There are two striking epidemiological features of testicular cancer. First, the incidence has increased strongly over the past few decades. Secondly, the incidence is greatest among younger men, and then declines from a certain age. We have constructed a statistical model to fit these observations. The idea of the model is that a subgroup of men is particularly susceptible to testicular cancer. In statistical terminology this is called a frailty model, since it focuses on varying frailty of the individuals. The frailty, or susceptibility, is considered as being established by birth, and due to a mixture of genetic and environmental effects. The strong increase in incidence over calendar time points to strong environmental effects, which are thought to operate in fetal life, causing damage to the fetus. Based on data from the Norwegian Cancer Registry we fit a frailty model to incidence data collected during 1953-93. The model gives a good fit and we discuss the interpretations of our findings.
We have identified 23 334 individuals (40%) of twins born in Norway 1905-45 where both twins were alive in 1960 without malignant disease. These were linked to the Cancer Registry of Norway. A reduced risk of malignant disease was demonstrated among twins for all tumour sites combined; standardized incidence rate (SIR): 0.90 (95% CI 0.85-0.94) in females and 0.95 (95% Cl 0.90-0.99) in males. In both sexes, we observed a significant reduced incidence of malignant melanomas of the skin. The incidence of colorectal cancer tended to be reduced for both sexes. In females, the incidence of tumours of the central nervous system and lungs were reduced. We consider our findings are real, but cannot explain them.
BACKGROUND: Concern has been raised that a low total serum cholesterol level, although beneficial for cardiovascular diseases, may increase the risk of cancer. This prospective cohort study analyses the hypotheses that a low total serum cholesterol level or its subfractions (serum low-density-lipoprotein cholesterol, high-density-lipoprotein cholesterol, and triglycerides) increase the risk of cancer of the colon and rectum. METHODS: Between 1977 and 1983, 62,173 men and women attended a health screening carried out by the Norwegian National Health Screening Service. The screening consisted of a questionnaire, anthropometric measurements, and samples of non-fasting blood drawn for analyses of serum total cholesterol, low-density-lipoprotein cholesterol, high-density-lipoprotein cholesterol, and triglycerides. RESULTS: During the 7- to 13-year follow-up, 186 patients were found to have colon cancer and 106 rectal cancer by linkage to the Norwegian Cancer Registry. Among men there were no associations between blood lipid and lipoprotein levels and risk of cancer of the proximal colon, distal colon, or the rectum. Among women there was a formal statistically significant inverse relationship between level of total cholesterol and low-density-lipoprotein cholesterol and risk of distal colon cancer, and a positive trend between total cholesterol level and rectal cancer. CONCLUSIONS: The statistically significant results among women were interpreted as incidental, and we conclude that blood lipid and lipoprotein levels were not associated with the risk of colon or rectum cancer in men or women in this cohort.
The aim of this study was to examine the blood pressure (BP) levels in patients treated for essential hypertension in 1816 patients in general practice in Norway. The study was based on an optical readable questionnaire filled out by the physician including information about systolic (S) and diastolic (D) BP, gender, age, body weight, smoking habits and all pharmaceutical treatment given. Sixty-four per cent of the patients were treated with one antihypertensive drug. Only 22.3% of the women and 30.7% of the men (p
Epidemiological studies have consistently shown elevated rates of breast cancer among female blood relatives of patients with ataxia telangiectasia (AT), a rare autosomal recessive disease. A large proportion of the members of AT families are carriers of AT-causing gene mutations in ATM (Ataxia Telangiectasia Mutated), and it has been hypothesised that these otherwise healthy carriers are predisposed to breast cancer. This is an extended and enlarged follow-up study of cancer incidence in blood relatives of 75 patients with verified AT in 66 Nordic families. Blood relatives were identified through population registry linkages, and the occurrence of cancer was determined from cancer registry files in each country and compared with national incidence rates. The ATM mutation carrier probabilities of relatives were assigned from the combined information on location in family, consanguinity, if any, and supplementary carrier screening in some families. Among the 1445 blood relatives of AT patients, 225 cancers were observed, with 170.4 expected, yielding a standardised incidence ratio (SIR) of 1.3 (95% confidence interval (CI), 1.1-1.4). Invasive breast cancer occurred in 34 female relatives (SIR, 1.7; 95% CI, 1.2-2.4) and was diagnosed in 21 women before the age of 55 years (SIR, 2.9; 95% CI, 1.8-4.5), including seven mothers of probands (SIR, 8.1; 95% CI, 3.3-17). When the group of mothers was excluded, no clear relationship was observed between the allocated mutation carrier probability of each family member and the extent of breast cancer risk. We concluded that the increased risk for female breast cancer seen in 66 Nordic AT families appeared to be restricted to women under the age of 55 years and was due mainly to a very high risk in the group of mothers. The findings of breast cancer risk in mothers, but not other likely mutation carriers, in this and other studies raises questions about the hypothesis of a simple causal relationship with ATM heterozygosity.
