All terms in NCIT
| Label | Id | Description |
|---|---|---|
| Retrovector Encoding Mutant Anti-Cyclin G1 | NCIT_C49082 | [A replication-incompetent, pathotropic, tumor matrix (collagen)-targeted, retroviral vector encoding an N-terminal deletion mutant form of the cyclin G1 gene with potential antineoplastic activity. Under the control of a hybrid long-terminal repeat/cytomegalovirus (CMV) promoter, retrovector encoding mutant anti-cyclin G expresses the mutant cyclin G1 construct, resulting in disruption of tumor cell cyclin G1 activity and decreased cellular proliferation and angiogenesis. This agent preferentially targets collagen of the tumor matrix because of the incorporation of the collagen-binding domain of von Willebrand factor (vWF) on the retrovector surface. Exploiting the collagen-targeting mechanism of vWF permits delivery of the retrovector to tumor sites where angiogenesis and collagen matrix exposure occur.] |
| DNA Vaccine | NCIT_C39619 | [DNA vaccines are used in vaccination in way that differs from those are designed to be inserted into germ line of vaccines. Therefore, this is a vaccine not a therapy for modifying genetic information (gene therapy). Direct innoculation of DNA vaccine causes expression of the recombinant DNA by cells in the inoculated host. This expression of the recombinant DNA produces protein of interest that promotes antibody, cytolytic T cell and protective immune responses.] |
| Hemiasterlin Analog E7974 | NCIT_C49083 | [An analog of the sponge-derived anti-microtubule tripeptide hemiasterlin with antimitotic and potential antineoplastic activities. Hemiasterlin analog E7974 binds to the Vinca domain on tubulin, resulting in inhibition of tubulin polymerization and microtubule assembly; depolymerization of existing microtubules; inhibition of mitosis; and inhibition of cellular proliferation. This agent may have more affinity for the beta-3 tubulin isotype.] |
| Vinca-Domain Binding Agent | NCIT_C67422 | [Any of a class of anti-mitotic compounds that bind to the vinca site of the beta tubulin subunit, a region located within the middle domain of the tubulin structure and corresponding with a residue sequence approximating 177-215. The agent binds to the vinca site to produce a conformational change in the protofilament structure and at high concentrations, to induce the formation of spirals and crystal aggregates; these changes impair the polymerization of tubulin dimers and thereby, prevent the assembly of microtubules. The subsequent decrease in the amount of formed microtubules causes disassembly of the mitotic spindle resulting from instability of the structure during the mitotic interphase, eventually leading to cell cycle arrest and/or apoptosis. Vinca-site binding agents include natural compounds isolated from the periwinkle (Catharanthus roseus, formally, Vinca roseus) plant and synthetic compounds.] |
| Melanoma of the Ciliary Body and Choroid pT2a TNM Finding v7 | NCIT_C88692 | [Tumor size category 2 without ciliary body involvement and extraocular extension. (from AJCC 7th Ed.)] |
| Imetelstat | NCIT_C49084 | [A synthetic lipid-conjugated, 13-mer oligonucleotide N3'-P5'-thio-phosphoramidate with potential antineoplastic activity. Complementary to the template region of telomerase (hTR) RNA, imetelstat acts as a competitive enzyme inhibitor that binds and blocks the active site of the enzyme (a telomerase template antagonist), a mechanism of action which differs from that for the antisense oligonucleotide-mediated inhibition of telomerase activity through telomerase mRNA binding. Inhibition of telomerase activity in tumor cells by imetelstat results in telomere shortening, which leads to cell cycle arrest or apoptosis.] |
| Telomerase Inhibitor | NCIT_C2826 | [Any substance that inhibits telomerase, a ribonucleoprotein enzyme complex that adds telomeric sequences to the 3-ends of eukaryotic chromosomes. Telomerase is quiescent in most normal cells but active in most tumors.] |
| Antisense Oligonucleotides | NCIT_C1291 | [Antisense Oligonucleotides, short synthetic segments of DNA or RNA, designed with a sequence complimentary to a specific mRNA that target and bind with mRNA, causing inhibition of translation or overexpression of the protein encoded by the mRNA.] |
