42 results about "Radiosensitivity" patented technology

The invention discloses a polyethylene glycol modified gold and manganese dioxide nano particle and a preparation method and application thereof, and belongs to the technical field of biological medicine, the polyethylene glycol modified gold and manganese dioxide nano particle (GMCN and PEG) has good biocompatibility under neutral physiological conditions, can relieve tumor hypoxia and increase generation of active oxygen in acidic TME, and has a good anti-tumor effect. The radiotherapy sensitivity is improved; and immune cell death is induced. Meanwhile, a cGAS-STING signal channel can be activated, dendritic cell maturation, macrophage M1 polarization and T cell infiltration are promoted, and the immunosuppression state in TME is counteracted. In addition, the GMCN-coated PEG also has an MR-CT bimodal imaging enhancement function, and integration of diagnosis and treatment is realized. The nano sensitizer disclosed by the invention has huge potential in the aspects of improving the radiotherapy curative effect, remodeling the tumor microenvironment, promoting the anti-tumor immunity, enhancing the biomedical imaging and the like.

The invention relates to rapamycin-loaded bionic nanoparticles as well as a preparation method and application thereof. The bionic nanoparticle loaded with the rapamycin comprises RZ NPs loaded with the rapamycin and a tumor cell membrane, the tumor cell membrane is coated with the RZ NPs loaded with the rapamycin; the rapamycin is modified in pores of the RZ NPs; and the RZ NPs has a crystal structure of ZIF8. The preparation method of the rapamycin-loaded bionic nano-particles comprises the following steps: preparing RZ NPs loaded with rapamycin, and modifying the RZ NPs by using a tumor cell membrane to prepare the RZM NPs. The RZM NPs provided by the invention has the capability of external irradiation sensitization on tumors, and due to the fact that rapamycin has potential influence possibility on cell cycles, tumor cells can be stagnated in a stage which is more sensitive to external irradiation, so that the radiotherapy effect is improved.

The invention belongs to the technical field of cancer immunotherapy, and particularly relates to iterative radiation-resistant tumor cell debris, a preparation method thereof and an application thereof in tumor resistance. The anti-radiation tumor cells generated by repeated radiation exposure show higher TMB (Tetramethylbenzidine) and induce stronger immunoreaction, so that a personalized vaccine is developed based on the method, and the frozen fragment vaccine is obtained by freeze thawing and inactivation of the radiation-resistant tumor cells. The RR-FDV exhibits enhanced immunogenicity as compared to a conventional radiosensitive counterpart. In the present disclosure, RR-FDV exhibits superior activation of antigen presenting cells, while in vivo, it recruits more dendritic cells to the vaccination site, promotes DC-mediated antigen presentation, and induces stronger antigen-specific T cell toxicity.

The present invention relates to an sgRNA sequence for targeted knockout of the IGFL3 gene and its application in enhancing the radiosensitivity of glioblastoma, belonging to the field of biotechnology. The sgRNA sequence is IGFL3-sgRNA-1 or IGFL3-sgRNA-3, and a CRISPR / Cas9 vector for targeted knockout of the IGFL3 gene is constructed using this sgRNA. The above vector was transfected into human glioblastoma cell line U251, and it was identified that the IGFL3 gene could be efficiently knocked out in this cell, and 2 U251 cell lines with knocked-out IGFL3 gene were screened. By targeted knockout of the IGFL3 gene, the radiosensitivity of human glioblastoma cell line U251 can be effectively enhanced. The present invention lays a foundation for studying the role of the IGFL3 gene in the radiosensitivity of glioblastoma, and also provides a powerful tool for developing this gene as a potential molecular target for enhancing the radiosensitivity of glioblastoma.

The invention discloses application of a detection reagent of interleukin-22 in preparation of a product for predicting radioactive intestinal injury sensitivity, and belongs to the technical field of medical detection. The expression level of IL-22 before radiation is related to the severity of intestinal injury after radiation, mice with high expression of IL-22 show more serious intestinal injury symptoms after radiation, IL-22 can be used as a biomarker for predicting sensitivity of radioactive intestinal injury, the risk of intestinal injury can be preliminarily evaluated by detecting the level of IL-22 before individual radiation, and the risk of intestinal injury can be further evaluated by detecting the level of IL-22 before individual radiation. Early warning is realized; the IL-22 can increase the radiosensitivity of intestinal tissues, the kit provided by the invention adopts a modern detection technology, such as enzyme-linked immunosorbent assay (ELISA), performs high-sensitivity and high-specificity detection on the IL-22, is simple and convenient to operate, and supports multiple sample types. The kit has important scientific research value and application prospect, and is expected to play a key role in prevention and treatment of radioactive intestinal injury along with the development of nuclear energy technology and radiotherapy.

