21 results about "Radiosensitivity" patented technology

This invention relates to the field of biomedical technology. The invention discloses a method for preparing nanomaterials that can improve the radiosensitivity of tumors and their applications, comprising: S1: dissolving tungsten and copper compounds in an organic solvent in a specific ratio to prepare a mixed solution; S2: transferring the solution to a reaction vessel, adding a surfactant or polymer, and reacting at a certain temperature to form rod-shaped initial nanomaterials; S3: cooling to room temperature, centrifuging and washing to obtain a moist material; S4: drying to obtain Cu-W. 18 O 49 Nanomaterials. The Cu-W of this invention 18 O 49 Nanomaterials can be injected intravenously or intratumorally to target tumors via the EPR effect. When combined with near-infrared light and X-ray therapy, the photothermal effect raises the temperature, improves hypoxia, and enhances the killing effect of radiotherapy. It is suitable for triple-negative breast cancer, etc., inhibiting tumors through the secondary electrons of tungsten, the Fenton reaction of copper ions, and the photothermal effect. It can be monitored by CT or photoacoustic imaging, and can activate the immune response when used in combination with immune checkpoint inhibitors.

According to the radioactive hydrogel and the preparation method and application thereof and the radioactive tumor treatment application, chitosan serves as a matrix and is crosslinked with genipin to construct a three-dimensional network, and stable loading and slow release of radionuclides can be synchronously achieved; the self-antibacterial and adhesion characteristics of the patch can reduce the infection risk and ensure the fixation of the patch, so that a safe, effective and easy-to-operate local treatment platform is provided, the prepared patch can be directly placed on a tumor bed after resection in an operation, beta or alpha rays released by radionuclides accurately and continuously act on an area where tumor cells are most likely to remain, and the effect of treating the tumor cells is achieved. Different from traditional external radiation radiotherapy, the hydrogel can continuously release radiation with a low dosage rate. The mode has a stronger biological effect (such as inhibition of reproliferation) on tumor cells, the radiosensitivity difference of different cell periods and time phases can be overcome, the killing effect is more thorough, and chitosan is proved to have certain antibacterial activity, tumor cell growth inhibition activity and immunomodulatory activity. A synergistic effect can be generated with radionuclide, and a microenvironment which is not beneficial to survival and relapse of tumor cells is constructed together with the radionuclide.

The application relates to an application of nilotinib or a pharmaceutically acceptable salt thereof in preparation of a radiotherapy synergistic and attenuated drug for rectal cancer, and belongs to the technical field of medicines.The technical problem to be solved by the application is that the existing radiotherapy combined scheme is difficult to simultaneously realize enhancement of tumor radiosensitivity and reduction of normal intestinal radiation injury.The new application provided by the application is that: as a ZAK alpha inhibitor, the nilotinib weakens radiotherapy resistance, enhances DNA damage accumulation and promotes apoptosis in tumor cells by inhibiting ionizing radiation-induced ZAK alpha-mediated ribosome toxicity stress response, and reduces radiation-induced apoptosis in normal intestinal epithelial cells and protects the intestinal mucosal barrier.In vitro and in vivo experiments prove that the nilotinib can effectively enhance the radiotherapy effect of colorectal cancer and significantly relieve radiation-induced intestinal injury under the same administration scheme, realizes the double functions of radiotherapy "synergism" and "attenuation" of a single drug, and has important clinical transformation value.

This invention discloses the application of disulfiram or its pharmaceutical salt in the preparation of radiosensitizers, wherein the radiosensitizer refers to a radiosensitizer for malignant tumors, specifically osteosarcoma. The radiation involved in the radiosensitizer is selected from alpha, beta, gamma, or X-ray radiation. This invention is the first to discover and confirm a novel use of disulfiram in enhancing the radiosensitivity of malignant tumors, significantly inhibiting the proliferation of osteosarcoma cells after radiotherapy and promoting cell death in vitro. It also demonstrates outstanding efficacy in inhibiting the growth of subcutaneously implanted osteosarcoma in mice after radiotherapy.

