作者: Robert A. Kratzke , Eiji Shimizu , Frederic J. Kaye
DOI: 10.1007/978-1-4615-3088-6_3
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摘要: While the last 15 years have not yielded substantial improvements in diagnosis and treatment of lung cancer, this same period has experienced an extraordinary expansion our understanding cancer initiation progression. These investigations provided strong support for a multistep mechanism tumor induction progression [1,2] that previously could only be inferred from experimental animal models epidemiologic analyses. This recent work also revealed that, many cases, structural alterations gene products (for example, myc ras or p53 Rb genes) might critical steps genesis wide range adult tumors differing histologie origins. observations blur distinction investigators focusing on specific models, while at time offer hope advances any particular type will far broader implications. In addition, now genetic basis been well established, we are witnessing resurgence interest mechanisms environmental carcinogens as tools new generation prevention strategies [3]. There is currently no doubt use tobacco single most important (although only) causative factor development [4,5], these patterns abuse spread there projected worldwide increase incidence malignancies paralleling seen North America Europe over 50 years. Therefore, challenge immediate future to apply molecular clues obtained laboratory into effective preventive therapeutic applications. The purpose chapter review some more experiments concerning genetics identification (and implications) somatic mutations limited number cellular genes referred either dominant recessive oncogenes.