The invention discloses application of 5 '-methylthioadenosine in preparation of a radiotherapy sensitizing drug, and belongs to the technical field of radiotherapy drugs. The invention provides an application of 5 '-methylthioadenosine in preparation of a prostatic cancer radiotherapy sensitization drug. Specifically, by adding 5 '-methylthioadenosine into prostatic cancer radiotherapy-resistant cells, it is found that the 5'-methylthioadenosine can inhibit growth of the prostatic cancer radiotherapy-resistant cells, induce apoptosis, retard the cell cycle in a radiotherapy-sensitive G2 / M period and improve the radiosensitivity of prostatic cancer cells, so that a new prostatic cancer radiotherapy sensitizer can be provided. Therefore, the radiotherapy effect is improved.

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 invention relates to a combined depolymerization therapy for enhancing colorectal cancer radiotherapy sensitivity, and belongs to the technical field of biological medicine. Specifically, the invention provides an application of an LDH / EDTA layered double hydroxide material in preparation of an anti-colorectal cancer drug used in combination with radiotherapy. In order to solve the problem that the curative effect of low-level colorectal cancer is low, the invention provides a combined therapy for enhancing the curative effect of radiotherapy through depolymerization treatment by using a zinc-aluminum layered dihydroxide material loaded with ethylenediaminetetraacetic acid. By adopting the method, the connection between cells can be efficiently destroyed, so that the tumor is loosened, the hypoxic environment of the tumor is improved, the sensitivity of the tumor to radiotherapy is finally enhanced, and the curative effect is further enhanced.

The invention belongs to the technical field of tumor radiotherapy related medicines. CCK8 and other experiments find that the DC and the affinity peptide thereof can enhance the radiosensitivity of tumor cells, so that candidate drugs can be provided for clinical tumor radiotherapy sensitization.

The present invention provides a rapid in vitro detection method for predicting the radiosensitivity of tumor patients for non-diagnostic purposes. The method includes: preprocessing cancer tissue samples and adjacent tissue samples; transferring tissue blocks into a well plate and grouping them; irradiating each group of tissue blocks at a second preset time according to the radiation time and a preset dose rate; detecting the absorbance values of each group and calculating the inhibition rate of the cancer tissue and the activity value of the adjacent tissue. Furthermore, the radiosensitivity corresponding to each radiation dose is predicted. The rapid in vitro detection method for predicting the radiosensitivity of tumor patients for non-diagnostic purposes provided by the present invention can rapidly and accurately predict the radiosensitivity of tissues, which is beneficial to providing a strong basis for routine clinical implementation.

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.

The invention relates to the technical field of medicines, in particular to application of diacetamide trinitrogen amidine in preparation of medicines for preventing, relieving or treating intestinal injury diseases caused by ionizing radiation. It is found for the first time that diacetamide triazamidine can effectively relieve intestinal injury caused by ionizing radiation and does not reduce the radiosensitivity of tumor cells, the compound can protect normal intestinal tissue, and meanwhile the limitation that a radiation protection medicine can possibly protect tumors is overcome; the invention provides a new treatment scheme for radioactive intestinal injury of organisms, and can be used for preventing, relieving or treating radioactive intestinal injury caused by radiotherapy. The invention develops new application of the diacetamide trinitrogen amidine and has a wide application prospect.

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 discloses application of glutamine in preparation of drugs for enhancing radiotherapy and killing wound pharyngeal squamous cell carcinoma, and relates to the technical field of biological medicines. According to the application disclosed by the invention, the tumor radiosensitivity is improved by taking glutamine as a target spot for the first time, a mechanism for improving the radiosensitivity of oropharyngeal squamous cell carcinoma by HPV infection is analyzed, the effectiveness of regulating the OPSCC radiosensitivity by glutamine is proved, and a new scheme is provided for developing tumor sensitization treatment medicines.

The invention relates to the technical field of radiotherapy drugs. The invention provides application of fusarium as a medicine for improving tumor radiotherapy sensitivity. Compared with the prior art, the medicine provided by the invention has the advantages of novel structure, unique action mechanism and large clinical transformation potential, and can provide a new medicine strategy for overcoming tumor radiation tolerance and improving radiotherapy curative effect.

