Multiple primary cancer of the breast and ovary were investigated as part of a survey being undertaken at the Birmingham and West Midlands Regional Cancer Registry. Population-based data relating to 17,756 registrations for breast and 3470 for ovarian cancer between 1950 and 1964 were analysed. On the basis of person-years at risk and incidence rates for the Region (1960-1962), an increased risk of a second primary tumour in the ovary was observed in patients diagnosed with a first primary in the breast before 45 years of age (O = 8; E = 1.83; P less than 0.001). No excess was found in patients diagnosed after 45 years of age (O = 15; E = 17.06). In patients with an index tumour of the ovary, the observed number of second primary tumours of the breast was not significantly different from the expected number (O = 19; E = 12.95). Complementary analysis (a combined assessment for the 2 sites) showed that the development of a first primary at either site before 45 years of age carried a 2.8-fold risk of a second primary tumour at the other site (O = 9; E = 3.21; P less than 0.01). After 45 years of age no increased risk was found (O = 32; E = 28.63). Over all ages a 1.3-fold risk was observed (O = 42; E = 31.54; P less than 0.05). No evidence of subfertility was found in the 9 patients in the high-risk premenopausal group who developed the 2 tumours. The results are more consistent with an aetiology of early exposure to an external carcinogen than with one of abnormal hormone production.

The metabolism of (2-14C) + (3',5',7,9-3H) folic acid was studied in normal rats, tumour-bearing rats and rats treated with methotrexate (MTX). The experiments were designed to investigate changes in the catabolism and folate. The breakdown of folate to scission products was again demonstrated to be a normal phenomenon. Catabolites excreted included p-acetamidobenzoate, p-acetamidobenzoyl-L-glutamate, 3H2O, urea and a number of pterins. The catabolic process was decreased in the presence of a tumour and increased by the administration of MTX. MTX also led to the excretion of 4 additional radioactive pterins not found in normal urine. The possible mechanisms of folate breakdown are discussed with reference to the point of action of MTX.

The incidence of childhood cancer in Queensland has been studied using the data of the population-based Queensland Childhood Malignancy Registry. During the 7-year period 1973-1979, 454 cases were registered, giving an annual age-specific incidence of 11.34/10(5) for the age group 0-14 years inclusive. There was a male/female ratio of 1.36. The commonest group of diseases was that of the leukaemias, followed by that of CNS tumours. The incidences of the various types of tumour in Queensland have been compared with those from other reported series. The incidence of leukaemia was midway between that of U.S. whites and that of Manchester, while the incidences of lymphoma and Wilms' tumour were much closer to those of the United States. Ewing's tumour was considerably commoner than osteosarcoma.

Cytoplasts and karyoplasts were obtained by ultracentrifugation of Hepatoma D23 cells on a Ficoll gradient containing cytochalasin B. Their nuclear and protein content and their metabolic activity were determined. Three i.p. injections of 2.3 x 10(7) cytoplasts were unable to protect syngeneic WAB/Not rats against an s.c. challenge of 10(4) D23 cells, whereas a similar amount of karyoplasts, or 3 injections of 10(6) irradiated D23 cells, were fully protective. Ability of cytoplasts to act as primary or secondary immunogen were also studied, and compared to that of 0.01% glutaraldehyde-treated cells, 43 degrees C heat-treated cells and 3M KCl-soluble extracts, these preparations also being of weak immunogenicity. Only heat-treated cells behaved as a primary immunogen, whereas none of the preparations provided a secondary stimulation. Moreover, when these preparations were fed in vitro to peritoneal-exudate cells before their injection into rats, cytoplasts and glutaraldehyde-treated cells showed no immunogenicity, whereas heat-treated cells induced full protection against tumour challenge. Therefore, in this tumour model, the in vivo persistence of immunogen and the presence of a nucleus are likely to be crucial in inducing transplantation resistance to tumour.