15 results about "Neoplastic growth" patented technology

The application discloses a LYTAG-Gem compound for enhancing the anti-tumor effect of gemcitabine and application thereof, relates to the technical field of biological medicine, and particularly relates to a gemcitabine (Gem) targeted delivery system based on a lysosome targeting chimera (LYTAC) and application thereof in enhancing the anti-tumor process. 2+ The system is assembled from heavy chain ferritin, Ni 2+ , NTA-PEG5000-DBCO and a targeting ligand TPP-1-N3 in a specific mass percentage, can efficiently load Gem and form a nano compound with a particle size of about 59-79 nm, the system targets tumor cells through heavy chain ferritin, and realizes site-specific release of Gem in cells by means of an endocytosis-lysosome pathway mediated by the LYTAC structure, in-vivo pharmacodynamic experiments show that the LYTAC-Gem compound can significantly inhibit the tumor growth of a KPC pancreatic cancer mouse model, molecular mechanism research further reveals that the LYTAC-Gem compound can down-regulate the expression of PD-L1 protein in tumor tissues, and it is indicated that the LYTAC-Gem compound has the potential to activate an anti-tumor immune response, and the application provides a novel targeted delivery strategy for overcoming the toxic side effects and tumor drug resistance of gemcitabine.

This disclosure provides methods for treating tumors, reducing tumor severity, inhibiting tumor growth, or inducing tumor necrosis, wherein the methods include: selecting a patient with cancer (e.g., liver cancer, lung cancer, or head and neck cancer) in need of treatment and administering neoadjuvant therapy to the patient in a combination of a therapeutically effective amount of a programmed death 1 (PD-1) inhibitor (e.g., cimiprimab or its bioequivalent) and radiation therapy (e.g., SBRT) or an anti-LAG-3 antibody (e.g., fenpromab), followed by surgical resection and optionally administration of a programmed death 1 (PD-1) inhibitor (e.g., cimiprimab or its bioequivalent) as postoperative adjuvant therapy. In some embodiments, the cancer is liver cancer, such as hepatocellular carcinoma (HCC).

This invention discloses a photoactivated nanoparticle-based drug delivery material for immunoadjuvants, its preparation method, and its applications. The drug delivery material is constructed from photosensitizer monomers, crosslinking monomers, and immunoadjuvant prodrug monomers within a confined space of a nanoemulsion via a copper-free click polymerization reaction to form crosslinked polymer nanoparticles. The nanoparticle size is controllable, and the composition is precisely defined. Under physiological conditions, the drug delivery material exhibits good colloidal stability and high drug loading. Upon near-infrared light irradiation, the generated ROS can cleave the thioketone bonds, causing the nanoparticles to depolymerize and achieving photo-triggered, controllable release of the immunoadjuvant. Under photodynamic action, this drug delivery material efficiently generates reactive oxygen species to induce immunogenic cell death in tumor cells. Simultaneously, the released immunoadjuvant activates the TLR7 / 8 pathway, promotes dendritic cell maturation, and enhances the systemic anti-tumor immune response, thereby inhibiting the growth of tumors in situ and at distant sites, and reducing the risk of metastasis and recurrence.

The invention relates to medical training aids. The claimed method includes preparing models of bone and cartilage structures and molds for blood vessel and thyroid models by 3D printing. A plastisol containing polyvinyl chloride is used for simulating a thyroid and blood vessels. This plastisol is poured into the molds for the blood vessel and thyroid models and held until it has cooled. A plastisol containing powdered graphite and a metal glitter for echogenicity is used for simulating lymph nodes and tumorous growths. Lengths of jute twine are laid in molds, into which a plastisol with added glitter is poured, the plastisol is held until it has cooled, and neck muscle models are cut out. A plastisol containing dyes is poured into a master neck mold to produce a skin model. The models of the muscles, vessels, thyroid, bone and cartilage structures, trachea, lymph nodes and tumorous growths are arranged in the master neck mold, into which a plastisol containing glitter is poured, the assembly is left to cool before being removed and the skin model is attached. The technical result is that the structure of the phantom more closely resembles the structure of a human thyroid.

The invention relates to the technical field of tumor immunotherapy, in particular to an RPL39L gene and application of a gene inhibitor of the RPL39L gene, and the RPL39L gene comprises an RPL39L gene knockout agent and small interfering RNA (Ribonucleic Acid) targeting the RPL39L gene. According to the invention, the cancer testosterone gene RPL39L is found to be ribosomeST for forming spermatogenic cell specific ribosomeST for the first time, and can regulate and control a plurality of downstream cancer testosterone genes. A gene inhibitor and small interfering RNA are designed for the RPL39L, the RPL39L is knocked out from various tumor cells such as osteosarcoma, colorectal cancer, leukemia and glioma by using a CRISPR / Cas9 technology, and the influence on the proliferation ability and migration ability of the tumor cells after the RPL39L is knocked out is proved in vitro; and shRNA of a target RPL39L coding region is designed, so that the expression level of the RPL39L in tumor cells is successfully inhibited, and the inhibition effect of the shRNA on the growth of the tumor cells is proved in vitro. The invention provides an effective means for inhibiting the expression of the cancer testosterone gene regulatory factor from the upstream, and has extremely important significance and application prospect in tumor treatment.

