Cancer genetics and cell and molecular biology. Is this the way forward?
Lung cancer, the most prevalent cancer in the western world, is predominantly caused by smoking and thus perceived as a "self-inflicted" disease. Nevertheless, only 20% of smokers develop lung cancer. This review examines the concept of high-risk populations and screening. It looks at developments in the molecular epidemiology of the disease that shed new light on genetic changes that may predispose individuals to malignancy. Improvements in existing drug therapy are discussed as well as important new therapeutic developments, including antigrowth factors (antagonists G and D), antimetastatic agents (matrix metalloproteinase inhibitors), and natural products, arising from a greater understanding of signal transduction pathways and the process of cell metastasis.
Smyth
J F
JF
Department of Clinical Oncology, University of Edinburgh, Scotland.
D000959:Antihypertensive Agents / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000627:therapeutic use; D003647:Debrisoquin / Q000627:therapeutic use; D005109:Extracellular Matrix / Q000201:enzymology; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy / Q000235:genetics*; D008666:Metalloendopeptidases / Q000037:antagonists & inhibitors; D009842:Oligopeptides / Q000494:pharmacology; D010455:Peptides / Q000494:pharmacology; D011230:Precancerous Conditions / Q000235:genetics
D000959:Antihypertensive Agents; D000970:Antineoplastic Agents; D009842:Oligopeptides; D010455:Peptides; C095573:arginyl-tryptophyl-N-methylphenylalanyl-tryptophyl-leucyl-methioninamide; D008666:Metalloendopeptidases; D003647:Debrisoquin