of the raw materials and the adoption of the special ratio and the production process, complex feed capable of meeting requirements on growth, gestation and lactation of the immunodeficient mice is provided.

A small percentage of cells within an established solid tumor have the properties of stem cells. These solid tumor stem cells give rise both to more tumor stem cells and to the majority of cells in the tumor that have lost the capacity for extensive proliferation and the ability to give rise to new tumors. Thus, solid tumor heterogeneity reflects the presence of tumor cell progeny arising from a solid tumor stem cell. We have developed a xenograft model in which we have been able to establish tumors from primary tumors via injection of tumor cells in the mammary gland of severely immunodeficient mice. These xenograft assay have allowed us to do biological and molecular assays to characterize clonogenic solid tumor stem cells. We have also developed evidence that strongly implicates the Notch pathway, especially Notch 4, as playing a central pathway in carcinogenesis.

The invention provides a construction method and application of a synovial sarcoma heterogenous transplanting mouse model. The method comprises the steps of firstly, collecting a synovial sarcoma patient tumor tissue block, and performing heterogenous in-situ transplanting of the fresh patient tumor tissue block into an immune deficiency mouse body under the sterile condition, wherein heterogenousin-situ planting includes the steps of selecting a 2-6-week old immune deficiency mouse, the mouse is consistent with the patient in gender, the collected fresh patient tumor tissue block is soaked with a sterile incubation solution containing fetal calf serum, the mouse is fixed after anesthesia, the patient tumor tissue block is planted into the joint capsule of the mouse, an incision is sewn,and the mouse is bred so that a tumor in the joint capsule can grow. Compared with subcutaneous modeling, the in-situ modeling condition is more real, the screened medicine scheme can be better used for the patient, and on the basis of the in-situ modeling theory, tumor metastasis is more likely to happen compared with subcutaneous modeling.