All terms in NCIT
| Label | Id | Description |
|---|---|---|
| True Histiocytic Lymphoma | NCIT_C35382 | [An antiquated term referring to large cell lymphomas.] |
| Hematopoietic and Lymphoid Neoplasm (Antiquated) | NCIT_C7340 | |
| Malignant Spindle Transitional Cell | NCIT_C60303 | |
| Malignant Transitional Cell | NCIT_C36778 | |
| Malignant Epithelial Spindle Cell | NCIT_C37109 | |
| Grade 2 Heartburn or Dyspepsia, CTCAE | NCIT_C60304 | |
| Heartburn or Dyspepsia, CTCAE | NCIT_C57818 | |
| Wheeze | NCIT_C60305 | |
| Two to 10 Mitoses per 10HPF | NCIT_C60306 | |
| Alvocidib | NCIT_C74940 | [The free base form of a synthetic N-methylpiperidinyl chlorophenyl flavone compound. As an inhibitor of cyclin-dependent kinase, alvocidib induces cell cycle arrest by preventing phosphorylation of cyclin-dependent kinases (CDKs) and by down-regulating cyclin D1 and D3 expression, resulting in G1 cell cycle arrest and apoptosis. This agent is also a competitive inhibitor of adenosine triphosphate activity.] |
| Cyclin-Dependent Kinase Inhibitor | NCIT_C2185 | [Any substance that inhibits cyclin-dependent kinase (CDK), an enzyme that catalyzes the addition of a phosphate group to a protein in the cell cycle regulation pathway. Inhibition of cyclin-dependent kinase results in cell cycle arrest and apoptosis.] |
| Enzyme Inhibition | NCIT_C40577 | [Enzyme Inhibition involves interference with, or restraint of, the function of a biological molecule that possesses catalytic activity.] |
| Cyclin-Dependent Kinase | NCIT_C17767 | [Cyclin-dependent kinases are eukaryotic, phosphoregulated protein kinases that associate with cyclins to control cell cycle progression.] |
| Negative Regulation of G2 to M Transition | NCIT_C19829 | [G2/M Arrest consists of cellular biochemical mechanisms, responsive to diverse conditions, that control cellular transition from the G2 to M phase of the cell cycle. Cdc2/cycB regulates this transition. During G2, Cdc2 is inactivated by Wee1 and Mt1 kinases. Activation of Cdc25 phosphatase activates Cdc2. If genome damage has occurred, activated DNA-PK/ATM/ATR kinases inactivate Cdc2/cycB by two channels. First, Cdc25 is inactivated by CHK kinases. Second, phosphorylated p53 dissociates from MDM2, is acetylated by p300/PCAF, binds DNA, and activates transcription of genes that inhibit Cdc2/cyclin (14-3-3s, GADD45, and p21Cip1).] |
| Negative Regulation of G1 Phase | NCIT_C19816 | [G1 Arrest consists of cellular biochemical mechanisms, responsive to diverse governing conditions (DNA damage, contact inhibition, growth factors, etc.), that control cellular progress through the G1 phase of the cell cycle. G1 progress is controlled by de/phosphorylated cyclin/CDK complexes. During G1, cycD/CDK phosphorylation of Rb/HDAC repressor permits E2F/DP1 transcription of genes that promote the G1/S switch and DNA replication. p53 induces p21 inhibition of cycD/CDK; Mdm2 inhibits p53/p21. TGF-b induces p15 inhibition of cycD/CDK. cAMP induces p27 inhibition of cycD/CDK. GSK3b induction of cycD degradation, and INK4, Kip, and Cdc25A regulate cycD/CDK activity.] |
| Protein Phosphorylation Inhibition | NCIT_C41600 | [Protein Phosphorylation Inhibition involves interference with, or restraint of, enzymatic activities involved in covalent transfer of a phosphate group from ATP to a protein via the action of a kinase. The major phosphoryl acceptors in proteins are serine, threonine, and tyrosine. Typically, such post-translational modifications regulate protein function.] |
| Epinephrine Hydrochloride | NCIT_C74941 | [The hydrochloride salt of the naturally occurring sympathomimetic amine with vasoconstricting, intraocular pressure-reducing, and bronchodilating activities. By stimulating vascular alpha-adrenergic receptors, epinephrine causes vasoconstriction, thereby increasing vascular resistance and blood pressure. When administered in the conjunctiva, this agent binds to alpha-adrenergic receptors in the iris sphincter muscle, resulting in vasoconstriction, a decrease in the production of aqueous humor, and a lowering of intraocular pressure. Through its beta1 receptor-stimulating actions, epinephrine increases the force and rate of myocardial contraction and relaxes bronchial smooth muscle, resulting in bronchodilation.] |
| Adrenergic Agonist | NCIT_C87053 | [Any agent that binds to and activates any of the adrenergic receptors.] |
| Anatomic Pathology Procedure | NCIT_C74942 | [A laboratory procedure that involves the examination of tissues or cells for diagnostic or research purposes.] |
| Laboratory Procedure | NCIT_C25294 | [Any procedure that involves testing or manipulating a sample of blood, urine, or other body substance in a laboratory setting.] |