79 results about "Inhibitory molecules" patented technology

We examined IQGAP1 copy gain and its relationship with clinicopathologic outcomes of thyroid cancer and investigated its role in cell invasion and molecules involved in the process. We found IQGAP1 copy number (CN) gain ?3 in 1 of 30 (3%) of benign thyroid tumor, 24 of 74 (32%) follicular variant papillary thyroid cancer (FVPTC), 44 of 107 (41%) follicular thyroid cancer (FTC), 8 of 16 (50%) tall cell papillary thyroid cancer (PTC), and 27 of 41 (66%) anaplastic thyroid cancer, in increasing order of invasiveness of these tumors. A similar tumor distribution trend of CN ?4 was also seen. IQGAP1 copy gain was positively correlated with IQGAP1 protein expression. It was significantly associated with extrathyroidal and vascular invasion of FVPTC and FTC and, remarkably, a 50%-60% rate of multifocality and recurrence of BRAF mutation-positive PTC (P=0.01 and 0.02, respectively). The siRNA knock-down of IQGAP1 dramatically inhibited thyroid cancer cell invasion and colony formation. Co-immunoprecipitation assay showed direct interaction of IQGAP1 with E-cadherin, a known invasion-suppressing molecule, which was upregulated when IQGAP1 was knocked down. IQGAP1, through genetic copy gain, plays an important role in the invasiveness of thyroid cancer and represents a useful prognostic marker and therapeutic target for this and other cancers.

Provided herein are methods for inhibiting tumor angiogenesis in a cancer patient, the method comprising administering to the subject an effective amount of a first isolated binding molecule which specifically binds to semaphorin-4D (SEMA4D) and an effective amount of a second isolated binding molecule which specifically binds to VEGF.

The present invention provides a gene delivery system containing nanoparticles. In more detail, the present invention provides a gene delivery system containing (a) a nanomaterial; (b) an oligonucleotide as an universal binding partner covalently linked to the surface of the nanomaterial; and (c) a cargo comprising (i) a complementary oligonucleotide containing a nucleotide sequence complementary to the universal binding partner as a binding counter-partner, and (ii) an inhibitory molecule having a nucleotide sequence complementary to a target gene of interest to be inhibited or an inducible molecule having a nucleotide sequence of a target gene of interest to be expressed. The present invention is a gene delivery system capable of feasibly deliver aptamer, siRNA, shRNA, miRNA, ribozyme, DNAzyme, PNA or gene as well as antisense oligonucleotide into the cells. In addition, the present invention is more efficient than the commercially available gene transfer reagent in respect to the degree of knockdown of target protein expression.

Provided herein are methods for inhibiting tumor angiogenesis in a cancer patient, the method comprising administering to the subject an effective amount of a first isolated binding molecule which specifically binds to semaphorin-4D (SEMA4D) and an effective amount of a second isolated binding molecule which specifically binds to VEGF.

The invention discloses a preparation method of a high-efficiency killer cell preparation adopting an immunodetection point dual-block CTL (cytotoxic lymphocyte). The preparation method comprises steps as follows: step 1), collecting mononuclear cells in peripheral blood; step 2), performing DC (dendritic cell) separation and T cell separation on the separated mononuclear cells with an adherence method; step 3), adding adhering DCs to a serum-free culture medium containing GM-CSF (granulocyte-macrophage colony-stimulating factor) and IL-4 (interleukin-4) for preparation of a DC vaccine; step 4), adding suspending T cells to CD3 and IL-2 for T cell culture and amplification; step 5), adding antigen-supported DCs to the amplified T cells for preparation of the CTL, and adding PD-1 (Programmed death 1) and CTLA-4 (cytotoxic t lymphocyte associated antigen-4) antibodies for preparation of the cell preparation with the dual-block CTL effect. According to the novel technology and the novel method provided by the invention, an immune brake effect is effectively regulated and T cell depletion is retarded by blocking inhibitory molecules on the tumor specific CTL surfaces, so that the tumor cytotoxicity of CTL effector cells is substantially improved.

The present invention provides RNA purification and / or analysis methods that use ammonium sulfate to mitigate or neutralize inhibitory effects of certain molecules. Exemplary inhibitory molecules that interfere with RNA function or analysis are those that bind to or cleave RNA, or stabilize RNA secondary structures.

Demineralized bone matric (DBM) and native bone morphogenetic protein (nBMP) are complex mixtures of non-collagenous bone proteins. These mixtures contain many of the BMPs that are available as recombinant molecules. Information regarding the presence in these materials of molecules that may affect the availability and activity of the BMPs is very limited. A chemical extraction of DBM, such as using alkali-urea produces a water soluble extractate which inhibits the osteogenic activity of DBM. Noggin, an extracellular BMP ligand antagonist is found in the water soluble extractate from DBM. Differential chemical extraction is a useful means of removing non-osteogenic, or osteogenic inhibitory molecules from DBM and nBMP.

The invention discloses microRNA (micro ribonucleic acid) for regulating gene expression of B7-H3 (a molecule of the B7 family). The microRNA is nucleic acid, functional segment or variant including a sequence of 5'-UGAGAUGAAGCACUGUAGCUC-3'. The microRNA is miR-143. Performed in-vitro biological function tests show that hsa-miR-143 is capable of inhibiting molecular expression of the B7-H3 by bonding with 3'-UTR (untranslated regions) of the B7-H3 gene, and antitumor effect is achieved by regulating a signal path of the B7-H3 and / or expression and functions of the miR-143.

Compositions and method for stimulating and controlling arteriogenesis and lymphatic vasculature by preventing and / or reducing the cellular interaction between RAF1 and AKT have been developed. The compositions include molecules that increase the bioavailability of non-phosphorylated RAF1, for example, the RAF1 Ser259 to Ala259 mutant in (RAF1 S259A), and AKT1 inhibitory molecules. Defects, disorders or diseases of insufficient blood or lymphatic vasculature are treated by administering to a patient in need thereof, a pharmaceutical composition comprising a molecule specifically blocking RAF1-AKT crosstalk in a pharmaceutically acceptable carrier or excipient in an amount effective to enhance the growth of blood or lymphatic vasculature in the patient. Compositions can be administered by injection or by controlled or sustained release devices, coating on devices or implants, microparticles, bulking agents or depots, or other techniques providing controlled or sustain release over a period of time effective to induce blood or lymphatic vasculature growth as desired.