Cancer Therapeutics, Molecular Targets, Pharmacology and Clinical Applications--First International Conference 19-21 February 2004, Florence, Italy.
The treatment of cancer is currently undergoing a conceptual revolution due to the discovery of cancer pathways and mechanisms of oncogenesis. There are presently two complementary approaches in the field of cancer chemotherapy. Firstly, the development of "classical" anticancer agents aimed at the inhibition of cellular proliferation as a whole and bearing global cytotoxic properties that are aimed not only at cancer cells but also at all actively proliferative cells of the organism. Secondly, the development of "targeted" agents, which inhibit specific cancer targets including cyclin-dependent kinases, tyrosine kinase receptors and metalloproteases involved in cell invasion. These new molecularly targeted therapies are still experimental, with the exception of two or three compounds that have been marketed recently; a number of molecules, however, appear promising. It is generally believed that the "cytostatic" properties of classical compounds (in contrast to the cytotoxic properties) will avoid the general toxicity symptoms that usually accompany cancer chemotherapy, and that many of them will find specific indications in the cancers bearing the alteration they target. This renewal in the concept of anticancer drug discovery and development explains the emergence of new research groups involved in this field, and the continued interest in organizing meetings devoted to this rapidly expanding field. In addition, identification of the molecular targets of classical as well as novel agents, together with the completion of genome sequencing, has allowed the emergence of the science of pharmacogenomics, which tries to relate gene structure and/or expression to the activity of anticancer drugs. It is anticipated that in a few years from now cancer chemotherapy will no longer be prescribed as a function of the localization of the tumor (breast or colon, for example), but as a function of the oncogenic alteration (mutated Ras tumor, ErbB-2 amplifying tumor, etc), wherever it is localized. The paradigm of antibiotics and infectious diseases may well serve as a guide for this evolution.
Roberts
Jacques
J
Institut Bergonie, 229 Cours de l'Argonne, 33076 Bordeaux Cedex, France. robert@bergonie.org
D000818:Animals; D000970:Antineoplastic Agents / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use*; D016503:Drug Delivery Systems / Q000379:methods*; D015507:Drugs, Investigational / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use*; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy* / Q000235:genetics
D000970:Antineoplastic Agents; D015507:Drugs, Investigational