This invention relates to the field of biomedical technology, providing a novel use for RBM25, specifically the application of RBM25 inhibitors in the preparation of tumor radiosensitizing drugs. The invention further provides a recombinant vector for an RBM25 inhibitor, and a tumor radiosensitizing drug with an RBM25 inhibitor or its recombinant expression vector as the active component. Through clonogenic assays, apoptosis assays, comet electrophoresis assays, and immunofluorescence assays, it was demonstrated that shRNA targeting the RBM25 gene can significantly inhibit the survival rate of colorectal cancer cells after irradiation, increase the degree of DNA damage after irradiation, and make cells more sensitive to radiation. The shRNA targeting the RBM25 gene provided by this invention can effectively improve the radiosensitivity of tumor cells during radiotherapy, especially effectively improving the radiosensitivity of colorectal cancer cells.

The invention discloses application of ribosomal proteins RPS10 and RPS27A in regulating cell growth and radiosensitivity, and belongs to the technical field of biology. In order to research the effects of specific RPs in the aspects of regulating and controlling cell proliferation, survival and radiosensitivity, peripheral blood of a human body is subjected to gamma-ray irradiation, complete transcriptome sequencing is performed on the peripheral blood before and after irradiation after irradiation, and it is found that the expression levels of various RPs genes such as RPS10, RPS27A, RPL27 and RPL35 are remarkably changed after irradiation; then, functional research is carried out on RPS10, RPS27A, RPL27 and RPL35 genes in HeLa cells, and it is found that the RPS10 and RPS27A genes have the important regulating effect on cell proliferation and survival.

The invention belongs to the technical field of biological medicines, and particularly relates to a targeted CANX and SIRT7 combined polypeptide inhibitor and application thereof in lung adenocarcinoma radiation resistance treatment. The polypeptide has a sequence TKPPSRRPKL (SEQ ID NO: 1), and can be competitively combined with CANX protein and block succinylation modification of SIRT7 on the CANX protein, so that the localization and function of CANX in MAM are recovered, mitochondrial metabolism reprogramming is reversed, and the radiosensitivity of lung adenocarcinoma cells is enhanced. Experiments show that the polypeptide can significantly inhibit the combination of CANX and SIRT7 in vitro and improve the radiosensitivity of radiation-resistant lung adenocarcinoma cells. The invention provides a new targeting strategy and drug candidate for treatment of lung adenocarcinoma radiation resistance.

The invention discloses a calcium ion binding protein marker combination for evaluating individual radiosensitivity and application of the calcium ion binding protein marker combination, and belongs to the technical field of biotechnology and nuclear radiation protection. Aiming at the technical problems that a genomics detection method and a functional experiment method for evaluating individual radiosensitivity have obvious limitation and the like at present, the invention is based on a C57BL / 6J mouse half lethal dose radiation experiment for the first time; a radiosensitivity prediction model based on the serum calcium ion binding protein combination (Ihh, NUCB1 and PROS1) is screened and established through a high-throughput mass spectrometry technology, and the clinical application value of the serum calcium ion binding protein combination (Ihh, NUCB1 and PROS1) as the radiosensitivity prediction marker is proved for the first time. A novel molecular marker is provided for professional radiation protection monitoring and formulation of a precise tumor radiotherapy scheme.

The invention relates to the field of medical image processing and artificial intelligence, in particular to a radiosensitivity prediction transfer learning system, which comprises a data preprocessing module for extracting and normalizing genome and PET image features of a patient; the topology maintaining feature decoupling network module constructs a feature space topological structure, and feature decoupling is achieved through manifold homeomorphic mapping; the multi-source-domain adaptive migration module guides adversarial learning based on geodesic distance, and constructs homotopy equivariant mapping to realize cross-domain feature migration; the prediction evaluation module is used for respectively constructing a parotid gland radioactive damage probability prediction network and a tumor recession rate prediction network; the clinical application interface module outputs a prediction result and provides radiotherapy scheme optimization suggestions, the problem of data heterogeneity between different platforms is effectively solved through a topology maintenance feature decoupling network, and the stability and accuracy of the model in cross-platform application are improved.

The invention discloses an identification and application method of UBA6 as a nasopharynx cancer radiosensitivity treatment target, and relates to the technical field of biomedical engineering. Comprising the following steps: S1, providing a cell line or tissue sample from nasopharyngeal carcinoma, wherein the sample is an in-vitro culture model or an in-vitro sample; s2, detecting the expression level of the UBA6 protein or gene in the sample through an immunology or molecular biological technology under an in-vitro condition; s3, based on the expression level, comparing the expression level with a pre-established radiosensitivity reference value, and identifying the sensitivity degree of the sample to ionizing radiation; and S4, on the basis of a phenotypic experiment, comparing with a non-treatment group, and proving that the growth of nasopharyngeal carcinoma cells can be inhibited by both the UBA6 knockout cells and the addition of UBA6 inhibitor inosine in the presence or absence of the UBA6 knockout cells, so that the radiotherapy treatment effect is improved.

