35results about How to "To achieve the effect of tumor treatment" patented technology

The invention provides two specific T cell receptors targeting G12V or G12C mutation epitopes of a KRAS gene and an anti-tumor application. The two T cell receptors respectively consist of an alpha peptide chain and a beta peptide chain. The invention also provides an antigen binding fragment of the T cell receptors, nucleic acid encoding the antigen binding fragment, a vector containing the nucleic acid, and a host cell containing the vector. The invention further provides a method for preparing a G12V mutation-specific T cell receptor of KRAS or an antigen-binding fragment thereof. The specific T cell receptor and the antigen binding fragment thereof can be used as immune effect activators to stimulate the immune response of the body, thereby generating the action effect of resisting tumors and other diseases.

The invention provides a preparation method of a carrier free nano drug for chemotherapy/light treatment. The drug is prepared by assembling a hydrophobic anticancer drug, a water soluble target, andan amphipathic photosensitizer through a self-assembly technology. The assembled carrier free nano drug is formed through phi-phi accumulation, hydrophobic force, and electrostatic force, is used forchemotherapy and light treatment, and solves the problems that in the prior art, the action mechanism of an artificially synthesized carrier is undefined, and metabolism and most of tumors cannot be inhibited effectively by a single treatment method and still grows slowly.

The invention relates to NIR-II conjugated nano particles and a preparation method and application thereof. The NIR-II conjugated nano particles comprise NIR-II conjugated small molecules and amphiphilic polymers; a structural formula of the NIR-II conjugated small molecules is as follows; and the amphiphilic polymers are self-assembled and encapsulated on the NIR-II conjugated small molecules. The nanoparticles have good biocompatibility, high NIR-II photothermal conversion efficiency, good photoacoustic imaging effect and NIR-II tumor photothermal therapy effect.

The invention discloses a mesoporous silicon nano assembly with tumor cell targeting and a preparation method thereof. The specific steps of the present invention are as follows: (1) first use the surfactant cetyltrimethylammonium bromide as a template, and tetraethyl orthosilicate as a silicon source, under alkaline conditions, at a temperature of 75-85°C The crude product is synthesized, and the surfactant is removed after post-treatment to obtain mesoporous silicon; (2) the mesoporous silicon and the drug are mixed in ethanol to obtain the drug-loaded mesoporous silicon; (3) the drug-loaded mesoporous silicon is treated with phosphate The buffer solution PBS is dispersed, added to the liposome membrane, first hydrated, and then homogenized to obtain the liposome-wrapped mesoporous silicon nanoparticles; (4) react the liposome-wrapped mesoporous silicon nanoparticles with HA Get the target material. The preparation method of the present invention is simple, and the obtained mesoporous silicon nano assembly can enhance the uptake of tumor cells to drugs from two aspects of targeting and preventing drug diffusion, so as to achieve the effect of treating tumors, and has obvious advantages in the treatment of tumors.

The invention discloses water soluble targeting-activated taxol derivatives as well as a preparation method and use thereof. The water soluble targeting-activated taxol derivatives have a following structural formula as shown in the specification, wherein the formula of taxol is also described in the specification, R1 is Ala, Thr, Val or Ile; R2 is Ala, Thr, Val or Asn; and n is equal to 1-150. Compared with taxol, the water soluble targeting-activated taxol derivatives provided by the invention become water soluble type anti-tumor targeting drugs, have specific activation characteristic and immunological enhancement characteristic, and good clinical application prospect, and is greatly improved in the drug action of inhibiting the tumor growth and metastasis, and greatly lowered in toxicity.

The invention belongs to the field of tumor gene therapy, and specifically relates to a recombinant mouse mIL-22BP vector and preparation methods and application of a liposome complex thereof. The invention, in view of the problem that a liposome complex having the murine IL-22BP gene has not been reported so far, provides the recombinant murine IL-22BP vector and the liposome complex thereof. Thevector contains a gene encoding mouse IL-22BP protein and can be used for expressing mouse IL-22BP protein in eukaryotic cells; after vector is combined with a cationic liposome to form the complex,the complex can well play a role of resisting colon cancer tumor tissue growth, has a tumor growth resisting effect, can be used for preparing drugs for diagnosis or treatment of tumors, and providesa new choice for tumor treatment.

