789 results about "Tumor inhibition" patented technology

The present invention relates to novel uses of AIM3 acting as a tumor suppressor, and more particularly to methods for using an AIM3 protein or a nucleic acid encoding the protein to activate ATM or ATR and to treat ATM- or ATR-mediated diseases. The AIM3 protein according to the present invention interacts directly with ATM/ATR so as to activate ATM/ATR and proteins regulated by ATM/ATR. Also, the AIM3 protein upregulates tumor suppressor gene p53 and its target genes so as to not only inhibit the proliferation of cells but also to induce apoptosis.

The present invention relates to oncogenes or tumor suppressor genes, as well as other genes, involved in prostate cancer and their expression products, as well as derivatives and analogs thereof. Provided are therapeutic compositions and methods of detecting and treating cancer, including prostate and other related cancers. Also provided are methods of diagnosing and/or prognosing prostate cancer by determining the expression level of at least one prostate cancer-cell-specific gene, including, for example, the ERG gene or the LTF gene alone, or in combination with at least one of the AMACR gene and the DD3 gene.

The invention discloses pyridylpyrimidyl amine compounds or pyridylpyridyl amine compounds disclosed as Formula I and application thereof in preparing antineoplastic drugs, belonging to the technical field of drugs. The compounds can selectively inhibit CDK4 and CDK6, enable G1-period tumor cells to stop growth and G1-period tumor cells to reduce, can effectively lower the phosphorylation of the tumor inhibiting protein Rb in the Ser780 site, and thus, can be used for various diseases caused by cell cycle control maladjustment participated by CDK4 and CDK6. The compounds are especially suitable for treating malignant tumors, and have the characteristics of high selectivity, high activity and high tumor cell proliferation resistance.

The invention belongs to the technical field of medicament, and particularly relates to preparation and application of phycocyanin extract. The phycocyanin extract is prepared by the following steps of: crushing spirulina cell walls of spirulina powder to obtain a crude extract by a repeated freeze-thawing method at the temperature of between 20 DEG C below zero and 4 DEG C; depositing the crude extract to obtain a crude protein extract by using 50 to 60 mass percent of ammonium sulfate; and then extracting and purifying the crude protein extract by adopting double aqueous phases, and removing salt by using excess infiltration to obtain phycocyanin extract solution. The phycocyanin extract mainly comprises phycocyanin, and the aqueous solution of the phycocyanin extract has the absorbance characteristics that A620/280 is slightly equal to 3.0+/-0.2 and A620/650 is slightly equal to 2.2+/-0.1. The phycocyanin extract is obtained by mainly combining the processes of ammonium sulfate deposition, double aqueous phase extraction, dialysis and salt removal and the like; and the phycocyanin extract administrated to S180 sarcoma mice with different dosages shows good tumor inhibiting effect and has no obvious toxicity on the spleen and the thymus gland.

The present invention relates to a harmine derivative compound and the application. The compound is produced through the structural modification of the 1st, 2nd, 3rd, 7th and 9th pint of the parent nuclear of the beta-carboline of the harmine; thus the novel harmine derivative compound is synthesized with the enhanced anti-tumor activity and no toxicity of the nervous system. Through the screening research of the vitro and vivo anti-tumor model, the harmine derivative compound is found to have the significant anti-tumor activity (the tumor-inhibition rate of the tumor-bearing mice model reaches as high as 63.5 percent), have no neurotoxicity, and have the prospects of clinical application. The preparation method of the compound is simple; the collection rate is high; and the compound is used for the drugs of treating various tumor diseases.

The invention discloses a micro-molecule polypeptide TAT-p53DM and an application thereof to preparing a medicine for treating or preventing ischemic stroke. A fusion protein polypeptide TAT-p53DM of a TAT protein transduction domain and p53DM is artificially synthesized; TAT carries p53DM protein polypeptide to pass through a blood brain barrier through blood so as to be taken by nerve cells; used in an in-vitro and in-vivo ischemic stroke model, the micro-molecule polypeptide TAT-p53DM is capable of effectively playing a biological role in blocking binding between death domain of death associated protein kinase 1 (DAPK1DD) and tumor suppression protein p53DNA binding motifs (p53DM), inhibiting signals capable of causing neuronal apoptosis and necrosis at DAPK1 downstream, and reducing ischemic stroke brain injury; moreover, molecular targets are provided for further developing medicines for clinically treating ischemic stroke.