| Melanoma of the Iris pT3a TNM Finding v7 | NCIT_C88679 | [Melanoma of the iris with tumor confluent with or extending into the ciliary body, choroid, or both, with sclera extension and secondary glaucoma. (from AJCC 7th Ed.)] |
| Melanoma of the Iris pT3 TNM Finding v7 | NCIT_C88678 | [Melanoma of the iris with tumor confluent with or extending into the ciliary body, choroid, or both, with sclera extension. (from AJCC 7th Ed.)] |
| Melanoma of the Iris pT1c TNM Finding v7 | NCIT_C88675 | [Melanoma of the iris with tumor limited to the iris with secondary glaucoma. (from AJCC 7th Ed.)] |
| Melanoma of the Iris pT1 TNM Finding v7 | NCIT_C88672 | [Melanoma of the iris with tumor limited to the iris. (from AJCC 7th Ed.)] |
| Melanoma of the Iris pT2 TNM Finding v7 | NCIT_C88676 | [Melanoma of the iris with tumor confluent with or extending into the ciliary body, choroid, or both. (from AJCC 7th Ed.)] |
| Melanoma of the Iris Pathologic Primary Tumor TNM Finding v7 | NCIT_C88669 | [A pathologic finding about one or more characteristics of melanoma of the iris, following the rules of the TNM AJCC v7 classification system as they pertain to staging of the primary tumor.] |
| Melanoma of the Iris pT2a TNM Finding v7 | NCIT_C88677 | [Melanoma of the iris with tumor confluent with or extending into the ciliary body, choroid, or both, with secondary glaucoma. (from AJCC 7th Ed.)] |
| Flavonoid Tablet | NCIT_C74030 | [A tablet formulation of flavonoids with antioxidant and potential chemopreventive activities. Polyphenolic, soluble plant pigment flavonoids inactivate oxygen radicals, prevent lipid peroxidation, and inhibit DNA oxidation. In vitro, these agents have been shown to increase the rate of apoptosis, and inhibit cell proliferation and angiogenesis. Furthermore, flavonoids can induce conjugating enzymes, such as glutathione transferases and glucuronosyltransferases.] |
| Fluciclatide F 18 | NCIT_C74031 | [A radiopharmaceutical compound of a small synthetic cyclic peptide containing an RGD-sequence (Arg-Gly-Asp) labeled with the positron-emitting isotope fluorine F 18 that may be used to selectively image tumor cells and tumor vasculature by PET imaging. The RGD motif of fluciclatide F 18 selectively binds to the alphaVbeta3 integrin receptor, commonly upregulated on the surfaces of tumor cells and endothelial cells of tumor vasculature. This agent may be of use in visualizing and quantifying the development of tumor vascularity in response to antiangiogenic agents.] |
| Fluorine F-18 HX4 | NCIT_C74032 | [A 2-nitroimidazole labeled with the positron-emitting radioisotope fluorine F 18. HX4, the 2-nitroimidazole moiety of [F-18]HX4, is selectively bioreduced and bound in hypoxic tumor cells, permitting the imaging of hypoxic tumor cells with positron emission tomography (PET).] |
| Gallium Ga 68 F(ab')2-Trastuzumab | NCIT_C74033 | [A radioimmunoconjugate consisting of a trastuzumab fragment labeled with the positron-emitting radioisotope gallium Ga 68 with radioisotopic and antibody activities. Upon administration, Ga-68-labeled F(ab')2-trastuzumab may bind to HER2-positive tumor cells, allowing radioimmunolocalization with positron emission tomography (PET). Trastuzumab is a recombinant humanized monoclonal antibody that selectively binds to the extracellular domain of human epidermal growth factor receptor 2 (HER2), overexpressed by many adenocarcinomas, particularly breast adenocarcinomas.] |
| Endothelin B Receptor Agonist SPI-1620 | NCIT_C74027 | [A highly selective peptide agonist of the endothelin-B receptor. Endothelin B receptor agonist SPI-1620 binds to endothelin-B receptors on endothelial cells in tumor blood vessels, which, unlike the angioarchitecture of normal blood vessels, are relatively devoid of smooth muscle. This agent may induce a transient, selective increase in blood flow to a tumor, which may result in an increase in the delivery of anticancer agents to the tumor and, so, an increase in anticancer agent efficacy.] |