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Summary.-A curvilinear dose response of myeloid leukaemia induction in the CBA male mouse was obtained after single whole-body X-irradiation at about 3 months of age. This strain has a very low spontaneous incidence of the disease and no cases were found in the unirradiated controls. The incidence was independent of dose rate over the range used (4.2-552 rad/min). Diagnosis required histopathological examination of various body tissues, the gross anatomical changes being easily confused with other haemopoietic disorders, but a few cases were recognized in life from blood samples. Curve-fitting to various models based on theories of radiocarcinogenic mechanism is described.

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In a preliminary investigation of 'hot particle' carcinogenesis uranium oxide particles were introduced into the lungs of rats either by intubation of a liquid suspension of the particles or by inhalation of an aerosol. Subsequently the animals were briefly exposed to slow neutrons in a nuclear reactor, resulting in localized irradiation of the lung by fission fragments emitted from 235U atoms in the oxide particles. The uranium used in the intubation experiments was either enriched or depleted in 235U. Squamous cell carcinomas developed at the site of deposition of the enriched uranium oxide in many cases but no lung tumours occurred in the rats with the depleted uranium oxide, in which the lung tissue was exposed to very few fission fragments. Only enriched uranium oxide was used in the inhalation experiments. Pulmonary squamous cell carcinomas occurred after the fission fragment irradiation but were fewer than in the intubation experiments. Adenocarcinomas of the lung were seen in rats exposed to uranium oxide without subsequent irradiation by neutrons in the reactor and in rats irradiated with neutrons but not previously exposed to uranium oxide. It is concluded that (i) fission fragments were possibly implicated in the genesis of the squamous cell carcinomas, which only developed in those animals exposed to enriched uranium oxide and neutrons and (ii) the adenocarcinomas in the rats inhaling enriched uranium oxide only were likely to have been caused by protracted irradiation of the lung with alpha-rays emitted from the enriched uranium.

SUMMARY.-The behaviour of the normal epidermis of mice on the first 5 days of exposure to a single application of carcinogens and cocarcinogens has been investigated by simple quantitative measurements of cell population, size of cells and thickness of the epidermis. Irritant substances and promoting agents both produce cellular hypertrophy but the respective responses can be distinguished by the massive and persistent hyperplasia associated with promoting activity and the much greater incidence of degenerate cells associated with irritant treatment. Urethane treatment is characterized by induction of a transient hypoplasia which is not in agreement with the level of cellular division. This response has also been demonstrated after treatment with mild carcinogens or low doses of potent carcinogens. Higher dose levels are followed by a reduction in the mitotic index after about 27 hours. The possibility of developing a preliminary screening test for carcinogenic substances is discussed in the light of these observations.