The invention provides an application of a long-chain non-coding RNA RP11-224O19.2 inhibitor in preparation of a drug for treating tumors. The invention further provides a drug for treating the tumors, and a kit for liver cancer screening and/or liver cancer prognosis diagnosis. The application shows that the RNA RP11-224O19.2 inhibitor has a significant treatment effect on the tumors. In addition, the expression level of RNA RP11-224O19.2 is detected, and the long-chain non-coding RNA RP11-224O19.2 inhibitor can be applied to auxiliary diagnosis and prognosis judgment of a clinical liver cancer and is good in application prospect.

The invention discloses a complex frequency ultrasonic tumor treatment head. The complex frequency ultrasonic tumor treatment head is characterized by comprising an ultrasonic transducer, the ultrasonic transducer comprises a double-end stud, a rear cover board, a front cover board and an insulation sleeve located on the middle section of the double-end stud, and the rear cover board and the front cover board are located on a front thread section and a rear thread section of the double-end stud respectively and compress a first insulation ceramic wafer, a rear piezoelectric ceramic stack, a second insulation ceramic wafer, a mass block, a third insulation ceramic wafer, a front piezoelectric ceramic stack and a fourth insulation ceramic wafer which are sequentially connected to the insulation sleeve in a sleeved mode. A signal generator is utilized for transmitting two signal frequencies, the two piezoelectric ceramic stacks at the two ends of the mass block in the transducer are made to vibrate at different frequencies, the transducer works at a double-frequency mode, the cavitation effect is enhanced through the low frequency generated by difference frequency in the double frequencies, tumor angiogenesis is induced to form thrombus, a tumor nutrition feeding channel is blocked, and the effect of treating a tumor is achieved. The complex frequency ultrasonic tumor treatment head is simple in structure, low in manufacturing cost, and easy and convenient to operate.

The invention discloses a novel Pt(IV) complex with a tumor targeting function. The complex has a structure represented by the formula (I) or the formula (II). The invention discloses a preparation method of the novel Pt(IV) complex. According to the preparation method, an asymmetric ammonia ligand of a Satraplatin carrier group is maintained, a biotin ligand with a targeting function is introduced into one axial end, chloride is introduced into the other end so as to reduce the negative value of the redox potential of the platinum complex, the reducing power is increased at the same time; ora hydroxyl group of the other end is maintained, thus after the Pt(IV) complex enters a human body, the Pt(IV) complex can preferably combine with a reducing agent in the human body, and the Pt(IV) complex is reduced to obtain Pt(II) complex so as to treat the tumors. The provided Pt(IV) complex has antitumor activity on specific tumors, and the toxic effect and side effect are reduced. At the same time, the raw materials are cheap and easily available, the preparation method is simple and is easy to perform, the conditions are mild, the operation is easy, and the preparation method is suitable for large scale production. Z is Cl<->.

The invention provides a cervical cancer therapeutic vaccine based on recombinant attenuated Listeria monocytogenes and a preparation method of the cervical cancer therapeutic vaccine, and relates tothe field of genetic engineering. The attenuated Listeria monocytogenes Lemo-C07 are taken as a background, and a virulence factor LLO protein of the strain carries two key mutant amino acid sites, sothat the virulence of the strain is greatly reduced, but part of the proliferation ability in the cells is still retained. According to the vaccine, on the basis of the attenuated Listeria monocytogenes, a molecular biological technique is utilized to integrate a full-length gene of a specific antigen E7 of the cervical cancer to the downstream part of an LLO gene of the Listeria monocytogenes, thereby constructing and obtaining the recombinant attenuated Listeria monocytogenes containing the tumor specific antigen E7. The vaccine has the capabilities of presenting the specific antigen and activating the anti-tumor cellular immunity of the body, and has the remarkable tumor treatment effect.

