80 results about "Chemotherapy resistance" patented technology

The invention relates to a method for establishing a paclitaxel (PTX)-resistant ovarian cancer cell model. The method comprises the following specific steps: intervening an OVCAR-3 cell and an SK-OV-3 cell by virtue of PTX, replacing a PTX-free culture medium, intervening the OVCAR-3 cell and the SK-OV-3 cell until growth of cells returns to be normal, namely, under the conditions that the cells stably grow, morphologies are full, no floating dead cells are produced and the passage density is 30%, enabling the cells to grow 90% in 3-5 days, starting to carry out normal passage and improving the concentration of PTX, wherein the intervention time for each time is 24 hours; and finally obtaining the PTX-resistant ovarian cancer cell model having the preservation numbers of CCTCC C2014203 and CCTCC C2014204. According to the method, by closely observing growth states of cells and selecting the intervention moment, the established cell model has higher level of drug-resistance coefficients and good resistance stability and can be used for the research on ovarian cancer drug-resistant mechanism, ovarian cancer drug-resistant reversion, prevention of chemotherapy resistance and the improvement on chemosensitivity.

Methods are provided for the prognosis, diagnosis and treatment of various pathological states, including cancer, chemotherapy resistance and dementia associated with Alzheimer's disease. The methods provided herein are based on the discovery that various proteins with a high level of sialylation are shown herein to be associated with disease states, such as, cancer, chemotherapy resistance and dementia associated with Alzheimer's disease. Such methods provide a lysosomal exocytosis activity profile comprising one or more values representing lysosomal exocytosis activity. Also provided herein, is the discovery that low lysosomal sialidase activity is associated with various pathological states. Thus, the methods also provide a lysosomal sialidase activity profile, comprising one or more values representing lysosomal sialidase activity. A lysosomal sialidase activity profile is one example of a lysosomal exocytosis activity profile. As such, the level of lysosomal exocytosis activity and/or lysosomal sialidase activity is predictive of a diagnosis and/or prognosis of cancer, chemotherapy resistance or dementia associated with Alzheimer's disease.

Toll-like receptors (TLR) are expressed by a variety of cancers, including melanoma and T-ALL. TLR signaling plays an important role in T cell malignancies and melanoma. The effects of stimulating or inhibiting the TLR/IL-1 receptor-associated kinases IRAK-1 and IRAK-4 in melanoma and T-ALL cells were evaluated. Pharmacological treatment with an IRAK-1,-4 inhibitor delays tumor growth and prolongs survival in vitro and in vivo, indicating that TLR signaling contributes to T-ALL and melanoma progression and interfering with this signaling is a novel therapeutic strategy to control T-ALL and melanoma proliferation.

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.

Disclosed are compositions, such as nucleic acids, vectors, cells, animal models and the like, useful to reduce tumor growth, cancer cell migration and various other cancer pathologies associated with EGFR (epidermal growth factor receptor) and MET (the receptor tyrosine kinase for hepatocyte growth factors) dyregulation, particularly in non-small cell lung carcinoma.

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 relates to application of miRNA in preparation of a diagnostic reagent for predicting platinum chemotherapy drug resistance of high-grade serous ovarian cancer. The miRNA comprises miR-1287, miR-3131, miR-335, miR-4419, miR-4468 and miR-96. The invention also provides application for analyzing and detecting platinum chemotherapy drug resistance of high-grade serous ovarian cancer onthe basis of the determination of the expression quantity of miR-1287, miR-3131, miR-335, miR-4419, miR-4468 and miR-96, and the application has better accuracy than the existing method for predictingplatinum chemotherapy drug resistance of high-grade serous ovarian cancer.

The invention discloses a chimeric antigen receptor and a gene and a recombinant expression vector thereof, an engineered CD33 targeting NKT cell and an application thereof. The chimeric antigen receptor is CD33ScFv-CD8-CD137-CD3zeta which is formed by connecting CD33ScFv, a hinge domain and a transmembrane domain of CD8, an intracellular signal structural domain of CD137 and an intracellular signal structural domain of CD3zeta in series. By adopting the chimeric antigen receptor CD33ScFv-CD8-CD137-CD3zeta modified NKT cell for treating CD33 positive acute myelogenous leukemia in a progressive stage, drug resistance and chemotherapy resistance caused by combined application of a CD33 monoclonal antibody and chemotherapy can be effectively avoided, and the cell has specific killing activity on leukemia cells.

