58 results about "Therapy resistant" patented technology

The present invention provides novel methods and kits for diagnosing the presence of cancer within a patient, and for determining whether a subject who has cancer is susceptible to different types of treatment regimens. The cancers to be tested include, but are not limited to, prostate, breast, lung, gastric, ovarian, bladder, lymphoma, mesothelioma, medulloblastoma, glioma, and AML. Identification of therapy-resistant patients early in their treatment regimen can lead to a change in therapy in order to achieve a more successful outcome. One embodiment of the present invention is directed to a method for diagnosing cancer or predicting cancer-therapy outcome by detecting the expression levels of multiple markers in the same cell at the same time, and scoring their expression as being above a certain threshold, wherein the markers are from a particular pathway related to cancer, with the score being indicative or a cancer diagnosis or a prognosis for cancer-therapy failure. This method can be used to diagnose cancer or predict cancer-therapy outcomes for a variety of cancers. The markers can come from any pathway involved in the regulation of cancer, including specifically the PcG pathway and the “stemness” pathway. The markers can be mRNA, microRNA, DNA, or protein.

Disclosed are methods of using proteasome inhibitors (PI) in combinations with other pharmaceutically active agents for treating viral hepatitis infections, for example, for treating therapy-resistant and -refractory viral hepatitis infections. Also disclosed are pharmaceutical compositions and kits of pharmaceutical compositions which can be used for treating viral hepatitis infections, for example, for treating therapy-resistant and refractory viral hepatitis infections.

The present invention relates to immunotherapy methods for treating hyperproliferative disease in humans, particularly to hyperproliferative disease that is refractory to therapy. More specifically, the invention is directed, in one embodiment, to methods for treating a subject with a hyperproliferative disease in which the expression of a self gene is upregulated in therapy-resistant hyperproliferative cells. In another embodiment, an adenoviral expression construct comprising a self gene under the control of a promoter operable in eukaryotic cells is administered to the therapy-resistant hyperproliferative cells. The present invention thus provides immunotherapies for treating therapy-resistant hyperproliferative disease by attenuating the natural immune system's CTL response against hyperproliferative cells or overexpressing mutant p53 antigens, for example.

The present application demonstrates that Salinosporamide A can be used to sensitize cancer cells to cancer therapy. Furthermore, the present application demonstrates that Salinosporamide A acts as a therapeutic agent to kill or inhibit cancer cells after sensitization of the cells by an antibody or other chemosensitizing reagents. The cancer cells can be either therapy-sensitive or therapy resistant. The present application further demonstrates that Salinosporamide A induces the expression of Raf kinase inhibitor protein (RKIP) and PTEN, tumor suppressor proteins, and inhibits the expression of YY1, a transcriptional regulator protein overexpressed in cancer cells and also inhibits the growth factor pleiotrophin (PTN).

The present invention provides novel methods and kits for diagnosing the presence of cancer within a patient, and for determining whether a subject who has cancer is susceptible to different types of treatment regimens. The cancers to be tested include, but are not limited to, prostate, breast, lung, gastric, ovarian, bladder, lymphoma, mesothelioma, medullablastoma, glioma, and AML. Identification of therapy-resistant patients early in their treatment regimen can lead to a change in therapy in order to achieve a more successful outcome. One embodiment of the present invention is directed to a method for diagnosing cancer or predicting cancer-therapy outcome by detecting the expression levels of multiple markers in the same cell at the same time, and scoring their expression as being above a certain threshold, wherein the markers are from a particular pathway related to cancer, with the score being indicative or a cancer diagnosis or a prognosis for cancer-therapy failure. This method can be used to diagnose cancer or predict cancer-therapy outcomes for a variety of cancers. The markers can come from any pathway involved in the regulation of cancer, including specifically the PcG pathway and the “stemness” pathway. The markers can be mRNA, microRNA, DNA, or protein.

