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Objective: To describe study design and procedures for a prospective randomized trial investigating whether radical prostatectomy (RP) ± radiation improves cause-specific survival in comparison with primary radiation treatment (RT) and androgen deprivation treatment (ADT) in patients with locally advanced prostate cancer (LAPC). Materials and methods: SPCG-15 is a prospective, multi-centre, open randomized phase III trial. Patients are randomized to either standard (RT + ADT) or experimental (RP with extended pelvic lymph-node dissection and with addition of adjuvant or salvage RT and/or ADT if deemed necessary) treatment. Each centre follows guidelines regarding the timing and dosing of postoperative RT and adjuvant treatment such as ADT The primary endpoint is cause-specific survival. Secondary endpoints include metastasis-free and overall survival, quality-of-life, functional outcomes and health-services requirements. Each subject will be followed up for a minimum of 10 years. Results: Twenty-three centres in Denmark, Finland, Norway and Sweden, well established in performing RP and RT for prostate cancer participated. Each country's sites were coordinated by national coordinating investigators and sub-investigators for urology and oncology. Almost 400 men have been randomized of the stipulated 1200, with an increasing rate of accrual. Conclusions: The SPCG-15 trial aims to compare the two curatively intended techniques supplying new knowledge to support future decisions in treatment strategies for patients with LAPC The Scandinavian healthcare context is well suited for performing multi-centre long-term prospective randomized clinical trials. Similar care protocols and a history of entirely tax-funded healthcare facilitate joint trials. [ABSTRACT FROM AUTHOR]

Background: For unknown reasons, the age-standardized incidence of testicular cancer has shown a rapid increase in virtually all countries (mostly Western) studied. For populations with a sufficiently long period of cancer registration, this development can be traced back to the first half of this century.Purpose: By evaluating data from six countries with long periods of cancer registration (Denmark, Norway, Sweden, the former German Democratic Republic [East Germany], Finland, and Poland), we sought to determine whether the increase in testicular cancer risk follows a birth cohort pattern and, if so, to quantify and compare any birth cohort effects.Methods: A total of 30,908 incident cases of testicular cancer, diagnosed from 1945 through 1989 in men who were 20-84 years of age, were identified in population-based cancer registries in the six countries. In addition to performing simple trend analyses, we fitted several Poisson regression models (with the explanatory variables age, time period [calendar time], and birth cohort) to the data. Individual models were estimated by the maximum likelihood method.Results: The age-standardized incidence of testicular cancer was found to vary among the six populations and, on the basis of total registration data, increased annually at rates ranging from 2.3% (in Sweden) to 5.2% (in East Germany). A comparison of several regression models indicated that birth cohort was a stronger determinant of testicular cancer risk than was calendar time for all six populations. Within each population, little variation in testicular cancer risk was observed for men born between 1880 and 1920; thereafter, the risk began to increase. Among men born in Denmark, Norway, and Sweden between 1930 and 1945 (the period encompassing the Second World War), the increasing trend in risk was interrupted (i.e., a leveling in risk occurred). After 1945, an uninterrupted increase in risk was observed for all six populations. With men born around 1905 as the reference group, the relative risk of testicular cancer for those born around 1965 varied from 3.9 (95% confidence interval [CI] = 2.7-5.6) in Sweden to 11.4 (95% CI = 8.3-15.5) in East Germany.Conclusions and Implications: The increasing trend in testicular cancer risk observed for these six populations follows a birth cohort pattern. This distinct risk pattern provides a framework for the identification of specific etiologic factors. [ABSTRACT FROM AUTHOR]

Background. Herpes simplex virus type 2 (HSV-2) is a common cause of acute and recurrent aseptic meningitis. Our aim was to determine the impact of antiviral suppression on recurrence of meningitis and to delineate the full spectrum of neurological complications. Methods. One hundred and one patients with acute primary or recurrent HSV-2 meningitis were assigned to placebo (n = 51) or 0.5 g of valacyclovir twice daily (n = 50) for 1 year after initial treatment with 1 g of valacyclovir 3 times daily for 1 week in a prospective, placebo-controlled, multicenter trial. The primary outcome was time until recurrence of meningitis. The patients were followed up for 2 years. Results. The first year, no significant difference was found between the valacyclovir and placebo groups. The second year, without study drugs, the risk of recurrence of verified and probable HSV-2 meningitis was significantly higher among patients exposed to valacyclovir (hazard ratio, 3.29 [95% confidence interval, 10.06-10.21]). One-third of the patients experienced 1-4 meningitis episodes during the study period. A considerable morbidity rate, comprising symptoms from the central, peripheral, and autonomous nervous system, was found in both groups. Conclusions. Suppressive treatment with 0.5 g of valacyclovir twice daily was not shown to prohibit recurrent meningitis and cannot be recommended for this purpose after HSV meningitis in general. Protection against mucocutaneous lesions was observed, but the dosage was probably inappropriate for the prevention of HSV activation in the central nervous system. The higher frequency of meningitis, after cessation of active drug, could be interpreted as a rebound phenomenon. [ABSTRACT FROM AUTHOR]

