Background: Epidemiologic studies have suggested that vitamin E and ␤-carotene may each influence the development of prostate cancer. In the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, a controlled trial, we studied the effect of ␣-tocopherol (a form of vitamin E) and ␤-carotene supplementation, separately or together, on prostate cancer in male smokers. Methods: A total of 29 133 male smokers aged 50-69 years from southwestern Finland were randomly assigned to receive ␣-tocopherol (50 mg), ␤-carotene (20 mg), both agents, or placebo daily for 5-8 years (median, 6.1 years). The supplementation effects were estimated by a proportional hazards model, and two-sided P values were calculated. Results: We found 246 new cases of and 62 deaths from prostate cancer during the follow-up period. A 32% decrease (95% confidence interval [CI] = −47% to −12%) in the incidence of prostate cancer was observed among the subjects receiving ␣-tocopherol (n = 14 564) compared with those not receiving it (n = 14 569). The reduction was evident in clinical prostate cancer but not in latent cancer. Mortality from prostate cancer was 41% lower (95% CI = −65% to −1%) among men receiving ␣-tocopherol. Among subjects receiving ␤-carotene (n = 14 560), prostate cancer incidence was 23% higher (95% CI = −4%-59%) and mortality was 15% higher (95% CI = −30%-89%) compared with those not receiving it (n = 14 573). Neither agent had any effect on the time interval between diagnosis and death. Conclusions: Long-term supplementation with ␣-tocopherol substantially reduced prostate cancer incidence and mortality in male smokers. Other controlled trials are required to confirm the findings. [J Natl Cancer Inst 1998;90:440-6]

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Summary Comparative genomic hybridization (CGH) was used to detect copy number changes of DNA sequences in the Ewing family of tumours (ET). We analysed 20 samples from 17 patients. Fifteen tumours (75%) showed copy number changes. Gains of DNA sequences were much more frequent than losses, the majority of the gains affecting whole chromosomes or whole chromosome arms. Recurrent findings included copy number increases for chromosomes 8 (seven out of 20 samples; 35%), 1q (five samples; 25%) and 12 (five samples; 25%). The minimal common regions of these gains were the whole chromosomes 8 and 12, and 1q21-22. High-level amplifications affected 8q13-24, 1q and 1q21-22, each once. Southern blot analysis of the specimen with high-level amplification at 1q21-22 showed an amplification of FLG and SPRR3, both mapped to this region. All cases with a gain of chromosome 12 simultaneously showed a gain of chromosome 8. Comparison of CGH findings with cytogenetic analysis of the same tumours and previous cytogenetic reports of ET showed, in general, concordant results. In conclusion, our findings confirm that secondary changes, which may have prognostic significance in ET, are trisomy 8, trisomy 12 and a gain of DNA sequences in 1 q.

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Fluctuating selection pressure may maintain phenotypic variation because of different types of individuals being adapted to different environmental conditions. We show that the extensive variation in the coloration of male pied flycatchers (Ficedula hypoleuca) can be maintained through differences in the reproductive success of male phenotypes under different conditions. The effects of weather conditions on the relative success of different male phenotypes varied between different phases of breeding. The reproductive output of black males was the highest when it was cold during egg‐laying but warm during the nestling period, whereas the fledgling production of brown males was highest when it was continuously warm. In addition, male forehead and wing patch sizes had context‐dependent effects on timing of breeding and nestling mortality, respectively. These results indicate that environmental heterogeneity plays a role in maintaining phenotypic variation. As melanin‐based coloration is heritable, climate change may alter phenotype frequencies depending on the patterns of warming.

Two lymphoblastoid cell lines have been established from patients who at the time of the initiation of the cultures did not show evidence of malignant diseases. WI‐L1 line originated from a lymph node biopsy of a patient who later developed a clinical course compatible with mycosis fungoides. WI‐L2 line was established from the spleen of a patient having hereditary spherocytic anemia. The lines were initiated by the organ culture method and then adapted to suspension cultures. The properties of these lines are similar to those derived from Burkitt's or leukemic patients and one (WI‐L1) contains a herpes‐type particle.

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