The present invention is directed to the administration of an HSV derived oncolytic virus and a PI3K/AKT/mTOR pathway inhibitor to treat various types of resistant tumors. Therapy-resistant tumor formation is one of the main causes for treatment failure in the clinic. The treatment methods and compositions disclosed herein sensitize resistant tumors to the treatment of herpes simplex virus (HSV)-based oncolytic virotherapy. Pre or co-treatment of resistant tumor cells with the mTOR inhibitor, rapamycin, or certain PI3K inhibitors, such as LY294002, can efficiently sensitize the tumors to HSV derived oncolytic viruses, whereby the replication and spread of the viruses are dramatically enhanced.

The present disclosure is directed to a composition for the sustained-release delivery of an active agent to a target cell of an individual. The compositions disclosed herein comprise of at least one porous particle; at least one polymer; and at least one active agent. In an embodiment, the porous particle comprises a plurality of microscale reservoirs. In an exemplary embodiment, the at least one active agent is covalently linked to the at least one polymer to form a polymer-active agent conjugate, and the polymer-active agent conjugate is contained in the plurality of microscale reservoirs of the porous particle. The present disclosure is also directed to a method of treating a tumor, comprising the step of administering to an individual the composition described supra. Additionally, disclosed herein is a method of eliminating tumor stem cells. Furthermore, there is provided a method of circumventing multi-drug resistance in a tumor cell.

The subject invention pertains to materials and methods for treating oncological disorders. The subject invention also pertains to materials and methods for preventing or reducing the development by cancer cells of resistance to an anticancer therapy, such as chemotherapy, radiotherapy and/or immunotherapy. In one embodiment, a patient is treated with an agent that inhibits cholesterol synthesis or that prevents or reduces the increase in cholesterol synthesis observed in therapy-resistant cancer cells. In another embodiment, a patient is treated with an agent that increases the expression, activity, or amount of a Bim protein in a cell. In another embodiment, a patient is treated with an agent to inhibit or reduce cancer cell adhesion to extracellular matrices or stromal cells. In another embodiment, a patient is treated with an agent to inhibit expression of a gene of function of a protein of the FANC/BRCA pathway. In a further embodiment, a patient is treated with an agent to prevent or reduce the DNA crosslink repair function of a cell.

The invention discloses enterococcus faecalis phage lyase and a coding gene and application thereof. The enterococcus faecalis phage lyase is a protein of the following (a) or (b): (a) protein composed by an amino acid sequence as shown in a sequence 1 of a sequence table; (b) protein which is derived by the sequence 1, has a function of cracking enterococcus faecalis, and is made by the fact that the amino acid sequence as shown in the sequence 1 is subjected to the replacement and/or deletion and/or addition of one or a few of amino acid residue(s). Experiments prove that the lyase protein can crack a variety of kinds of enterococcus faecalis and can be closely combined with the specificity of sensitive bacteria. In addition, animal experiments prove that the lyase has a better treatment effect on the infection caused by enterococcus faecalis, and timely and effective dosage after infection has a certain meaning for reducing the mortality of mice. According to the invention, a foundation for antibiotic replacement therapy resistant to enterococcus faecalis is laid.

In one embodiment, the invention provides a method of treating a subject suffering from a breast cancer tumor which is non-responsive or intrinsically resistant to anti-estrogen therapy comprising administering a therapeutically effective amount of an inhibitor of alternative (ALT) non-homologous end joining (NHEJ) factor to the subject.

In another embodiment the invention provides a method of treating a subject who suffers from a pancreatic cancer which is non-responsive to chemotherapy and/or radiation comprising co-administering a therapeutically effective amount of PARP1 inhibitor and a DNA ligase IIIα inhibitor to the subject. Related diagnostic methods, nucleic acid arrays, devices and kits are also provided.

The invention discloses a novel brain glioma molecular typing method which comprises the following steps: step 1, collecting data, acquiring gene expression profiles and clinical information data from a database, and collecting four independent immunotherapy queues from a public database, including (1) Roh queues: an anti-CTLA4 treatment queue and an anti-PD1 treatment queue; (2) GSE100797: an adoptive T cell treatment queue; and (3) GSE78220: an anti-PD1 treatment queue. the GRI values are obtained through a large amount of data, brain glioma molecules of different patients can be divided, the accuracy of brain glioma molecule division is improved, doctors can be assisted in conducting different types of division on the patients conveniently, scientific treatment is conducted on the patients through different treatment modes, the treatment rehabilitation rate of the patients is increased, and the treatment cost of the patients is reduced. The problem that the traditional brain glioma molecular typing accuracy is low is solved.

