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Although the peak of lung cancer incidence among men in North America, Australia, New Zealand, and northwestern Europe was reached in the 1980s, the rate for men in southern and eastern Europe and for women continued to increase, at least until the 1990s. In other parts of the world, where smoking is still increasing, mortality due to lung cancer will increase dramatically in the next decades. The geographic variation and trends in incidence were closely associated with past smoking behavior. The trend toward smoking more low-tar filter cigarettes probably caused the increase in the incidence of adenocarcinoma. This tumor type is already the major histological subtype in North America and may also become the major type in other countries in the near future. Lymphatic and hematogenous metastases are often present at the time that lung cancer is diagnosed, and prognosis is still very poor. The prognosis for non-small-cell lung cancer has only slightly improved, while considerable progress has been made in the short-term survival of small-cell lung cancer since the introduction of chemotherapy in the 1970s. Due to a growing proportion of elderly lung cancer patients, more patients present with serious comorbidity at diagnosis of cancer. This may complicate treatment and indicates the need for adapted guidelines for these patients, who usually are not entered in clinical trials.

Carcinogens have clearly shown to be present in cigarette smoke. Their activation to highly reactive metabolites contributes to the potential insults to DNA, RNA, and proteins- altering a system of “gatekeepers and caretakers” and permitting cells to transform into clones that develop into a neoplasm. Alterations in the detoxification and repair capacity pathways contribute to the perpetuation of DNA damage to linger and burden the system. Further studies are needed to link carcinogens to their full responsibility in tumorigenesis in relation to tobacco. However, there is little doubt that they play an important role in the process.

Many lung cancer models are available, but none accurately reflect every aspect of human lung cancer. Each has its own advantages and disadvantages that should be understood and evaluated before their use. In selecting the best model system, consideration should be given to the genetic stability and heterogeneity of the transplanted cell line, its immunogenicity within the host animal, and the appropriate biologic endpoints. There is increasing pressure on the research community to reduce, or even eliminate the use of animals in research. However, relevant animal model systems provide the appropriate interface between the laboratory bench and a patient’s bedside for continued progress in cancer research and drug development. As in many other diseases, even more sophisticated lung cancer models will be needed in the future, as the complexities of this devastating disease are slowly unraveled.

In contrast to most other organs, the lungs are prone to a very wide range of epithelial tumors, varying in their location and histology. These tumors show varying degrees of relationship to smoke exposure, with the central carcinomas showing the greatest relationship. The molecular lesions from in these tumors share certain common elements and exhibit characteristic changes. Their precursor lesions also differ, with some being well defined and others being poorly understood because of the difficulty of identifying them prior to surgical resection of an existing tumor. Thus, their natural history is also poorly understood. The advent of newer diagnostic procedures such as fluorescence bronchoscopy and high-resolution CT scanning will aid in their diagnosis and permit us to study their natural history.