A large-scale trial has been started in the United Kingdom with the aim of evaluating the effectiveness of different methods for the early detection of breast cancer. Two populations, each of 25,000 women aged 45-64 are invited for annual screening by mammography and/or clinical examination. Two further populations, one of 25,000 and one of 40,000 women in the same age range, are invited for education sessions in breast self-examination, and 4 control populations, totalling 120,000 women, are offered no additional services beyond conventional diagnostic facilities. All breast histology, both benign and malignant, in all women in the study is recorded, as are the findings, management and follow-up of all breast cancers. Changes in the populations, and deaths from all causes, are also recorded. This is essentially a non-randomized trial, though in one of the screening centres, where an education programme about breast cancer is provided for the whole population, only women registered with certain randomly selected general practices are invited to be screened. The principal means of evaluation will be the comparison of the mortality rates from breast cancer in each of the study populations. Costs, in terms of use of health resources, unnecessary surgery and radiation hazard, will be assessed. Additional aspects of the trial include studies of women's attitudes to early detection, and of the aetiology of breast cancer.

Cells from patients with chronic lymphocytic leukaemia (CLL) do not respond in the mixed lymphocyte culture (MLC) but are able to stimulate the response of normal lymphocytes. Mixed lymphocyte cultures were performed using cells from 24 patients with CLL and cells from 16 normal donors. The stimulatory capacity of 8 of these CLL cells was reduced when a common DR antigen was shared with the normal responding cell. We suggest that cells from certain selected CLL patients may be used in the mixed-lymphocyte reaction for determining the D-locus specificity of normal donors. CLL cells when expressed 1 DR antigen only, induced more clearly defined typing responses than cells with 2 DR antigens. There was no correlation between the ability of a CLL cell to induce a typing response and the T-cell status of the patient. However, a correlation with clinical course was suggested, because most cells which induced a typing response were obtained from patients who had received intensive treatment for the disease.

3M-KCl extracts of the hepatoma D23 contain antigens that inhibit the complement-dependent cytotoxicity for D23 hepatoma cells of serum from D23 tumour-bearing rats (D23 TBS). Inhibition was not due to a general anticomplementary activity of the extracts. Although a minor part (25%) of the protein of D23-KCl extract was insoluble in PBS, this part contained most of the inhibitory activity. Fractionation of the PBS-soluble material of the extract on Concanavalin A-Sepharose showed that the inhibitory activity did not bind to the lectin. Analysis of D23-KCl extracts on a Sepharose CL-4B column showed that the antigens involved in the cytotoxicity were heterogeneously distributed in the high-mol. wt region (greater than 200,000). Precipitation with 10% trichloroacetic acid (TCA) of D23 KCl extracts revealed that most of the antigenicity was insoluble in TCA. Heating of D23 KCl extracts at 100 degrees C did not affect the antigenicity. Enzyme treatment of D23 extra nuclear membranes (D23 ENP) revealed that the inhibitory activity was not sensitive to proteolytic digestion, while treatment with phospholipase A2, C or D abrogated partly the inhibitory activity. The lipid nature of the antigenicity was indicated by its solubility in organic solvents as chloroform or n-butanol. Images Fig. 3

Resistance to the cytocidal action of Adriamycin (ADR) was induced in rat hepatocytes by incorporation of the carcinogen 2-acetylaminofluorene (AAF) into the rat diet. Using a quantitative assay in primary monolayer culture, it was demonstrated that resistance to ADR is an early phenotypic change that is induced during chemical carcinogenesis in the rat, and appears to be stable.

The Familial Atypical Multiple Mole-Melanoma Syndrome (FAMMM) is characterized by an autosomal dominantly inherited susceptibility to multiple atypical naevi. Patients with this hereditary phenotype show a strong susceptibility to cutaneous malignant melanoma (CMM). Our investigation of an extended Dutch kindred showing the FAMMM phenotype revealed a proband with bilateral intraocular malignant melanoma (IOM) and multiple CMM. The family revealed an array of tumours which included carcinoma of the lung, skin, larynx, and breast in addition to CMM and IOM, which were transmitted vertically through 3 generations. There was male-to-male transmission, and the number of affected males and females was about the same, which was consistent with an autosomal dominant inheritance. Thus the FAMMM syndrome not only indicates a potential for CMM, but a susceptibility to other systemic cancers as well. These observations, though limited to a single kindred, merit a painstaking evaluation of cancer of all anatomical sites in other kindreds showing the FAMMM syndrome. Such studies could yield clues to cancer aetiology, pathogenesis, and control. Images Fig. 2 Fig. 3 Fig. 4

The levels of T, B and null lymphocytes in the peripheral blood, draining lymph nodes, and tumour masses at different growth stages in dogs transplanted with canine transmissible venereal sarcoma (CTVS) were determined by immunofluorescence techniques. The tumours were classified at excision into "progressor", "steady state", and "regressor" stages of growth. The percentage of B cells in the lymphocytes infiltrating into the progressively growing tumours (n = 10, 37.3 +/- 7.4%) was significantly higher (P less than 0.025) than that in regressing tumours (n = 21, 26.1 +/- 1.9%). In contrast, the percentage of T cells in the lymphocytes infiltrating into the regressing tumours (n = 21, 61.2 +/- 2.6%) was significantly higher (P less than 0.005) than that in the progressively growing tumours (n = 10, 34.0 +/- 5.1%). The tumours at the steady-state growth stage (n = 9) had 50.8 +/- 5.7% infiltrating T-cells, which was significantly higher (P less than 0.005) than the progressors and lower (P less than 0.005) than the regressors. The percentage of null cells of progressors (n = 10, 26.0 +/- 6.9%) was significantly (P less than 0.025) higher than in regressors (n = 21, 13.5 +/- 2.9%). The draining lymph nodes of progressor dogs (n = 5) had significantly fewer (P less than 0.025) B cells (8.2 +/- 2.3%) than in normal (n = 5, 16.1 +/- 3.1%), regressors (n = 12, 19.1 +/- 1.7%) and steady-state dogs (n = 5, 15.8 +/- 2.6%). Although there was slight lymphopenia and fluctuation of null cells, no significant differences in T- and B-lymphocyte levels were noted in the peripheral blood of the tumour dogs (n = 44) studied.

The antitumour effects of ICRF-159 and related analogues were evaluated using the B16 melanoma. Treatment of mice with ICRF-159 inhibited tumour growth, while each of the analogues, trans-4,4(1)-(1,2-cyclopropandiyl) bis (2,6-piperazinedione) (trans-5), and cis-4,4(1)-(1,2-cyclopropandiyl) bis (2,6-piperazinedione) (cis-7) independently accelerated primary tumour growth. Pretreatment of B16 melanoma cultures either with ICRF-159 or the analogue cis-7 decreased the yield of lung-colonies following i.v. injection of tumour cells. In contrast, pretreatment of tumour cells with the trans-5 analogue led to an increase in lung colonies. The effect on colony formation in vitro of these analogues correlated with increased growth in vivo, and not with lung colony formation.