The invention provides an SLC16A3 inhibitor based on ferroptosis regulation and application of the SLC16A3 inhibitor in lung adenocarcinoma, and relates to the technical field of biological treatment drugs. The SLC16A3 inhibitor is a drug MSC-4381, the drug MSC-4381 is an effective SLC16A3 inhibitor, the SLC16A3 inhibitor can be used for inhibiting lactic acid transporter SLC16A3, breaking the redox steady state of tumor cells, inducing ferroptosis and remarkably enhancing the curative effect of the drug gefitinib, and in an in-vivo and in-vitro model, cell proliferation, migration and invasion can be inhibited through SLC16A3 knock-down or pharmacological inhibition, so that the SLC16A3 inhibitor can be used for preventing and treating the tumor cells. The MSC-4381 and the gefitinib are combined to promote lipid peroxidation and iron ion accumulation, the tumor growth can be obviously delayed through drug combination of the MSC-4381 and the gefitinib, the effect can be partially reversed through the Ferrostatin-1, the ferroptosis-dependent mechanism of the MSC-4381 and the gefitinib is verified, and transcriptional regulation and control of the SLC16A3 by the HIF1A and influence on ferroptosis resistance are clear. The invention provides a feasible combined medication strategy, verifies the significant tumor inhibition effect of the HIF1A-SLC16A3 axis in cell and animal models, reveals the key effect of the HIF1A-SLC16A3 axis in lung adenocarcinoma drug resistance formation, and provides a new combined treatment strategy and a new molecular target.

The present application relates to the technical field of biological medicine, and particularly relates to a tumor microenvironment responsive iron overload hydrogel, a preparation method and application thereof. The hydrogel anchors deferoxamine conjugate in the hydrogel network through thiol-maleimide click chemistry, does not affect intracellular Fe 2+ The Fenton reaction process occurs, and the excreted Fe 3+ is specifically captured and locked, iron ion loss and systemic diffusion are effectively prevented, and a long-acting iron overload microenvironment is constructed locally in the tumor; iron oxide nanoparticles release Fe 2+ in response to a weak acid microenvironment, hydroxyl radicals are catalytically generated, and the effect of the iron death inducer on the antioxidant pathway is synergistic, effectively inducing tumor cell ferroptosis and overcoming treatment resistance; the hydrogel has excellent biocompatibility, blood compatibility and targeted tumor inhibition activity, inhibits the growth of solid tumors while reducing systemic toxic side effects, and thus realizes efficient and safe local treatment of tumors.

The invention relates to a degradable magnesium metal catgut embedding set, preparation and application in tumor inhibition, and relates to the field of medical instruments, the degradable magnesium metal catgut embedding set comprises a degradable magnesium metal wire, a fixing sleeve and a rebound catgut embedding needle provided with a needle tube inner cavity; the rebounding catgut embedding needle comprises a lining core seat, a rebounding plastic part, a lining core, a needle seat and a stainless steel needle tube, the rebounding plastic part comprises a rebounding part and circular ring parts arranged at the two ends of the rebounding part, the circular ring part at one end of the rebounding part is arranged on the needle seat in a sleeving mode, and the circular ring part at the other end of the rebounding part is arranged on the lining core seat in a sleeving mode so as to be used for fixing the lining core seat. The lining core is inserted into the stainless steel needle tube, the lining core is connected with the stainless steel needle tube in a sliding mode, the degradable magnesium metal wire is arranged in an inner cavity of the needle tube of the rebounding catgut embedding needle, and the fixing sleeve is arranged at the needle point of the rebounding catgut embedding needle in a sleeving mode. The application has the effects of improving the accuracy of the tumor catgut embedding position and reducing and inhibiting tumor growth.

@biotinThe invention discloses a preparation method and application of a lipid bispecific antibody nanosheet capable of activating a cGAS-STING pathway to enhance anti-tumor immune response of cDC1 and PD-1 + T cells in the field of biological medicine, and the preparation method comprises the following steps: firstly, preparing an Mg0.2 Co0.8 (OH) 2 nanosheet, then wrapping the prepared Mg0.2 Co0.8 (OH) 2 nanosheet with liposome, then coupling biotin with a monoclonal antibody, and finally preparing the lipid bispecific antibody nanosheet capable of activating the cGAS-STING pathway to enhance the anti-tumor immune response of the cDC1 and PD-1 + T cells. Streptavidin is coupled with lipidosome of a nano cobalt magnesium tablet, LMC is finally fused with alphaCLEC9A (at) biotin and alphaPD-1 (at) biotin, Co < 2 + > and Mg < 2 + > released by MC enter cytoplasm, a cGAS-STING pathway is synergistically activated, DC is promoted to secrete IFN-1 and costimulatory molecules, and the antigen presentation capacity is enhanced; the bispecific antibody is combined with CLEC9A + cDC1 and PD-1 + T cells at the same time, promotes physical crosstalk of the CLEC9A + cDC1 and PD-1 + T cells in tumors and drainage lymph nodes, and activates CD8 + T cells to proliferate and differentiate into effector T cells; in a TC-1 tumor-bearing mouse, LMC-NBiE promotes CD8 + T cell infiltration and tumor cell apoptosis and inhibits tumor growth by inducing high expression of CLEC9A + cDC1 and cross presentation of tumor antigens.