The invention belongs to the field of hepatitis B prevention and treatment, and in particular relates to a hepatocyte nuclear factor 4a specificity short hairpin RNA with an inhibition effect for hepatitis B virus replication and applications thereof. The technical problem to be solved by the invention is to provide a novel effective choice for HBV resistant treatment. The technical scheme of the technical problem solved by the invention is to provide a specificity short hairpin RNA aiming at the hepatocyte nuclear factor 4a and a carrier capable of expressing the sequence. The shRNA sequence and the expression carrier thereof provided by the invention are testified to be able to inhibit internal HBV transcription and copy effectively and have no obvious side effects, and provide a novel effective choice for HBV resistance, and have favorable application prospects in preparing HBV-resistant medicaments.

The present invention provides, for the first time, the finding that organic cation transporters (OCTs) are major determinants of the anticancer activity of platinum-based drugs such as oxaliplatin, and therefore have clinical significance for selecting oxaliplatin as the preferred therapy for a cancer that expresses one or more OCTs, such as colorectal cancer or liver cancer. In addition, the OCT genotype can also be used to predict oxaliplatin response or to select therapy. The present invention also provides methods of treating or inhibiting cancers that expresses one or more OCTs by administering a therapeutically effective amount of a platinum-based drug such as an oxaliplatin analog having an organic non-leaving group with an increased size. The present invention further provides methods of sensitizing a therapy resistant cancer to a platinum-based drug such as oxaliplatin by administering a therapeutically effective amount of a nucleic acid encoding an OCT. Compositions, kits, and integrated systems for carrying out the diagnostic, prognostic, and therapeutic methods of the present invention are also provided.

The invention provides a curative effect prediction method, system and device for breast cancer liver metastasis anti-HER-2 treatment and a medium, and belongs to the technical field of medicine. The method comprises the following steps: acquiring a to-be-recognized abdomen enhanced CT image of a subject, namely an anti-HER-2 treated breast cancer liver metastasis patient; and inputting a to-be-identified abdomen-enhanced CT image to the curative effect prediction model, and performing quantitative analysis operation on the to-be-identified abdomen-enhanced CT image by the curative effect prediction model to obtain a curative effect prediction result of the breast cancer liver metastasis anti-HER-2 treatment of the subject. According to the method, the value of the radiomics characteristics based on the abdominal enhanced CT in predicting the anti-HER-2 treatment effect of the BCLM is researched for the first time, so that reference information and related clinical guidance opinions are provided for predicting the anti-HER-2 treatment effect of an HER-2 positive BCLM patient and a total treatment scheme.

The present invention relates to the treatment of therapy-resistant neoplasias. The compounds and methods of the invention are particularly useful for the treatment of taxol-resistant human cancers, particularly cervical and breast cancer. Components of the compositions of the present invention show strong synergy with one another allowing them to be used in relatively low amounts for the treatment of stage IV or recurrent cancer which may have grown resistant to the traditional chemotherapeutic agents. These compositions comprise oridonin.

The present invention provides MEL-18, which is a biomarker for human epidermal growth factor receptor2 (HER2)-positive cancer and anti-HER2 therapy, and a use thereof. According to the present invention, MEL-18 is a prognostic factor or predictor for a response of subjects to an anti-HER2-targeted drug in HER2-POSITIVE cancer and may be used in companion diagnostics for HER2-targeted drugs in subjects with HER2-positive cancer. Therefore, HER2-positive cancer may be more effectively treated by overcoming resistance to HER2 therapeutic agents and enhancing therapeutic efficacy by determining whether ADAM10/17 inhibitors are administered or co-administered with HER2-targeted drugs.

The present disclosure provide for methods of using 6-thio-2′-deoxyguanosine (6-thio-dG) to treat telomerase-positive cancers that exhibit (a) one or more TERT promoter mutations, and/or (b) enriched telomere transcriptional signature(s). In particular, melanomas, including those who are not sensitive or have become resistant to immune checkpoint inhibition and/or MAPKi therapy are targets for this therapy.