Santa Clara, CA, United States
Santa Clara, CA, United States
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Patent
Crown Bioscience | Date: 2017-02-08

The present disclosure provides methods of detecting a fusion gene of HNF4G and RSPO2 in a nucleic acid-containing sample, and a primer set, a probe set and a kit for detecting the fusion gene are also provided. Animal models for a human disease positive for the fusion gene are also provided herein. In addition, the present disclosure relates to the methods for assessing and identifying an agent effective on the fusion gene of HNF4G and RSPO2 or a human disease positive for a fusion gene of HNF4G and RSPO2 and thereby treating said disease are also provided.


Patent
Crown Bioscience | Date: 2017-02-08

The present invention provides a method for predicting the responsiveness of a cancer cell to an MEK inhibitor, comprising detecting the presence of at least one mutation in one or more genes selected from the group consisting of ADAM12, COL14A1, TNN and TP53, in the cancer cell. The present invention also provides a method for predicting the responsiveness of a cancer cell to an ERK inhibitor, comprising detecting the presence of at least one mutation in one or more genes selected from the group consisting of ADAM12, PEX5L, TNN and TP53, in the cancer cell.


Patent
Crown Bioscience | Date: 2015-04-03

A method for predicting the responsiveness of a cancer cell to an MEK inhibitor, comprising detecting the presence of at least one mutation in one or more genes selected from the group consisting of ADAM12, COL14A1, TNN, and TP53, in the cancer cell, by contacting a nucleic acid sample derived from the cancer cell with at least one oligonucleotide which allows specific detection of the mutation; wherein presence of mutation in ADAM12, COL14A1, TNN, TP53 and/or any combination thereof is indicative of decreased responsiveness of the cancer cell to the ERK inhibitor.


The present invention relates to methods for treating gastric neoplasias, in particular treating patients who have been previously determined to have an EGFR biomarker. Gastric carcinoma (GC) is one of the most common and deadest cancers with 1 million diagnoses and 0.7 million deaths each year worldwide, with high incidence in Eastern Asia.


The present invention provides an immuno-deficient animal useful as an animal model for a human disease associated with a first mutation of a target gene, wherein the animal comprises (a) a first human xenograft comprising the target gene comprising the first mutation; (b) a second human xenograft comprising the target gene but lacking the first mutation, wherein the first human xenograft and second human xenograft are isogenic. Also provided here are methods of producing the animal model and methods of using such animal model.


Patent
Crown Bioscience | Date: 2015-04-06

The present disclosure provides an immuno-deficient animal useful as an animal model for a human disease, wherein the animal comprises: (a) functional human immune cells; and (b) a human xenograft comprising a pathogenic human cell or tissue, wherein the human immune cells and the human xenograft meet at least one of the following criteria: i) the human xenograft expresses a threshold level of a therapeutic target for the human disease; ii) the human immune cells match with the human xenograft for at least one human leukocyte antigen (HLA) marker; and iii) the human xenograft cells expresses a desired level of the matched HLA marker. Also provides is a method of producing the animal model and use of the animal models.


The present teachings relate to methods of screening for a therapeutic agent, selecting a treatment and monitoring a treatment for a human disease or infection and methods for producing a mouse model for human disease or infection wherein the mouse has a functioning human immune system. The method includes administering a test substance to an immunocompromised NOD/SCID mouse with a reconstituted human immune system and is also engrafted with a substance containing a diseased or infectious cell derived from a human diseased or infected patient and a step of assessing improvement in the disease or infection of the mouse and/or to monitor a side effect of the test substance.


The present teachings relate to methods of screening for a therapeutic agent for human acute myelogenous leukemia (AML) and methods for treating AML. The method includes administering a test substance to an immunocompromised NOD/SCID mouse engrafted with a substance containing a leukemic cell derived from a human AML patient and a step of assessing improvement in leukemia in the mouse and/or to monitor a side effect of the test substance. The method can further include monitoring a side effect of the test substance in the mouse.


The present invention provides a method for using non-human animals to mimick human clinical trial comprising: (a) obtaining cells or tissues from n human subjects suffered from a disease, wherein n>1; (b) establishing a control group and a treatment group, wherein i) the control group comprises i control non-human animals, wherein in, wherein cells or tissue from each human subject are grafted to at least one control non-human animal; ii) the treatment group comprises j treatment non-human animals, wherein jn, wherein cells or tissue from each human subject are grafted to at least one treatment non-human animal; and iii) each control non-human animal or treatment non-human animal is grafted with cells or tissues from one human subject; (c) administering a first agent to the control group and administering a second agent to the treatment group, wherein the first agent is different from the second agent; (d) obtaining the end point of the control group and the treatment group; and (e) comparing the end point of the control group to the end point of the treatment group.


Gene expression signature predictive of cancer patient response to multi-kinase inhibitor is disclosed. Also disclosed are methods predicting the efficacy of the multi-kinase inhibitor for treating cancer in a patient. Also disclosed are methods for distinguishing responders from non-responders to a multi-kinase inhibitor in treating cancer. Also disclosed are methods for treating a cancer patient with a multi-kinase inhibitor.

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