The invention discloses an application of a plasma activation solution in preparation of a drug for enhancing hypoxia tumor radiotherapy sensitivity. Atmospheric pressure plasma generated at low power activates a culture solution DMEM, and acts on tumor cells in a hypoxic state, so that the hypoxic state of the tumor cells can be improved, the activity and clone ability of the hypoxic tumor cells can be inhibited, and the growth of tumors can be inhibited by cooperating with radiotherapy. The plasma activating solution can inhibit the activity of hypoxic colorectal cancer cells and regulate the cell cycle, so that the hypoxic colorectal cancer cell cycle is collected in the G2 / M period, the radiotherapy effect is enhanced, and the plasma activating solution has good safety when being applied in vivo.

This invention discloses a method, system, and device for computer-aided screening of drugs that enhance radiosensitivity in non-small cell lung cancer (NSCLC) based on miR-320a and RAD51. This invention provides a computer-readable storage medium and a method for screening drugs that enhance radiosensitivity in NSCLC based on miR-320a and RAD51. This invention offers an efficient, accurate, and rapid screening method for the research and development of related drugs that enhance radiosensitivity in NSCLC, with broad application prospects.

The present invention provides the application of the K568 site mutation of Ku80 protein in regulating tumor cell proliferation and radiosensitivity, belonging to the field of biotechnology. The present invention provides the application of a substance capable of causing site-directed mutation at the K568 site of Ku80 protein in the body or cells in any one of the following: inhibiting tumor cell proliferation; inhibiting DNA damage repair in tumor cells; treating tumors; enhancing tumor radiosensitivity; preparing tumor chemotherapy drugs. The experiments of the present invention prove that the K568 site mutation of Ku80 protein can reduce tumor cell viability, inhibit tumor cell proliferation, promote tumor cell apoptosis, inhibit DNA damage repair in tumor cells after radiotherapy, enhance radiosensitivity, and can be used as a target to study related drugs for treating tumors, having potential clinical application value.

There exist in NATURE a number of microscopic organisms that exhibit survival traits under extreme conditions. Several exhibit survival traits under extensive radiation fields. One such organism is Deinococcus Radiodurans. (refer to Refs 1 a and 1 b of PRIOR ART) We believe that this survival trait is genetically based. We claim that this genetic trait can be utilized for enhancement of radiation susceptibility and resistance and can be encapsulated in a pharmaceutical. This is partially confirmed in Ref 1c for a human cell system (refer to the PRIOR ART section), and justifies our Patent. We claim as our invention a pharmaceutical selectively utilizing the Deinococcus Radiodurans genes, and DNA / RNA genetic as well as chemical repair system, for the application to radiation treatment of human Glioblastoma Brain Cancer. We claim that we can utilize this pharmaceutical for the targeted enhancement of radiation susceptibility and resistance in the cancerous and healthy tissues, using energetic Protons or Carbon lons and the associated Bragg Peak selected energy deposition for these regions. We claim that this pharmaceutical can also be utilized with other focused radiation modalities such as X-Rays or electron beams, but not as effectively. We specifically select the DR1709 Deinococcus Radiodurans gene for this application and the DrRRA(DR2418) Deinococcus Radiodurans gene for this application. We do not exclude other Deinococcus Radiodurans genes, and DNA / RNA genetic as well as chemical repair systems not known at this time to this inventor currently or in the future. We do not exclude genes of other micro-organisms that survive under extreme conditions. However, only the application of radiation resistant micro-organism genetic material to create a pharmaceutical for the control of radiation resistance and susceptibility is being patented with a specific organism and gene set as the basis of this Patent (i.e., Deinococcus Radiodurans) and the application to the radiation treatment of human Glioblastoma Brain Cancer.

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 present invention provides the use of the FKBP5 gene as a molecular marker for photon radiation resistance in nasopharyngeal carcinoma, belonging to the field of biomedicine. Through protein profiling, gene sequencing, and clinical sample gene chip testing, the present invention analyzes and screens genes differentially expressed in nasopharyngeal carcinoma radiation-resistant and radiation-sensitive cell lines. The findings indicate that FKBP5 expression is significantly higher in radiation-resistant nasopharyngeal carcinoma cells than in radiation-sensitive nasopharyngeal carcinoma cells. Inhibiting FKBP5 expression significantly enhances nasopharyngeal carcinoma radiosensitivity and cell lethality.

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.

This invention discloses the application of hsa-miR-92b-5p as a biomarker for radiosensitivity in low-grade gliomas. The inventors found that high expression of hsa-miR-92b-5p indicates radioresistance in patients with low-grade gliomas, a high risk of recurrence after radiotherapy, and a poor prognosis. hsa-miR-92b-5p can serve as a biomarker for radioresistance in low-grade gliomas, enabling personalized radiotherapy for these tumors, improving treatment efficacy, and avoiding ineffective treatment.