THE demonstration that isoniazid (INH) is carcinogenic for the lungs of mice (Juhasz, Balo and Kendrey, 1957) raised a new type of cancer problem. Most known carcinogens are avoidable as human hazards and many are subject to restrictive legislation. However, INH is a valuable life-saving drug in the control of tuberculosis, and the assessment of it as a potential carcinogenic hazard for man is therefore a matter of unusual concern. Moreover, it must be noted that the induction of pulmonary alveolar adenoma or adenocarcinoma in mice by a variety of chemically dissimilar carcinogens (e.g. urethane and 4-nitro-quinoline-N-oxide) is most striking in those strains, such as A and BALB/c, which have a high spontaneous incidence of such tumours. Tumours of similar histogenesis can be induced experimentally in rats but they very rarely occur spontaneously. In terms of initiators and promoters, mice of different strains behave as though they have variable amounts of some inborn initiator which determines the response of their alveolar cells to a variety of carcinogenic promoters. Apart from known genetic factors no " initiator " a