Background: Previous studies on the association between maternal age and risk of childhood leukemia found inconsistent results. Objectives: We aimed to assess whether there is an association between maternal age and risk of childhood leukemia and whether such an association is modified by maternal year of birth. Methods: By linking nationwide Swedish registers, we analyzed leukemia incidence among all children between 1 and 5 years of age born between 1960 and 1999. We estimated incidence time trends by child year of birth (overall and stratified by maternal age) and incidence rate ratios (RRs) for maternal age groups stratified by maternal birth cohort. We tested the interaction between maternal age and child year of birth through the likelihood ratio test between nested Poisson regression models. Results: We observed 1,562 leukemia cases. The overall annual percent change (APC) was 1.00 [95% confidence interval (CI) , 0.51 to 1.49]. Stratifying by maternal age classes, APCs decreased from 1.66 (0.68 to 2.65) for mothers < 24 years to 0.23 (-0.93 to 1.40) for mothers > 35 years at delivery. RRs for children born to the oldest with respect to the youngest mothers were 2.42 (1.31 to 4.67) , 1.68 (1.00 to 2.72) , 1.34 (0.87 to 2.01) , and 0.87 (0.46-1.54) for mothers born in 1930-1934, 1940-1944, 1950-1954, and 1960-1964, respectively. Conclusions: Childhood leukemia risk increased with maternal age for mothers born in the past, whereas maternal age had no effect on this risk for mothers born more recently. This finding may explain the inconsistency of previous studies and suggests that leukemia risk may be related to an environmental factor to which women's exposure has changed over time. [ABSTRACT FROM AUTHOR]

We aimed to investigate the role of perinatal determinants on the risk for germ-cell testicular cancer, with respect to the aetiological heterogeneity between seminomas and non-seminomas. A case-control study of 628 case patients with testicular cancer (308 seminomas and 320 non-seminomas) and 2309 individually matched controls was nested within a cohort of boys born from 1920 to 1980 in two Swedish regions (Uppsala-Orebro Health Care Region and Stockholm). Cases were diagnosed from 1958 to 1998 and were identified through the Swedish National Cancer Registry. Perinatal information on cases and controls was collected through charts available at maternity wards. Gestational duration, categorised in three categories (<37, 37-41, >41 weeks), was negatively associated with the risk for testicular cancer (P value for linear trend=0.008). A protective effect of long gestational duration and an increased risk for high birth weight were found for seminomas. Non-seminomas were associated with short gestational duration, particularly among those with low birth order (odds ratio: 3.02, 95% confidence intervals: 1.53-5.97) and high maternal age (odds ratio: 2.33, 95% confidence intervals: 1.19-4.55). No significant differences were found in tests for heterogeneity between the two histological groups. Our data support the hypothesis that intrauterine environment affects the risk for germ-cell testicular cancer. Seminomas and non-seminomas seemed to have similar risk patterns, although they are not entirely congruent. [ABSTRACT FROM AUTHOR]

Examines the relationship between body size and testicular cancer. Increase in the number of testicular cancer; Influence of disease on body weight; Determination of body size; Use of incidence ratio to measure relative risks; Univariate characteristics of the cohort and rates of testicular cancer; Inverse association of testicular cancer with body mass index.

We have previously found an increased risk of breast cancer among women born preterm. To confirm or refute the results, an enlarged study was conducted. The results from this study do not confirm the initial findings and suggest that preterm birth can be ruled out as a risk factor for breast cancer.British Journal of Cancer (2003) 89, 1664-1666. doi:10.1038/sj.bjc.6601357 www.bjcancer.com [ABSTRACT FROM AUTHOR]