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Anticancer Drugs in Clinical Use - DNA as Target for Anticancer Agents (CROSBI ID 618273)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | domaća recenzija

Jadrijević-Mladar Takač, Milena ; Kos, Ivan Anticancer Drugs in Clinical Use - DNA as Target for Anticancer Agents // Program and Book of Abstracts, CROPBSA-CEEPUS Summer University on Tumors / Juretić, Dubravka (ur.). Zagreb: Farmaceutsko-biokemijski fakultet Sveučilišta u Zagrebu, 2004. str. 14-15

Podaci o odgovornosti

Jadrijević-Mladar Takač, Milena ; Kos, Ivan

engleski

Anticancer Drugs in Clinical Use - DNA as Target for Anticancer Agents

Cancer is a leading cause of death throughout the world. More than ten million new cancer cases occur annually and disease causes over six million deaths a year. The global burden of this disease continues to rise. Evidence indicates that up to 80% of human cancer is potentially preventable since the factors that determine the incidence are largely environmental. These exogenous etiologic factors include dietary factors, cigarette smoking, radiation, occupational and environmental chemicals, socio-economic factors, specific parasites, bacteria, viruses and exogenous hormones in women. In addition, endogenous factors, such as hereditary, immunological and hormonal factors and gene/environment interactions play critical roles in individual suspectibility. However, the exogenous factors are clearly most amenable to interventions targeted at primary prevention of cancer. The specific approach used to treat cancer depends upon the specific type, location, and storage of the cancer. Regardless of the specific details, there are several fundamental techniques available to treat cancer including surgery, radiation therapy, immunologic treatment, and chemical based approaches. Generally, a combination of these methods is used, and in most therapeutic approaches to the treatment of cancer there will be a chemical component. The DNA molecule is essential for the growth of all living cells, and so far it has been the main target for anticancer drug action. Some of these drugs act directly on the DNA molecule, either by drug induced DNA damage or by some kind of alteration of DNA, whereas other drugs prevent nucleic acid synthesis by inhibiting one or more enzymes involved in the DNA synthesis, or by disturbing the DNA function by incorporation of ''wrong pieces'' into the DNA molecule. The DNA interacting drugs prevent cell growth, but not only cancer cell growth. Unfortunately, the growth of normal cells is also blocked. The cytotoxic effect is most serious on rapidly dividing cells, i.e. in addition to tumour cells the cells of normal bone narrow, gut, skin epithelium, and mucosa of the mouth. The lack of selectivity of cancer drugs is one of the main problems in cancer chemotherapy. All the known abnormal biological phenomena of cancer cells (e.g. excessive cell proliferation, loss of tissue-specific characteristics, invasiveness, and metastasis) seem to based on normal biological function of the cells, e.g. by use of normal enzyme systems. The abnormality of malignant tumour growth is connected to the regulation of cell growth and caused by mutations in control genes, which are converted to oncogenes. The introduction of gene therapy might be a very important step forward in the treatment of cancer in the future. In most gene therapies full, healthy genes are introduced as substituents for wrong versions, but blocking of bad genes by a drug might also be possible. It should be noticed that most anticancer drug interfering with DNA or DNA synthesis also exhibits a variety of actions on other targets in cells. The classification of anticancer drugs is based on the mode of action of the specified anticancer agents, which is generally believed to be responsible for the cytotoxic activity. Anticancer drugs that are in clinical use have three different target levels for their action, and they are as it follows: 1.DNA as target for anticancer drugs (alkylating agents, metal complexes binding to DNA, degradation of DNA, intercalating agents and antisense agents) 2.Drugs interfering with DNA synthesis (inhibitors of: tetrahydrofolate synthesis, purine and pyrimidine synthesis, DNA/RNA polymerases and ribonucleotide reductase), and 3.Mitotic apparatus as target for drugs (drugs interfering with the vinca alkaloid binding site of tubulin, drugs interfering with the colhicine binding site of tubulin, and drugs interfering with the assembled microtubules, taxol). One of the most serious problems in cancer chemotherapy is the development of the drug resistance. Multidrug resistance (MDR) is characterized by cross-resistance to a group of structurally and mechanistically distinct antitumour agents including the anthracyclines (daunomycin and adriamycin), the vinca alkaloids (vincristine and vinblastine), colchicine and podophyllotoxins, and actinomycin D. However, this resistance does not extend to all anticancer agents, for example antimetabolites (e.g. methotrexate, cytarabine, and thioguanine) and alkilating agents (carmustine and cyclophosphamide) are not affected. Drugs can influence the functioning of the DNA molecule in different ways. Damage to DNA, where covalent bond formation is involved, is performed by category of compounds usually called akylating agents, including some anticancer antibiotics, and by cis-platinum complexes. Breakdown of the DNA molecule (DNA strand scission) is caused by other antibiotic agents. The intercalating agents disturb DNA function by intercalating between the base pairs, but normally without bond breakage or formation. Antisense anticancer agents are designed to perform their action on nucleic acids (cancelling of specified base sequences) by combination of intercalating and alkylating abilities, in addition to hydrogen bonding and hydrophobic interactions. References 1.World Health Organization, World Cancer Report 2003, Iarc Press, Lyon, France, 2003. 2.Callery, P., gannet, P., Cancer and cancer chemotherapy. In Foye's Principles of Medicinal Chemistry, edited by D. A. Williams, T. L. Lemke, 5th Ed., Lippincott Williams and Wilkins, Baltimore 2002, 924-951. 3.Larsen, K. I., Anticancer agents. In Textbook of Drug Design and Development, edited by P. Krogsgaard-Larsen, T. Liljifors, U. Madsen, 2nd ed., Harvard Academic Publishers, Amsterdam, The Netherlands, 1996, 460-507. 4.Lown, J. W., The chemistry of DNA damage by antitumour drugs. In Molecular aspects of Anti-cancer Drug Action, edited by S. Neidle, M. J. Warning, The Macmillan Press, London 1983, 283, 314. 5.www.immunomedics.com

Anticancer drugs; DNA; Cancer chemotherapy

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Podaci o prilogu

14-15.

2004.

objavljeno

Podaci o matičnoj publikaciji

Program and Book of Abstracts, CROPBSA-CEEPUS Summer University on Tumors

Juretić, Dubravka

Zagreb: Farmaceutsko-biokemijski fakultet Sveučilišta u Zagrebu

Podaci o skupu

CROPBSA-CEEPUS Summer University on Tumors

pozvano predavanje

21.07.2004-28.07.2004

Zadar, Hrvatska

Povezanost rada

Farmacija