The invention provides a water-soluble fullerene derivative, composite and the applications in the preparation process of medicament used for inhibiting growth and transfer of tumor; the derivative is fullerols presented by a general formula: C60OxHy; wherein, y is more than 10 and less than or equal to x; x is less than 50 and more than or equal to y; alternatively, the derivative is fullerene carboxyl derivative presented by the general formula C60(C(COOH)2)n; wherein, n is equal to 1-3; the tumor inhibiting composite comprises the grains of the water-soluble fullerene derivative and pharmaceutically acceptable carrier. The invention has the advantages that: compared with cyclophosphamide, cisplatin, paclitaxel, and the like, which are generally applied to clinic at present; the fullerols and carboxylic fullerene nano grains have small dosage, low toxicity and can inhibite the growth and transfer of the tumor.

The present invention provides methods and compositions for the suppression of oncogenic transformation, tumorigenesis and metastasis. The present invention discloses functional domains of E1A responsible for the suppression of transformation, and provides mini-E1A constructs that can be used for tumor suppression. The invention also discloses methods for the novel use of mini-E1A in combination with chemotherapeutic drugs and/or tyrosine kinase inhibitors.

The invention discloses a method for refrigerating, vacuum-drying and purifying ganoderma spore powder, which comprises the following steps of: adding water into ganoderma spore powder raw material while stirring and uniformly dispersing the ganoderma spore powder raw material; standing, removing upper layer floating matter and removing deposit; filtering intermediate solution and removing impurities; filtering and pressing filtrate, smashing the filtrate, adding purified water, mixing the filtrate with the purified water uniformly to obtain mixed suspension and carrying out refrigeration vacuum drying process to obtain the ganoderma spore powder. The method enhances the cleanliness, purity and bioactivity, keeps physical properties such as color, fragrance and flavor and the like, and can ensure that ganoderma spore biological protective film which can cause immuno reaction on human body is fully removed and the ganoderma spore powder truly becomes a kind of purely natural safe green food; and the obtained ganoderma spore powder has a low moisture content and is beneficial to long-time storage of product. The ganoderma spore powder refrigerated and dried by adopting the method is loose in texture. The method is beneficial to reduction of wall damaging times and improvement on the wall damaging rate, and can remarkably improve the tumor inhibition rate of the ganoderma spore powder.

Mutations to the tumor suppressor protein p53 have been observed in 40-60% of all human cancers. These mutations are often associated with high nuclear and cytoplasmic concentrations of p53. Since many tumors exhibit highly elevated p53 levels, the protein is an attractive target for cancer immunotherapy. Unfortunately, p53 is an autoantigen that is likely to be tolerated as a self-protein by the immune system. The present invention is based on the discovery that this self-tolerance can be overcome by administration of recombinant modified vaccinia Ankara (MVA) containing a nucleic acid that encodes p53 (rMVAp53). The invention discloses a method of generating a p53-specific CTL-response to tumor cells expressing mutated p53 by administering a composition comprising rMVAp53. Administration of rMVAp53 decreases tumor development, tumor growth, and mortality in a variety of malignant cell types. These effects are enhanced by administration of CTLA-4 blocker and/or CpG oligodeoxynucleotide immunomodulators.

Relating to the technical field of pharmaceutical preparations, the invention provides an antibody composition preparation composed of Trastuzumab and Pertuzumab. The antibody composition preparation has better tumor treatment activity. Compared with the independent treatment of Trastuzumab and Pertuzumab, the composition preparation shows a synergistic effect of the two antibodies, and can reach a tumor control rate of 92.43%. And the preparation provided in the invention has better stability, thus being in favor of long-term preservation of the antibody composition preparation. The antibody composition preparation provided in the invention is applicable to preparation of drugs treating diseases or symptoms suited to anti-HER2 antibody therapy. During application, the antibody composition preparation disclosed in the invention is used with a chemotherapeutic agent jointly or sequentially.

The invention discloses an acid sensitive polymer prodrug, nanoparticles of the prodrug and application of the nanoparticles. In the acid sensitive polymer prodrug, a polymer precursor is a vinyl ether-functionalized water-soluble A-B type two-block polymer; drug molecules are linked with the A-B type two-block polymer through an acetal bond; the acid sensitive polymer prodrug is self-assembled in water solution to form predrug micellar nanoparticles in which a polyethylene glycol hydrophilic chain segment serves as an outer surface and an anti-cancer drug bound to a polymer main chain through the acetal bond serves as a hydrophobic core. The pH sensitive prodrug and the nanoparticles of he prodrug are simple in preparation method, and good in tumor inhibitory effect; the nanoparticles also can efficiently encapsulate another hydrophobic anticancer drug; the kill capability to the cancer cell is enhanced; and the efficiency of endocytosis of the cell to the nanoparticles can be enhanced by coupling specific target molecules onto the surfaces of the nanoparticles. Thus, the inhibitory effect on the tumor cell is enhanced.

