18 results about "Platinum chemotherapy" patented technology

The invention discloses an eccDNAcircATP6V0A1 serving as a predictive marker of cis-platinum drug resistance of hypopharyngeal cancer and an application of the eccDNAcircATP6V0A1. The nucleotide sequence of the predictive marker eccDNA is as shown in SEQ ID NO. 3. According to the invention, a hypopharyngeal carcinoma cisplatin drug-resistant cell line model FaDu / DDP is cultured for the first time, meanwhile, a differential eccDNA expression profile and a circRNA expression profile in hypopharyngeal carcinoma cells FaDu and hypopharyngeal carcinoma cisplatin drug-resistant cells FaDu / DDP are disclosed and analyzed in a combined manner, and the eccDNA circATP6V0A1 is further screened and verified as a predictive marker of hypopharyngeal carcinoma cisplatin drug resistance through combined analysis. And a new treatment strategy diagnosis and treatment thought is provided for cis-platinum chemotherapy of hypopharyngeal carcinoma patients clinically.

The invention provides a chemotherapy combined medicine and application thereof. The chemotherapy combined medicine comprises a first medicine and a second medicine, the first drug is a platinum chemotherapeutic drug or adriamycin, and the second drug is a zinc nitroprusside nano-drug; the zinc nitroprusside nano-drug is formed by coordination self-assembly of sodium nitroprusside and a zinc ion source compound. The zinc nitroprusside nano-drug has glutathione responsiveness and can release nitric oxide and zinc ions. In the platinum chemotherapy combined medicine, the cis-platinum and the ZnNO play a synergistic interaction role.

The invention provides application of a USP9X inhibitor in preparation of a medicine for treating ovarian cancer and application of the USP9X inhibitor in preparation of a combined medicine for improving the medication effect of an ovarian cancer chemotherapy medicine. On one hand, the USP9X inhibitor is independently used to significantly inhibit development of ovarian cancer, and on the other hand, the USP9X inhibitor significantly improves the chemotherapy effect and improves the chemosensitivity of tumors to first-line chemotherapy drugs such as paclitaxel (PTX), cis-platinum (CDDP) and carboplatin. The pharmaceutical mechanism of the USP9X inhibitor in ovarian cancer treatment is found for the first time. According to the present invention, the single drug treatment of the USP9X inhibitor and the combined treatment of the USP9X inhibitor and the chemotherapeutic drug can significantly reduce the USP9X and Hif2alpha protein levels, and the half-life period detection of the protein finds that the USP9X inhibitor can promote the degradation of the Hif2alpha-dependent proteasome so as to provide the antitumor effect;

The present invention provides a polypeptide for enhancing the sensitivity of gastric cancer to cisplatin chemotherapy and its application, belonging to the technical field of biomedicine. The polypeptide of the present invention is derived from the 2nd - 17th positions of the precursor protein thymosin β4 (TYB4). Through experiments, it is found that the polypeptide is closely related to drug resistance in gastric cancer cells. After being treated with the polypeptide of the present invention, the cisplatin-treated drug-resistant gastric cancer cells show significant induction of apoptosis in drug-resistant gastric cancer cells, inhibit the activity and migration of drug-resistant gastric cancer cells, and have no obvious toxic and side effects on normal gastric mucosal cells. The polypeptide of the present invention has the advantages of low immunogenicity, strong tissue permeability, low production cost, and being easy to modify to enhance in vivo stability and biological activity. Therefore, its application in the anti-tumor field has broad clinical application prospects and provides a new direction for the development of gastric cancer treatment drugs.

The invention relates to a pharmaceutical composition and application thereof in preparation of drugs for treating chemotherapeutic drug-resistant solid tumors, the pharmaceutical composition comprises a targeted CDK9 degradation agent and platinum chemotherapeutic drugs, and the targeted CDK9 degradation agent is a compound shown in a general formula (I), a tautomer, a diastereomer, a racemate and a pharmaceutically acceptable salt thereof. The pharmaceutical composition provided by the invention has drug resistance to some platinum chemotherapeutic drugs, and the drug resistance mechanism of solid tumor cells or local advanced solid tumor cells is not clear; particularly, the compound has the effects of remarkably inhibiting the clone formation capability, effectively promoting cell apoptosis and reversing the drug resistance of solid tumors on esophageal squamous carcinoma cells resistant to platinum chemotherapeutic drugs.