This invention relates to the field of tumor treatment technology, and more particularly to the application of PCSK9 inhibitors in the preparation of drugs that enhance the radiosensitivity of solid tumors. The invention utilizes PCSK9 antibodies in combination with radiotherapy, and experiments were conducted in in vitro tumor cell and mouse tumor-bearing models. The results showed that PCSK9 monoclonal antibodies can inhibit cell proliferation and enhance radiotherapy-induced apoptosis. Furthermore, mice given PCSK9 antibodies in combination with radiotherapy exhibited significantly lower tumor growth rates than mice receiving only radiotherapy. This finding provides a new drug option for enhancing tumor radiosensitivity.

The invention discloses an application of a reagent for inhibiting or down-regulating an RIPK1 gene in preparation of a tumor radiotherapy sensitizing drug. The reagent for inhibiting or down-regulating the RIPK1 gene refers to a reagent for inhibiting or down-regulating the expression of the RIPK1 gene. The invention provides a reagent for inhibiting or down-regulating RIPK1 gene expression, namely siRNA of a targeted RIPK1 gene, and a clone formation experiment, an apoptosis experiment, a comet electrophoresis experiment and an immunofluorescence experiment prove that the siRNA of the targeted RIPK1 gene can remarkably inhibit the survival rate of colorectal cancer cells after irradiation, increase the damage degree of DNA after irradiation and enable the cells to be more sensitive to radiation. The siRNA of the targeted RIPK1 gene provided by the invention can effectively improve the radiosensitivity of tumor cells in the radiotherapy process, and especially can effectively improve the radiosensitivity of colorectal cancer.

The invention relates to the technical field of medicine preparation, in particular to application of cytokinin oTR in preparation of a medicine for enhancing tumor cell radiosensitivity. By constructing a stable tumor radiation resistance cell model and combining molecular biology experiments and statistical analysis, it is proved that cytokinin oTR can regulate and control expression of SIRT1 and miR-34a in radiation resistance cells in a time-dose dependence mode, and the radiotherapy sensitization effect is achieved through a p53 / miR-34a / SIRT1 pathway.

The one or more embodiments of the specification provide a cell radiosensitivity determination method, comprising: adopting a preset cell cycle arrest method to process a plurality of cell test groups of target cells respectively, to obtain a plurality of cell test groups with different G1 phase proportions; wherein the G1 phase proportion is the proportion of cells in the G1 phase in the cell test group; performing a radiation operation on the plurality of cell test groups, and determining a cell biological index in each cell test group after the radiation operation; based on the G1 phase proportion of each cell test group and the corresponding cell biological index, constructing a data model for indicating the corresponding relationship between the G1 phase proportion and the cell biological index of the target cell, for evaluating the radiation sensitivity of the target cell.

The invention discloses an application of a reagent for inhibiting or down-regulating expression of a micropeptide IRIMP in preparation of a tumor radiotherapy sensitizing drug. The invention provides a reagent for inhibiting or down-regulating expression of micropeptide IRIMP, namely siRNA of targeted micropeptide IRIMP, clone formation experiments, apoptosis experiments, cell cycle experiments, comet electrophoresis experiments and immunofluorescence experiments prove that the siRNA of targeted micropeptide IRIMP can significantly inhibit the survival rate of colorectal cancer HCT116 cells after irradiation, the DNA damage degree after irradiation is increased, and the survival rate of colorectal cancer HCT116 cells after irradiation is obviously improved. And the cells are more sensitive to radiation. The siRNA of the targeted micropeptide IRIMP provided by the invention can effectively improve the radiosensitivity of tumor cells in the radiotherapy process, and especially can effectively improve the radiosensitivity of colorectal cancer.