The invention relates to the technical field of medicines, and provides a docetaxel and sulforaphane loaded hyaluronic acid modified poly(lactic-co-glycolic acid) copolymer self-assembled nano-particle, a preparation method thereof and an application of the self-assembled nano-particle in preparing a medicine for treating breast cancer. The microscopic structure of the nano-particle comprises a hydrophobic PLGA (poly(lactic-co-glycolic acid)) core and a hydrophilic HA (hyaluronic acid) shell, wherein the PLGA core is used for wrapping a medicine DTX (docetaxel) or SFN (sulforaphane), and the hydrophilic shell HA can target a breast cancer stem cell highly expressing a CD44 receptor. In-vitro cytotoxicity tests indicate that the drug-loaded nano-particle can play a good role in resisting differentiation of mammary gland cells and breast cancer stem cells when compared with free medicines; in-vivo tumor inhibition experiments indicate that the drug-loaded medicine is more effective than free medicines and combined free medicines, and has a small systematic toxicity. The nano-particle can play a role in simultaneously performing target differentiating on mammary gland cells and breast cancer stem cells, and a new strategy is provided to treatment of breast cancer.

The invention belongs to the technical field of medicine, and relates to diphenyl selenide, diphenyl selenoxide, diphenyl selenone compounds and related compounds thereof, wherein the structure is represented by the following formula. The present invention further provides pharmaceutically acceptable non-toxic salts and hydrates formed by the compounds represented by the structure formula, wherein the pharmaceutically acceptable non-toxic salts comprise salts formed by the derivatives and acids or bases. Pharmacological activity experiment results show that the derivatives have good tumor inhibition activity, and can be used as tumor cell proliferation inhibitors and tumor vascular disrupting agents to be used for antitumor drug preparation.

The invention provides a nanogel with hydrophilic and hydrophobic reversal, charge reversal and intracellular redox responsiveness on the basis of pH regulation. The nanogel is prepared by cross-linking of thermo-sensitive monomer with controllable radical polymerization, amphoteric ionic monomer and amido-containing pH sensitive monomer through a disulfide-bond-containing cross-linking agent. The invention further provides a nanogel drug carrier system with smart response to tumor microenvironment and its preparation method. On the condition of blood pH 7.4, the nanogel is in a hydrophilic swelling state that is favorable for avoiding being phagocytosed by the reticuloendothelial system (RES) and accordingly, the nanogel has blood long circulation capacity; on the condition of tumor tissue subacidity, the state of the nanogel is reversed into a hydrophobic shrinking state that is favorable for the nanogel to realize effective concentration, depth penetration and be absorbed effectively by tumor cells on the tumor location. Besides, in the intracellular lysosome environment, negative charge of the nanogel is reversed into positive charge, which is favorable for the nanogel to escape from the lysosome; and then the nanogel releases drugs responsively in cytoplasm high-GSH environment, thereby achieving a good tumor inhibition effect.

The invention relates to a tumor inhibitory peptide capable of being specifically bound with PD-1 and an application thereof. The inhibitory peptide can be bound with an extracellular region of a PD-1 protein receptor and can effectively close a PD-1 protein at protein level and cellular level and prevent the PD-1 protein from being bound with a ligand PD-L1. The polypeptide has good biological activity. The polypeptide can be used in tumor immunotherapy alone or combined with an anti-PD-1 monoclonal antibody or other anti-tumor drugs as well as diagnosis and screening of a PD-1 positive tumor patient, namely the polypeptide can be applied to preparation of drugs used for treating tumor and autoimmune diseases.

This invention relates to the engineering of animal cells, preferably mammalian, more preferably rat, that are deficient due to the disruption of tumor suppressor gene(s) or gene product(s). In another aspect, the invention relates to genetically modified rats, as well as the descendants and ancestors of such animals, which are animal models of human cancer and methods of their use.

Compositions suitable for use as adjuvants in the preparation of vaccines, particularly those vaccines useful in the treatment of cancer, are provided. Methods for inhibiting tumor growth in an animal are also disclosed. Methods for immunizing an animal against cancer, such as prostate cancer, are also described. The adjuvants described are comprised of an extracellular matrix material, such as small intestinal submucosal (SIS) tissue. The preparations may take the form of sheets, gels, liquids (injectable), trocar, or other solid or semi-solid preparation. The invention provides for enhanced tumor inhibition of 2-fold or greater, compared to vaccine preparations without the extracellular matrix material, or from 4- to 5-fold, compared to preparations without the adjuvant promoting extracellular materials.