The invention provides an anti-tumor ANXA1 derived polypeptide and an application thereof. A series of experiment results prove that the ANXA1 is combined with the EphA2 to protect the EphA2 from being ubiquitinated and degraded by the E3 ubiquitin ligase Cbl, and 20-30 amino acids (namely EYVQTVKSSKG) and 28-30 amino acids (namely SKG) at the N end of the ANXA1 are key regions for combining the ANXA1 and the EphA2. In order to block the combination of ANXA1 and EphA2, 20-30 amino acid polypeptides at the N end of the ANXA1 are synthesized in vitro, the cell-penetrating peptide TAT is used forentering the tumor cells, so that the combination of the ANXA1 and the EphA2 in the tumor cells can be obviously blocked, the combination of Cbl and EphA2 is increased, the ubiquitination degradationof the EphA2 is promoted, the in-vitro and in-vivo growth of the tumor cells is inhibited, and a remarkable anti-tumor effect is achieved. Therefore, the EYVQTVKSSKG polypeptide can be used for preparing antitumor drugs, and has important clinical application value.

The invention provides a T cell epitope specific T cell receptor m2P8D TCR of a human papilloma virus E6 gene, a humanized form h2P8D TCR of the T cell epitope specific T cell receptor m2P8D TCR, andantigen binding fragments of the m2P8D TCR and the h2P8D TCR, and provides nucleic acids encoding the m2P8D TCR, vectors containing the vectors, wherein the two T cell receptors are respectively composed of alpha and beta peptide chains, and also provides nucleic acids encoding the two T cell receptors, a vector containing the nucleic acids, a host cell containing the vector, and anti-tumor applications of the two T cell receptors. The invention further provides a T cell epitope specific T cell receptor m2P8D TCR of the human papilloma virus E6 gene, a humanized form h2P8D TCR of the human papilloma virus E6 gene and preparation methods of the T cell epitope specific T cell receptor m2P8D TCR and the humanized form h2P8D TCR. The two specific T cell receptors and the antigen binding fragments thereof can be used as immune effect activators to stimulate the immune response of the body, thereby generating the action effect of resisting tumors and other diseases.

The invention relates to the field of medicines, and in particular relates to polypeptide which can inhibit MYC carcinogenic protein and treat tumor. The sequence of the polypeptide is as shown in SEQ ID NO.1. The polypeptide has the application of tumor treatment. The application includes tumor treatment in multiple administration modes, including subcutaneous or intramuscular injection, intravenous injection or intravenous drip, and the like. The polypeptide has the beneficial effects that in-vitro proliferation activity of multiple tumor cells can be inhibited, MYC protein expression in tumor cells can be promoted, telomerase activity of a tumor cell can be inhibited, growth of tumor inside tumor model naked mice can be inhibited, and the survival rate of tumor-bearing mice can be increased. An effect of treating tumor can be achieved.

The invention discloses an application of a CAR-T cell targeting AXL, a third generation of CAR-T cell targeting AXL is prepared by using scFv protein targeting AXL, and the CAR-T cell is applied to tumor treatment, so that the problem that a tumor specific target is difficult to find when CAR-T is used for treating solid tumors is solved, target missing is effectively avoided, the probability of side effects is reduced, and the solid tumor treatment effect is improved. Based on high expression of the AXL in lung cancer, the AXL has a specific killing effect on lung cancer tissues with positive expression of the AXL, so that the treatment on the lung cancer is realized; especially, the cell acts on lung cancer cells which are resistant to EGFR-TKI due to up-regulation of AXL, and can significantly improve the treatment effect of lung cancer and overcome the poor treatment effect caused by drug resistance in cooperation with EGFR-TKI drugs in treatment of lung cancer.

The invention discloses a target spot for treating tumors, application of the target spot and a tumor treatment preparation. A series of studies find that PRMT5 and CD38 in nasopharynx cancer, cervical cancer and lung cancer cells interact with each other, and PRMT5 enables CD38 protein to generate arginine methylation, so that the self enzyme activity of CD38 is influenced. Particularly, the 58th amino acid of the CD38 protein is subjected to arginine methylation. In-vivo and in-vitro experiments prove that the 58th arginine of the CD38 protein is changed into a glycine mutant which enters tumor cells, so that PRMT5 cannot enable the 58th arginine of the CD38 protein to be methylated and inhibit the self enzyme activity of the CD38, and further the proliferation and in-vivo tumorigenicity of the tumor cells are promoted by influencing an NAD-SIRT1-p53 axis, so that the effect of treating tumors is achieved. The anti-tumor CD38 is obvious in fixed-point target effect and free of obvious toxic and side effects.