The present invention relates to a drug delivery system with a micelle structure comprising a PEG2000-DSPE polymerized lipid and an APTEDB-PEG2000-DSPE polymer, and a preparation method thereof. The drug delivery system targets extra-domain B of fibronectin (EDB-FN), which is overexpressed in a brain tumor, and can pass through the blood-brain barrier (BBB) or the blood-brain tumor barrier (BBTB) to deliver a drug specifically to the brain tumor cells. In addition, the present invention can provide a pharmaceutical composition for diagnosing or treating a brain tumor, comprising the drug-loaded drug delivery system as an active ingredient. The composition can be accumulated inside the brain tumor and incorporated into the tumor cells to specifically inhibit tumor growth, and thus can be efficiently utilized for diagnosing or treating a brain tumor.

The invention discloses a composition, which comprises engineering bacteria for expressing TLS induced protein and mesenchymal stem cells, and can effectively induce TLS formation, inhibit tumor growth, improve systemic immunity, inhibit distant metastasis and prevent tumor recurrence in tumor tissues, thereby providing a new technical path for enhancing the universality and accessibility of immunotherapy. And an innovative platform is provided for the research on a combined treatment scheme of tumor immunotherapy.

Brain tumors remain the leading cause of cancer-related deaths in children and often are associated with long-term sequelae among survivors of current therapies. Telomerase and telomeres play important roles in cancer, representing attractive therapeutic targets to treat children with poor-prognosis brain tumors such as diffuse intrinsic pontine glioma (DIPG), high-grade glioma (HGG) and high-risk medulloblastoma (MB). It has shown that DIPG, HGG and MB frequently express telomerase activity. It is now shown that the telomerase-dependent incorporation of 6-thio-2′deoxyguanosine (6-thio-dG), a telomerase substrate precursor analog, into telomeres leads to telomere dysfunction-induced foci (TIFs) along with extensive genomic DNA damage, cell growth inhibition and cell death of primary stem-like cells derived from patients with DIPG, HGG and MB. Importantly, the effect of 6-thio-dG is persistent even after drug withdrawal. Treatment with 6-thio-dG elicits a sequential activation of ATR and ATM pathways and induces G2 / M arrest. In vivo, treatment of mice bearing MB xenografts with 6-thio-dG delays tumor growth, increases in-tumor TIFs and apoptosis. Furthermore, 6-thio-dG crosses the blood-brain barrier and specifically targets tumor cells in an orthotopic mouse model of DIPG. Together, these findings suggest that 6-thio-dG is a promising approach to treat therapy-resistant telomerase-positive pediatric brain tumors.

The application discloses a Dendrobium candidum composite extract with anti-lung cancer activity and a preparation method thereof, wherein the mass ratio of the Dendrobium candidum binzyl extract and the Dendrobium candidum polysaccharide is 1:1-1:2. The composite extract prepared by the application can inhibit the growth of Lewis lung cancer, and the effect is better than that of the binzyl or polysaccharide alone, and the composite extract plays a better synergistic effect, and is expected to be prepared into an anti-lung cancer drug. The application also establishes a detection method of the Dendrobium candidum composite extract, and the quality of the composite extract can be well detected.

The application discloses a construction method of a choroid melanin in-situ tumor animal model, and belongs to the technical field of biological medicine. The construction method comprises the following steps: providing tumor cells, wherein the tumor cells are mouse melanoma B16 cells; mixing luciferase-labeled tumor cells and biological gold medal matrix glue at 0-4 DEG C, and then injecting the mixture into the choroid layer through the suprachoroidal space of a mouse, so that the choroid melanin in-situ tumor animal model is obtained. The biological gold medal matrix glue is used as a carrier, the adhesion of the matrix glue and the cells is strong, and the cells can be uniformly dispersed in the matrix glue, so that the cells can be uniformly dispersed in the matrix glue. The matrix glue can be gelled in 1-3 minutes at room temperature, and can be rapidly solidified at 37 DEG C, so that the cells can be fixed in the choroid layer, and the real anatomical site of human choroid melanoma occurrence can be simulated. In addition, the matrix glue can provide a good nutrient environment for tumor growth, so that a single solid tumor can be formed by a tumor cell line in a short time.