Blocking and suppressing mechanisms of chemoprevention by dietary constituents. 2000

M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
MRC Toxicology Unit, CMHT Hodgkin Building, University of Leicester, Lancaster Road, PO Box 138, Leicester, UK. mmm2@le.ac.uk

Many dietary constituents are chemopreventive in animal models, and experiments with cultured cells are revealing various potential mechanisms of action. Compounds classified as blocking agents can prevent, or greatly reduce, initiation of carcinogenesis, while suppressing agents affect later stages of the process by reducing cell proliferation. Many compounds have both types of activity. Blocking mechanisms include alteration of drug metabolising activities and scavenging of reactive oxygen species. Mechanisms which suppress tumorigenesis often involve modulation of signal transduction pathways, leading to altered gene expression, cell cycle arrest or apoptosis. As our knowledge of how these dietary components affect cell biochemistry improves, so the likelihood of success in chemoprevention trials and in provision of dietary advice to the general population to optimise the chances of preventing disease is increased.

UI MeSH Term Description Entries
D007211 Indoles Benzopyrroles with the nitrogen at the number one carbon adjacent to the benzyl portion, in contrast to ISOINDOLES which have the nitrogen away from the six-membered ring.
D009369 Neoplasms New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms. Benign Neoplasm,Cancer,Malignant Neoplasm,Tumor,Tumors,Benign Neoplasms,Malignancy,Malignant Neoplasms,Neoplasia,Neoplasm,Neoplasms, Benign,Cancers,Malignancies,Neoplasias,Neoplasm, Benign,Neoplasm, Malignant,Neoplasms, Malignant
D002453 Cell Cycle The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE. Cell Division Cycle,Cell Cycles,Cell Division Cycles,Cycle, Cell,Cycle, Cell Division,Cycles, Cell,Cycles, Cell Division,Division Cycle, Cell,Division Cycles, Cell
D003474 Curcumin A yellow-orange dye obtained from tumeric, the powdered root of CURCUMA longa. It is used in the preparation of curcuma paper and the detection of boron. Curcumin appears to possess a spectrum of pharmacological properties, due primarily to its inhibitory effects on metabolic enzymes. 1,6-Heptadiene-3,5-dione, 1,7-bis(4-hydroxy-3-methoxyphenyl)-, (E,E)-,Curcumin Phytosome,Diferuloylmethane,Mervia,Turmeric Yellow,Phytosome, Curcumin,Yellow, Turmeric
D004032 Diet Regular course of eating and drinking adopted by a person or animal. Diets
D004791 Enzyme Inhibitors Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. Enzyme Inhibitor,Inhibitor, Enzyme,Inhibitors, Enzyme
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D015398 Signal Transduction The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. Cell Signaling,Receptor-Mediated Signal Transduction,Signal Pathways,Receptor Mediated Signal Transduction,Signal Transduction Pathways,Signal Transduction Systems,Pathway, Signal,Pathway, Signal Transduction,Pathways, Signal,Pathways, Signal Transduction,Receptor-Mediated Signal Transductions,Signal Pathway,Signal Transduction Pathway,Signal Transduction System,Signal Transduction, Receptor-Mediated,Signal Transductions,Signal Transductions, Receptor-Mediated,System, Signal Transduction,Systems, Signal Transduction,Transduction, Signal,Transductions, Signal
D016166 Free Radical Scavengers Substances that eliminate free radicals. Among other effects, they protect PANCREATIC ISLETS against damage by CYTOKINES and prevent myocardial and pulmonary REPERFUSION INJURY. Free Radical Scavenger,Radical Scavenger, Free,Scavenger, Free Radical,Scavengers, Free Radical
D016588 Anticarcinogenic Agents Agents that reduce the frequency or rate of spontaneous or induced tumors independently of the mechanism involved. Anti-Carcinogenic Agents,Anti-Carcinogenic Drugs,Anti-Carcinogenic Effect,Anti-Carcinogenic Effects,Anticarcinogenic Drugs,Anticarcinogenic Effect,Anticarcinogenic Effects,Anticarcinogens,Agents, Anti-Carcinogenic,Agents, Anticarcinogenic,Anti Carcinogenic Agents,Anti Carcinogenic Drugs,Anti Carcinogenic Effect,Anti Carcinogenic Effects,Drugs, Anti-Carcinogenic,Drugs, Anticarcinogenic,Effect, Anti-Carcinogenic,Effect, Anticarcinogenic,Effects, Anti-Carcinogenic,Effects, Anticarcinogenic

Related Publications

M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
June 2001, The Lancet. Oncology,
M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
January 1996, Preventive medicine,
M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
January 2000, Drug metabolism and drug interactions,
M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
April 1990, The American journal of pathology,
M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
January 2011, Molecular nutrition & food research,
M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
April 2001, Proceedings of the National Science Council, Republic of China. Part B, Life sciences,
M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
December 2015, Molecules (Basel, Switzerland),
M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
November 2018, International journal of molecular sciences,
M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
December 2012, Anti-cancer agents in medicinal chemistry,
M M Manson, and A Gescher, and E A Hudson, and S M Plummer, and M S Squires, and S A Prigent
February 2006, Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology,
Copied contents to your clipboard!