91 results about "Chemotherapy resistant" patented technology

Oligonucleotide microarrays were used to profile and compare gene expression patterns between uterine serous papillary carcinoma and ovarian serous papillary carcinoma or normal endometrial epithelial cells. mRNA fingerprints readily distinguish the more biologically aggressive and chemotherapy resistant USPC from OSPC or NEC. Plasminogen activator inhibitor is the most highly up-regulated gene in OSPC relative to USPC, whereas the c-erbB2 gene product (HER-2/neu) is strikingly overexpressed in USPC relative to OSPC and may therefore represent a novel diagnostic and therapeutic marker for this highly aggressive subset of endometrial tumors.

Gene expression profiling and hierarchial clustering analysis readily distinguish normal ovarian epithelial cells from primary ovarian serous papillary carcinomas. Laminin, tumor-associated calcium signal transducer 1 and 2 (TROP-1/Ep-CAM; TROP-2), claudin 3, claudin 4, ladinin 1, S100A2, SERPIN2 (PAI-2), CD24, lipocalin 2, osteopontin, kallikrein 6 (protease M), kallikrein 10, matriptase and stratifin were found among the most highly overexpressed genes in ovarian serous papillary carcinomas, whereas transforming growth factor beta receptor III, platelet-derived growth factor receptor alpha, SEMACAP3, ras homolog gene family, member I (ARHI), thrombospondin 2 and disabled-2/differentially expressed in ovarian carcinoma 2 (Dab2/DOC2) were significantly down-regulated. Therapeutic strategy targeting TROP-1/Ep-CAM by monoclonal chimeric/humanized antibodies may be beneficial in patients harboring chemotherapy-resistant ovarian serous papillary carcinomas. Claudin-3 and claudin-4 being receptors for Clostridium Perfringens enterotoxin, this toxin may be used as a novel therapeutic agent to treat ovarian serous papillary tumors.

The invention belongs to the production technology for antitumor drugs, and discloses uses of sorafenib and sorafenib salts in preparing drugs for reversing BCRP protein-mediated multidrug resistance of tumors. According to the present invention, the sorafenib and the sorafenib salts are combined with antitumor drugs, such that the sensitivity of multidrug resistant tumor cells to the antitumor drugs are recovered; the prepared drugs are applicable for providing combination chemotherapy for the clinical chemotherapy resistant patients or preventing the drug resistance of the tumor cells from generation.

Compositions and methods for treating ovarian cancer are provided. Methods include combined treatment with chemotherapeutic agents and anti-STn antibodies. Chemotherapy resistant ovarian cancer cells may be reduced. Chemotherapy resistant ovarian cancer cells may include cancer stem cells.

Embodiments of the disclosure include compositions and methods useful for treating cancers that are sensitive to a chemotherapy, such as temozolomide. The methods allow effective cell immunotherapy to be used with chemotherapy when the cell immunotherapy is susceptible to being rendered ineffective by the chemotherapy. In specific aspects, the cancer is being treated by temozolomide (TMZ) and tumor antigen-specific T-cells that are resistant to TMZ.

Provided is a mosaic mouse model for use in determining the potency of an shRNA in vivo for reducing survival of cancer cells of chemotherapy-resistant leukemia. The syngeneic mouse recipient is transplanted with tet-on competent leukemia cells carrying a bicistronic nucleic acid construct comprising a promoter operably linked to a fusion gene associated with chemotherapy-resistant leukemia, and a sequence encoding a reverse tet-transactivator protein, such that both coding sequences are co-expressed from the promoter. Also provided are methods of treating soft tissue cancers.

The invention discloses application of a PARP1 inhibitor in the preparation of a medicine for reversing drug resistance of tumor cells to amethopterin and belongs to the technical field of tumour biotherapy. It is found by the inventor through researches that as for malignant cells with MTX resistance and DHFR gene high-amplification, by specifically inhibiting the key protein RARP1 of A-NHEJ pathway, DHFR gene copy number can be reduce and DMs in cells can be decreased so as to reverse drug resistance of tumors and enhance efficiency of tumor therapy. Therefore, on the basis of the above researches, the invention brings forward the application of the PARP1 inhibitor in the preparation of a medicine for reversing the drug resistance of tumor cells to MTX by reducing DHFR gene copy number. The invention provides a new targeting therapeutic scheme for the MTX as the main therapeutic drug and for the biotherapy of malignant tumors which are easy to resist drugs and also provides a scientific basis for effectively fighting against MTX drug resistance. In addition, the invention is also of great positive significance for deeply understanding the nature of chemotherapy resistance and finding resistance target for individualized treatment.

The invention provides methods of using expression levels of one or more stroma signature genes as selection criteria for determining a patient with cancer that is chemotherapy-resistant who may benefit from a particular anti-cancer therapy, such as stroma-targeted therapy, anti-angiogenic therapy, and/or immunotherapy. The present invention also provides methods of using expression levels of one or more stroma signature genes as a selection criterion for treating cancer patients, such as ovarian cancer patients, with a stroma-targeted agent.

The invention belongs to the technical field of biology, particularly relates to the field of medical diagnosis, in particular to application of TRERNA1 gene to prediction and improvement of sensitivity of liver cancer drug sorafenib. The prognosis of hepatocellular carcinoma and the evaluation of chemotherapy resistance of liver cancer are marked, and the expression level of TRERNA1 genes is detected by utilizing an RNA in-situ hybridization technology or qPCR, so that the prognosis and chemotherapy resistance of the hepatocellular carcinoma can be obtained, the introduction way of the TRERNA1 is simple, the whole prediction and evaluation process is simple and easy, and the feasibility is high.