This invention relates to the application of *Bifidobacterium longum* BL21 in the preparation of formulations to alleviate multi-organ damage induced by cisplatin chemotherapy, namely, a novel microbial strategy for preventing or alleviating multi-organ damage induced by cisplatin chemotherapy. This invention creatively discovers that *Bifidobacterium longum* BL21 can alleviate kidney damage, intestinal damage, and bone marrow suppression without interfering with the antitumor activity of cisplatin. Specifically, it can reverse the increase in serum creatinine and blood urea nitrogen levels caused by cisplatin chemotherapy, reverse the increase in inflammatory factor levels in kidney tissue caused by cisplatin chemotherapy, and alleviate oxidative stress damage in kidney tissue caused by cisplatin chemotherapy; it can reverse the increase in intestinal permeability caused by cisplatin chemotherapy, reverse the downregulation of intestinal tight junction protein expression caused by cisplatin chemotherapy, reverse the increase in serum endotoxin levels caused by cisplatin chemotherapy, and reverse the decrease in beneficial intestinal bacteria caused by cisplatin chemotherapy; it can improve hematopoietic dysfunction caused by cisplatin chemotherapy and restore white blood cell count.

The invention discloses application of a CDK4 / 6 inhibitor in preparation of medicines for preventing or treating ototoxicity caused by platinum chemotherapy and radiotherapy. Through combined use of the CDK4 / 6 inhibitor and anti-cancer treatment, cochlea hair cell loss can be significantly reduced, a hearing threshold is reduced, and the anti-tumor effect of cis-platinum / radiotherapy is not affected. The device is especially suitable for breast cancer, head and neck cancer and other tumor patients needing long-term use of platinum drugs or radiotherapy.

The invention provides application of an inhibitor for targeted inhibition of MACIR expression or function in preparation of a tumor chemotherapy sensitizer and a composition of the inhibitor. The tumor chemotherapy sensitizer is specifically a tumor platinum chemotherapy sensitizer. According to the application, the MACIR is identified as a novel adapter protein of FIGNL1-FIRRM unfolding enzyme, the effect of the MACIR in RAD51 filamentous structure dissociation is clarified, and the fact that the MACIR is used as a key protein in a DNA repair pathway for cross-linking (ICLs) damage among DNA chains and can influence the sensitivity of tumor cells to platinum drugs is revealed.

The invention relates to the technical field of tongue squamous cell carcinoma cis-platinum chemotherapy treatment, and provides application of a DNPEP inhibitor in preparation of a medicine for reducing the tolerance of cis-platinum to tongue squamous cell carcinoma cells. The DNPEP inhibitor is applied to preparation of the medicine for reducing the tolerance of the cis-platinum to the tongue squamous carcinoma cells, and the tolerance of the tongue squamous carcinoma cells to the cis-platinum is reduced by inhibiting expression of DNPEP in the tongue squamous carcinoma cells. The DNPEP can be used as a treatment target for overcoming the chemotherapy drug resistance of the tongue squamous carcinoma, and the DNPEP inhibitor and cis-platinum are combined for treating the tongue squamous carcinoma, especially for treating patients with cis-platinum resistance type tongue squamous carcinoma.

The invention relates to the technical field related to medical medicines, discloses application of glycyrrhizic acid in inhibiting ototoxicity caused by cis-platinum chemotherapy, and aims to provide novel medical application of glycyrrhizic acid, namely the glycyrrhizic acid can be used for reducing ototoxicity side effects caused by CDDP. After a C57BL6 / J mouse is administered according to a model, ABR waveform of a CDDP group mouse is disordered, a hearing threshold is obviously increased, and an I-wave incubation period is prolonged; after the GL is given to the mouse, ABR waveform differentiation of each frequency is good, the hearing threshold value is obviously reduced, and the I-wave incubation period is shortened. Hamp, Hamp; e staining results show that CDDP destroys the morphological structure of cochlear vascular lines, resulting in cytoplasm reduction, vacuole increase, cell nucleus fixation and constriction and boundary fuzziness; the GL intervention enables the whole cytoplasm of the cochlea vascular lines of the mouse to be fuller, the vacuoles to be obviously reduced, the cell nucleus to be complete and the boundary to be clearer, which indicates that the GL inhibits the cochlea vascular line injury caused by the CDDP. EB staining finds that red fluorescence in the CDDP group microvessels is weak, and a large amount of EB exudes, which prompts that the permeability of BLB is increased.

Acquired hearing loss due to chemotherapy or noise exposure is a major health problem, and Cisplatin chemotherapy often causes permanent hearing loss in cancer patients. However, there are no FDA-approved drugs for the treatment or prevention of Cisplatin- or noise-induced hearing loss. In one aspect, use of Niclosamide, Ingenol, and Elesclomol as an active agent to treat a hearing impairment and to prevent a hearing impairment, and methods of treating and / or preventing hearing impairments or disorders using the compositions are disclosed. This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention.