Patients who are homozygous for ataxia-telangiectasia (AT) have an exceptionally high incidence of cancer. Heterozygous individuals for the disease have been reported to be at an increased risk of cancer, particularly breast cancer in female carriers. We have analyzed eight Norwegian families with AT for cancer incidence in the parents, in the parents' sibs, grandparents, and grandparents' sibs. Two of the obligate heterozygote females have had premenopausal breast cancer. This incidence is significantly higher than expected for that group. No increase in the cancer incidence was observed in the parents' sibs, the grandparents, or the grandparents' sibs. Since the incidence of AT is low, data from many sources have to be combined to allow any conclusion.
We examined the relation between breast cancer, parity, and age at first and last births in a large national cohort of young women in Norway. We estimated relative incidence rates by Poisson regression analyses of person-years at risk with parity and age at last (most recent) birth as time-dependent variables. A total of 1,071,795 women were included in follow-up, contributing a total of 16,643,883 person-years in the age range 20-54 years. Follow-up times ranged from 1 month to 34.5 years. A total of 4,302 women were diagnosed with breast cancer during follow-up. With adjustment for age at first and last births, high parity was associated with an overall reduced risk of breast cancer (incidence rate ratio = 0.46; 95% confidence interval = 0.36-0.59 for women with five or more children vs uniparous women). Among women age 20-29 years, however, the results suggested an increase in risk with increasing parity (incidence rate ratio = 1.25; 95% confidence interval = 0.64-2.45 for women with three children vs uniparous women). The protective effect of high parity was particularly strong among women with first birth before the age of 20 years and rather weak among those with first birth at age 30 years or more. Low ages at first and last births were both associated with reduced breast cancer risk in analyses with adjustment for the other factor, with the association with age at last birth being slightly stronger.
It has been suggested that World War II influenced breast cancer risk among Norwegian women by affecting adolescent growth. Diet changed substantially during the war, and the reduction in energy intake was assumed to be larger in non-food-producing than in food-producing municipalities. In the present study, we have looked at the influence of residential history in areas with and without food production on the incidence of breast cancer in a population-based cohort study consisting of 597,906 women aged between 30 and 64 years. The study included 7311 cases of breast cancer, diagnosed between 1964 and 1992. The risk estimates were calculated using a Poisson regression model. The results suggest that residential history may influence the risk of breast cancer, where the suggested advantageous effect of World War II seems to be larger in non-food-producing than in food-producing areas. Breast cancer incidence was observed to decline for the post-war cohorts, which is discussed in relation to diet.
The incidence, mortality and survival of breast cancer patients from 1970 to 1993 were studied using data from the Cancer Registry of Norway. The age-adjusted incidence rate increased from 62.0 to 76.9 per 100,000 person-years during the period, and more than 2000 cases are now registered annually. The increase tends to be highest in the age group below 40 years. The increase is mainly found in cases with localized tumours at the time of diagnosis. The mortality rate has been almost unchanged in the period; the age adjusted mortality rate is 27.0 per 100,000 person-years at the end of the study period. The 5-year overall survival has increased among cases with axillary lymph node metastases at the time of diagnosis; the other stages show only little improvement.