The invention belongs to the traditional Chinese pharmacology field, and concretely relates to a method for constructing the pharmacological mechanism of a Jinlong capsule through a biological and genetic engineering process. The method analyzes the system biology of a processed gene chip result and constructs the pharmacological mechanism of the Jinlong capsule by utilizing a Thomson Reuters Genego database through the hybridization, detection and analysis of the gene chip via omics and the system biology process. The invention also discloses a use of the Jinlong capsule as a brain tumor resistance medicine and in chemotherapeutic drug tolerance activity reversion. And the pharmacological mechanism of the Jinlong capsule as the brain tumor resistance medicine and in the chemotherapeutic drug tolerance activity reversion is constructed through the method.

The invention provides a kit for predicting the lung adenocarcinoma progression, prognosis and drug resistance of lung-adenocarcinoma patients using HOXB13 combined with HOXB13 downstream target genedetection. The kit includes q-PCR primers of HOXB13, ABCG1, EZH2 and IL6. The kit can be used for effectively detecting HOXB13 and the transcriptional expression levels of the HOXB13 downstream targetgenes (ABCG1, EZH2 and IL6), and the expression sum of the four molecules is used for predicting the drug resistance and disease prognosis of the lung-adenocarcinoma patients. Moreover, the molecularcombination predicts that the discovery of the chemotherapy resistance and the poor prognosis lays a foundation for extensive clinical application of the molecular combination.

The invention belongs to the technical field of medical biology, and particularly relates to an ovarian cancer marker and application thereof. The invention proposes that the expression level of PRPF6 in ovarian cancer is closely related to FIGO staging and is irrelevant to age, differentiation degree and lymph node metastasis for the first time. The expression levels of the PRPF6 gene and the encoded protein thereof in the ovarian cancer drug-resistant cells/tissues are detected through PCR, immunohistochemistry and other methods, high expression of the PRPF6 in the drug-resistant cells/tissues is found, and it is clear that the PRPF6 can be used as the ovarian cancer paclitaxel drug-resistant marker. By inhibiting the expression level of the PRPF6, the drug resistance of paclitaxel can be inhibited, the invasion and migration of ovarian cancer cells can be reduced, cell apoptosis can be induced, and tumor growth can be inhibited, so that the PRPF6 inhibitor can be used as a potential target spot for the paclitaxel chemotherapy drug resistance treatment of the ovarian cancer, and a reference basis is provided for clinical diagnosis and treatment of the chemotherapy drug resistance type ovarian cancer. The method has wide application prospects and huge potential social benefits.

The invention particularly relates to application of METTL3 in AML chemotherapy drug resistance, and belongs to the technical field of molecular biology and medicine. The clinical treatment effect of AML is poor, the prognosis condition is poor, and relapse and refractory cases cannot be relieved through conventional therapy. The invention provides a molecular marker for detecting the chemotherapy sensitivity of acute myelogenous leukemia by analyzing the expression difference of METTL3 in bone marrow of a patient relatively sensitive to AML chemotherapy and a patient resistant to AML chemotherapy. Through AML chemotherapy sensitive cell strains, chemotherapy drug-resistant cell strains and animal models, the AML chemotherapy drug-resistant treatment effect of the METTL3 inhibitor is proved. The research of the invention also proves that METTL3 can mediate AML chemotherapy resistance by regulating AML cell homing.

The invention discloses an in-vitro drug sensitivity detection device for drug resistance of the pancreatic cancer hepatic metastasis chemotherapy, and belongs to the technical field of in-vitro drug sensitivity detection devices. A culture dish is kept at the same and appropriate temperature through a constant-temperature assembly, a positioning lifting frame assembly is started, and a liquid guide pipe assembly is accurately aligned to the upper portion of the culture dish; then a corresponding electric adjusting assembly is started to drive a T-shaped piston rod assembly to operate, the T-shaped piston rod assembly is matched with a one-way valve assembly to guide liquid into a piston cavity firstly, then the T-shaped piston rod assembly is matched with a liquid guide pipe assembly to enable the liquid to flow into the culture dish for quantitative and accurate liquid adding, and meanwhile timing is conducted through a timer; and reminding is carried out when the measurement time is up.

The invention relates to application of miR-1914* and/or miR-1915 as drug resistance markers of a colorectal cancer chemotherapy drug as well as application of the miR-1914* and/or the miR-1915 in preparing a drug with the functions of inhibiting transfer, invasion, apoptosis and proliferation of the colorectal cancer. According to the invention, the miR-1914* and the miR-1915 exist in blood plasma, can be detected, are in a down-regulated trend in the blood plasma of a colorectal cancer drug resistant patient, have relative tissue specificities, are related to colorectal cancer first-line chemoresistance, and meanwhile also influence patient prognosis. The miR-1914* and the miR-1915 can be used singly or used together, and play a relatively important role in the colorectal cancer first-line chemoresistance, and particularly, the effect of combined use is better.

The use of at least one flavonoid of natural or synthetic origin in association with cyclophosphamide and/or methotrexate to increase the effectiveness of chemotherapeutic treatments used in human and veterinary medicine for the treatment of tumors is described, in particular in case of resistance to the chemotherapeutic agents currently in use. At least one flavonoid herein described is selected from the group comprising or, alternatively, consisting of rutin, oxerutin, diosmin, troxerutin and hesperidin.