The present invention relates to monitoring of ErbB receptor levels in methods and kits for determining the prognosis of cancer in a subject or improving the effectiveness of a cancer treatment. The invention also provides a method for predicting the recurrence of clinical signs of a cancer in a subject. In some embodiments, the invention provides methods for predicting the development of resistance to a chemotherapy regimen. In other embodiments, the invention provides methods for improving the effectiveness of a cancer treatment in a subject by monitoring levels of ErbB-2, ErbB-3 and/or ErbB-4. Preferably, the subject in the methods of the invention has been previously treated with a chemotherapy regimen for an ErbB-1 positive tumor.

A new method of therapy using the subcutaneous mode of administration of formulations based upon harringtonines including their salts and tautomeric forms having the formula 1 where: R.sup.1 is H, OH, OMe, O--(C.sub.1-C.sub.30)alkyl, O-aryl-(C.sub.1-C.sub.3- 0)-alkyl, O--(C.sub.2-C.sub.30)-alkenyl, O--(C.sub.3-C.sub.30-cycloalkyl or null and R.sup.2 is H or OH, or R.sup.1, R.sup.2 form together --O--. R.sup.3 .dbd.R.sup.4 50 OMe or R.sup.3 and R.sup.4 form together --OCH.sub.2O--, n is 0 to 8, R.sup.5 is H, OH, OMe, O--(C.sub.1-C.sub.30)-alkyl, O-aryl-(C.sub.1-C.sub.30)-alkyl, O--(C.sub.2-C.sub.30)-alkenyl, O--(C.sub.3-C.sub.30)-cycloalkyl or O-aryl, Z.dbd.O, S, or NH, and 2 or Z--R.sup.8 is NR.sup.12R.sup.13, R.sup.12 and R.sup.13 representing respectively R.sup.9 and R.sup.10, R.sup.9, R.sup.10, R.sup.11 are independently H, C.sub.1-C.sub.30 alkyl, C.sub.3C.sub.30 cycloalkyl, aryl, aryl-(C.sub.1-C.sub.30)-alkyl, C.sub.2-C.sub.30 alkenyl, C.sub.2-C.sub.30 alkynyl, C.sub.1-C.sub.30trihalogenoalkyl, C.sub.1-C.sub.30alkylamino-(C.sub.1-C.s- ub.30)alkyl, C.sub.1-C.sub.30 dialkylamino(C.sub.1-C.sub.30)-alkyl, or amino-(C.sub.1-C.sub.3)-alkyl, or 3 where R.sup.14, R.sup.15, R.sup.16 are independently H, halogen, C.sub.1-C.sub.30 alkyl, C.sub.3-C.sub.30 cycloalkyl, aryl, aryl-(C.sub.1-C.sub.30)-alkyl, C.sub.2-C.sub.30 alkenyl or C.sub.2-C.sub.30 alkynyl, C.sub.1-C.sub.30trihalogenoalkyl, m is 0 to 4, each of these groups including or not heteroatom(s) or their combination with another antitumor agent or a mixture of antitumor agents useful for the treatment of a disease in humans or animals, particularly cancers, leukemias, lymphomas, parasite diseases or chemotherapeutic resistance to other agents, In using a formulation specifically adapted for subcutaneous administration.

The invention discloses a tumor drug-resistant target site and application of the tumor drug-resistant target site. The invention discloses influence of NAC1 (Nucleus Accumbens-1) on tumor medicine treatment, and thus provides a purpose of an NAC1 inhibitor in medicine for reducing or eliminating tumor chemotherapy drug resistance and application of the NAC1 inhibitor as a tumor drug-resistant mark and a drug-resistant tumor prediction and diagnosis and drug-resistant tumor medicine design and screening target. The invention provides a novel mechanism for overcoming tumor drug resistance and improving the curative effect, and provides a novel target for resisting tumor drug resistance.