This invention belongs to the field of immunoassay and discloses an antigenic peptide phosphorylated at amino acid position 433 of CRTC2, a specific antibody, and its applications. Mass spectrometry analysis reveals for the first time the role of the CRTC2 Ser433 phosphorylation site in radiotherapy resistance, indicating that the phosphorylation level of CRTC2 Ser433 can serve as an indicator for predicting the radiosensitivity of liver cancer patients. Using the CRTC2 Ser433 phosphorylated antigenic peptide: CPHHRRVPLpSPLS, a specific phosphorylated antibody (CRTC2P-Ser433 antibody) is prepared for the first time. Radiosensitivity can be predicted through immunohistochemical staining scores, demonstrating both specificity and ease of detection.

The invention discloses an apolipoprotein marker combination for evaluating individual radiosensitivity and application thereof, and belongs to the technical field of biotechnology and nuclear radiation protection. Aiming at the technical problems that a genomics detection method and a functional experiment method for evaluating individual radiosensitivity have obvious limitations and the like at present, the invention screens and establishes a radiosensitivity prediction model based on serum apolipoprotein combinations (APOA1, APOA2 and APOA4) through a high-throughput mass spectrometry technology on the basis of a C57BL / 6J mouse half lethal dose radiation experiment for the first time; the clinical application value of the apolipoprotein combinations (APOA1, APOA2 and APOA4) as the radiosensitivity prediction marker is confirmed for the first time, and a novel molecular marker is provided for professional radiation protection monitoring and formulation of a precise tumor radiotherapy scheme.

The present invention relates to a composition for preventing, alleviating, or treating radiation-resistant breast cancer and enhancing radiation sensitivity, the composition comprising β-sitosterol as an active ingredient. Specifically, treating radiation-resistant breast cancer cells with the β-sitosterol according to the present invention induces ferroptosis, thereby increasing the level of apoptosis, and treating radiation-resistant breast cancer cells with a combination of β-sitosterol and irradiation significantly increases the radiation sensitivity of the radiation-resistant breast cancer cells. Therefore, β-sitosterol can be effectively used in a health functional food or pharmaceutical composition for preventing, alleviating, or treating radiation-resistant breast cancer, a composition for enhancing the radiation sensitivity of radiation-resistant breast cancer, and the like.

In the invention, mRNA of CXCL5, CD68, MATN1, SERPING1, SNCG, VTN, FBXO4 and SYTL4 genes, or proteins coded by the genes, show different expression levels between radiation-resistant colorectal cancer cells and radiation-sensitive colorectal cancer cells, and are closely related to the reduction of the survival rate in colorectal cancer patients. Therefore, according to the present invention, an agent for measuring the expression level of mRNA of a gene selected from the group consisting of CXCL5, CD68, MATN1, SERPING1, SNCG, VTN, FBXO4, and SYTL4 or a protein encoded by the gene effectively diagnoses radiation resistance in colorectal cancer or predicts radiation therapy for colorectal cancer. This makes it possible to determine whether to perform radiation therapy and the optimal radiation dose, thereby improving the efficiency and outcome of radiation therapy for colorectal cancer.

The invention discloses a lung cell radiosensitivity detection method and device and a storage medium, relates to the technical field of information processing, and mainly aims to improve the detection efficiency and detection accuracy of the lung cell radiosensitivity. Comprising the following steps: acquiring a plurality of gene expression data corresponding to unradiated lung cells; determining the contribution degree of each piece of gene expression data in the plurality of pieces of gene expression data to radiosensitivity detection, and screening out key gene expression data related to radiosensitivity detection from each piece of gene expression data based on the contribution degree; and based on a preset sensitivity prediction model and the key gene expression data, predicting the radiation sensitivity of the non-radiated lung cells. The method is suitable for detection scenes of lung cell radiosensitivity.

Use of a K568 site mutation in a Ku80 protein for regulating tumor cell proliferation and tumor cell radiosensitivity, belonging to the technical field of biotechnology. Use of a substance capable of inducing a site-directed mutation at a K568 site of a Ku80 protein in an organism or a cell in any one of the following items: preparing a product for inhibiting proliferation of a tumor cell; preparing a product for inhibiting DNA damage repair in the tumor cell; preparing a product for treating a tumor; preparing a product for enhancing radiosensitivity of the tumor; and preparing a chemotherapeutic drug for tumor. Experimental results demonstrate that the K568 site mutation in the Ku80 protein reduces tumor cell viability, inhibits tumor cell proliferation, and promotes tumor cell apoptosis. Such a site also suppresses DNA damage repair in the tumor cell following radiotherapy, thereby enhancing radiosensitivity.