Geschwulste * Tumors III : Modelle experimenteller Carcinogenese / Models of experimental Carcinogenesis

organ systems. Bronchogenic carcinoma in man develops as a result of chronic exposure to carcinogenic inhalants. Extensive studies on cigarette smokers 3 and 4 uranium miners have shown that a number of morphological abnormalities can be recognized in the bronchial mucosa prior to deve10pment of frank neopla- 5 sia. Similar lesions are experimentally induced in dogs exposed to tobacco smoke . Thus it appears that aseries of sequential histological and cytological changes develop, which with continued exposure to tobacco smoke eventually progress to invasive carcinoma. It is conceivable that some early epithelial lesions may become stationary or may even revert when carcinogen exposure is discontinued, 6 since the lung cancer risk of ex-smokers appears to dec1ine . This points to the potential practical usefulness of morphogenetic studies of experimentally induced respiratory tract neoplasms, provided the proper experimental model c1ose1y resembling human bronchogenic carcinoma is available, since it is much easier to reconstruct the deve10pment of sequential changes leading to invasive carcinoma in experimental than in human material. It should also be possible experimentally to distinguish between reversible and irreversible carcinogen-in- duced lesions and between toxic and carcinogenic changes. Knowledge obtained from such studies could he1p to improve the diagnosis of precancerous lesions and preinvasive carcinoma. As in most other areas of disease control, problems of early diagnosis and effective therapy are also c1ose1y linked in the treatment of lung cancer.

organ systems. Bronchogenic carcinoma in man develops as a result of chronic exposure to carcinogenic inhalants. Extensive studies on cigarette smokers 3 and 4 uranium miners have shown that a number of morphological abnormalities can be recognized in the bronchial mucosa prior to deve10pment of frank neopla­ 5 sia. Similar lesions are experimentally induced in dogs exposed to tobacco smoke . Thus it appears that aseries of sequential histological and cytological changes develop, which with continued exposure to tobacco smoke eventually progress to invasive carcinoma. It is conceivable that some early epithelial lesions may become stationary or may even revert when carcinogen exposure is discontinued, 6 since the lung cancer risk of ex-smokers appears to dec1ine . This points to the potential practical usefulness of morphogenetic studies of experimentally induced respiratory tract neoplasms, provided the proper experimental model c1ose1y resembling human bronchogenic carcinoma is available, since it is much easier to reconstruct the deve10pment of sequential changes leading to invasive carcinoma in experimental than in human material. It should also be possible experimentally to distinguish between reversible and irreversible carcinogen-in­ duced lesions and between toxic and carcinogenic changes. Knowledge obtained from such studies could he1p to improve the diagnosis of precancerous lesions and preinvasive carcinoma. As in most other areas of disease control, problems of early diagnosis and effective therapy are also c1ose1y linked in the treatment of lung cancer.