Today, despite current advances in combinatorial therapies such as surgery, radiotherapy and chemotherapy, aggressive cancers remain fatal. Cancer stem-like cells (CSCs) may account for chemotherapy resistance and thus represent a promising therapeutic target. In this context, the present inventors identified essential intracellular pathways favoring the self-renewal and survival of CSCs. More precisely, the present inventors showed that the cytokine co-receptor GP130 acts as a co-receptor for Apelin/APJ signaling and that the interaction of Apelin with APJ/GP130 activates a dual signaling pathway involving the Akt/mTOR and STAT3 transcription factor, thereby promoting CSCs survival and self-renewal. They therefore propose to block these pathways in order to treat patients suffering from tumors containing CSCs, such as glioblastomas. In another aspect, the invention relates to the use of the Apelin expression level for evaluating the survival probability of a subject suffering from glioblastoma.

The invention relates to application of a reagent for detecting PITX1 (paired-like homeodomain 1) expression in the preparation of a gastric cancer prognosis evaluation kit, belongs to the technical field of biology and particularly relates to the field of medical diagnosis. The invention discloses application of a reagent for detecting PITX1 expression in the preparation of a gastric cancer prognosis evaluation kit. Predicted gastric cancer prognosis and chemotherapy resistance condition can be acquired by marking gastric cancer prognosis prediction and gastric cancer chemotherapy evaluation, and by using immunohistochemical method to detect the expression level of PITX1 gene; the PITX1 gene is simple to introduce; the whole predictive evaluation is simple and easy and is highly feasible.

Cancer is one of the major causes of death worldwide. Although many advances have been made in the treatment and management of the disease, the existence of chemotherapy-resistance means there is still a great need to develop new strategies and drugs for its treatment. Provided herein are synthetic derivatives of combretastatin A-4, in particular those in which the aromatic rings are locked into a non-isomerisable active conformation, thus resulting in improved, stable compounds. The novel compounds are structurally related to combretastatin A-4 (CA-4) and lock the rings into the known active conformation by means of a four membered nitrogen containing heterocyclic ring, such as a beta-lactam ring, incorporated into the standard CA-4 structure. The compounds exhibit potent anti-cancer activity.

The invention provides methods for decreasing one or more symptoms of cancer in a patient requiring the steps of determining the activation or inactivation of the MK2 signaling pathway and, based on these determinations, administering either a MK2 inhibitor or a combination of a MK2 inhibitor and a chemotherapeutic agent, or a chemotherapeutic agent to the patient. The invention further provides methods for identifying a cancer patient that may selectively benefit from the administration of a chemotherapeutic agent, or the administration of a MK2 inhibitor or the combination of a MK2 inhibitor and a chemotherapeutic agent, requiring the steps of determining the activation or inactivation of the MK2 signaling pathway. The invention additionally provides methods and kits for diagnosing a chemotherapy-sensitive or chemotherapy-resistant cancer in a subject that require the step of (or reagents for) determining the activation or inactivation of the MK2 signaling pathway. The invention also provides methods of treating a cancer patient diagnosed as having a chemotherapy-sensitive or a chemotherapy-resistant cancer.

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 discloses application of RBMS3 as a molecular target for tumor drug resistance detection, treatment and prognosis. Inventors find that RBMS3 deletion can promote tumor cisplatin-resistance and tumor recurrence. In the prior art, most tumor therapeutic schedules are surgical resection with adjuvant chemotherapy, and chemotherapy resistance becomes an important factor affecting the prognosis of tumor patients. A specific molecular marker is disclosed and can be used as an important molecular marker for predicting tumor drug resistance. The target gene can be detected at DNA level,and DNA is stronger in stability than RNA or proteins, and can improve the accuracy and limitation of diagnosis. A targeted therapeutic schedule is provided for the treatment of the tumor patients. Abetter therapeutic effect on patients with no RBMS3 deletion tumors can be obtained by use of cisplatin alone; and a better therapeutic effect on patients with RBMS3 deletion tumors can be obtained bycombined use of cisplatin and PRI-724.

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 provides compositions comprising wilforlide A for overcoming drug resistance in cancer therapy, particularly in the treatment of cancers which have exhibited resistance to treatment by chemotherapeutic drugs. Methods and compositions for treating a cancer are disclosed. The method administers to a patient in need thereof a combination of wilforlide A and a chemotherapeutic drug. Wilforlide A and chemotherapeutic drug are administered in a combined amount effective to treat the can cer. The cancer being treated is at least in part resistant to treatment by the chemotherapeutic drug alone.

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.

Disclosed are methods for the use of Jumonji C demethylase inhibitors for the radiosensitization of cancers cells and the treatment and prevention of chemotherapy resistance in cancer.