This invention discloses a biomarker for predicting the sensitivity / prognosis of non-small cell lung cancer (NSCLC) treated with platinum-based chemotherapy drugs, and its application, belonging to the field of tumor biology technology. The biomarker is MT-ND6. MT-ND6 is an indicator of NSCLC's sensitivity to platinum-based chemotherapy, helping to avoid unnecessary treatment, reduce ineffective treatment, and minimize unnecessary chemotherapy side effects. The biomarker MT-ND6 can also serve as an independent marker distinguishing NSCLC tumor tissue from adjacent normal tissue; the expression level of MT-ND6 protein in tumor tissue is significantly higher than in normal tissue, demonstrating diagnostic value. This invention also discloses a detection reagent, a method for screening the biomarker, and a method for predicting / evaluating the sensitivity / prognosis of NSCLC treated with platinum-based chemotherapy drugs. The biomarker of this invention can be used to prepare diagnostic products for NSCLC, and has broad application prospects.

According to the application of the fumaric acid Vonoprasone as the colorectal cancer oxaliplatin chemotherapy adjuvant drug, the fumaric acid Vonoprasone assists colorectal cancer chemotherapy by enhancing the colorectal cancer oxaliplatin chemotherapy sensitivity. The invention relates to a drug combination of fumaric acid Vonoprasone used in a colorectal cancer oxaliplatin chemotherapy process.

The specification relates to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) for use in the treatment of EGFR TKI-naïve patients with locally-advanced or metastatic EGFR mutation-positive non-small cell lung cancer (NSCLC), wherein the EGFR TKI is administered in combination with pemetrexed and platinum chemotherapy.

The invention discloses an application of TBX1 / TBX1 methylation in treatment of esophageal cancer. Researches prove that after TBX1 methylation silencing, the proliferation effect of ESCC cells can be improved, and the drug resistance of cisplatin chemotherapy of the ESCC cells is improved; the treatment effect of cis-platinum in ESCC cells can be remarkably improved by recovering TBX1 expression in vivo and in vitro. In combination with clinical sample analysis, it is found that TBX1 promoter hypermethylation has universality in ESCC platinum chemotherapy tumor-resistant tissue, so that TBX1 promoter methylation can be used as an epigenetic biomarker for predicting ESCC platinum chemotherapy sensitivity, and TBX1 is expected to be used as a platinum-resistant ESCC chemotherapy sensitization target.

The invention belongs to the technical field of medicinal chemistry, and particularly relates to a metal platinum heterozygote for synergistically regulating polyamine uptake and PD-L1 glycosylation modification as well as a preparation method and application of the metal platinum heterozygote. The compound 5a takes oxaliplatin as a parent nucleus, has a cyclopropyl terminal fragment structure, shows the highest cytotoxicity and remarkable cell selectivity on non-small cell lung cancer, is good in stability, can reduce tumor progression and prolong the lifetime, and is a chemotherapy candidate drug for treating non-small cell lung cancer. The compound 5a provided by the invention has a good tumor killing effect in vitro, inhibits migration of tumor cells and induces apoptosis of the tumor cells. According to the present invention, the MAN2A1 coding the N-carbohydrate chain maturase is determined as the key immunomodulatory gene, and the compound 5a can simultaneously inhibit the polyamine uptake, mediate the modification of the N192 site high mannose type N-carbohydrate chain in PD-L1 through the MYCN / ODC / AKT / NF-[kappa] B pathway, target the non-small cell lung cancer metastasis, and rescue the immunosuppression of platinum-containing chemotherapy.

The invention discloses application of a kit for detecting GSTP1 gene polymorphism in preparation of a product for evaluating myelosuppression risk of a platinum chemotherapy-induced lung cancer patient, and belongs to the technical field of drug-induced myelosuppression risk evaluation. The reagent for detecting the polymorphism of the GSTP1 rs1695 gene can be used for detecting the genotype of the GSTP1 rs1695 gene of a lung cancer patient; according to the invention, the genotype of the GSTP1 rs1695 gene of the lung cancer patient is obtained by detecting the polymorphism of the GSTP1 rs1695 gene of the lung cancer patient, and the risk of myelosuppression during the period of using platinum drugs by the lung cancer patient is judged according to the genotype of the GSTP1 rs1695 gene of the lung cancer patient. By detecting the GSTP1rs1695 genotype, myelosuppression high-risk patients can be recognized in advance, so that the chemotherapy regimen is optimized. For example, for AG / GG type patients, reduction of the dosage of platinum drugs or combination of granulocyte colony stimulating factors (G-CSF) can be considered to reduce the occurrence of severe myelosuppression.

Provided herein are compositions, systems, kits, and methods for reducing chemoresistance (e.g., to platinum containing chemotherapeutics) and treating certain diseases, using nucleic acid sequences (e.g., aptamers and antisense sequences) that bind to certain mRNAs (e.g., WTAP), or bind a SEFIR domain of an ACT1 protein, or bind to or inhibit mRNA sequences that bind to Act1 protein.