Adult height and body weight are positively associated with breast cancer risk after menopause, but few studies have investigated these factors according to molecular breast cancer subtype. A total of 18,562 postmenopausal Norwegian women who were born between 1886 and 1928 were followed up for breast cancer incidence from the time (between 1963 and 1975) height and weight were measured until 2008. Immunohistochemical and in situ hybridization techniques were used to subtype 734 incident breast cancer cases into Luminal A, Luminal B [human epidermal growth factor receptor 2 (HER2-)], Luminal B (HER2+), HER2 subtype, basal-like phenotype (BP) and five-negative phenotype (5NP). We used Cox regression analysis to assess adult height and body mass index (BMI) in relation to risk of these subtypes. We found a positive association of height with risk of Luminal A breast cancer (ptrend , 0.004), but there was no clear association of height with any other subtype. BMI was positively associated with risk of all luminal breast cancer subtypes, including Luminal A (ptrend , 0.002), Luminal B (HER2-) (ptrend , 0.02), Luminal B (HER2+) (ptrend , 0.06), and also for the HER2 subtype (ptrend , 0.04), but BMI was not associated with risk of the BP or 5NP subtypes. Nonetheless, statistical tests for heterogeneity did not provide evidence that associations of height and BMI differed across breast cancer subtypes. This study of breast cancer risk among postmenopausal women suggests that height is positively associated with risk of Luminal A breast cancer. BMI is positively associated with risk of all luminal subtypes and for the HER2 subtype.
BACKGROUND: Birth size, and particularly birth length, is positively associated with breast cancer risk in adulthood. The objective of this study was to examine whether birth size is associated with survival among breast cancer patients. METHODS: Information on birth size (weight, length and ponderal index (kg/length (m3)) was collected from birth archives for 331 breast cancer patients who were diagnosed at two university hospitals in Norway (Bergen and Trondheim). The patients were followed from the time of diagnosis until death from breast cancer, death from another cause, or to the end of follow-up, and birth size was related to survival, using Cox regression analysis. RESULTS: Breast cancer patients with birth length > or = 52 cm had nearly twice the risk of dying (hazard ratio, 1.92, 95% confidence interval, 1.09-3.41) from breast cancer compared to women with birth length less than 48 cm, after adjustment for place of birth and year of diagnosis.Similar analyses related to birth weight and ponderal index showed no clear association with breast cancer survival. CONCLUSIONS: Poorer outcome of breast cancer patients with high birth length may reflect effects of factors that stimulate longitudinal growth and simultaneously increase the risk of metastases and fatal outcome. It is possible that the insulin-like growth factor (IGF) system is involved in the underlying mechanisms.
Leukemia incidence in childhood has been shown to increase with birth weight. The purpose of this paper is to study whether the incidence of other childhood cancers also increases with birth weight.
The Norwegian Medical Birth Registry was linked to the Norwegian Cancer Registry. The data consisted of 1.65 million children, of whom 3252 had a cancer diagnosis before age 16 years. The diagnoses were divided into 1010 leukemia cases, 870 cancer cases of the central nervous system (CNS), and 1370 remaining cancers.
The increase in hazard rate for all cancers with a 1 kg increase in birth weight was 1.23 (95% confidence interval = 1.14-1.32) after adjustment. For leukemia the increase was 1.29 (1.14-1.47), for CNS cancers 1.07 (0.93-1.23), and for the remaining cancer diagnoses 1.29 (1.16-1.40).
There seems to be a general relationship between heavier birth weight and cancer incidence in childhood.
BACKGROUND: Prospective studies have indicated that elevated blood glucose levels may be linked with increased cancer risk, but the strength of the association is unclear. We examined the association between blood glucose and cancer risk in a prospective study of six European cohorts. METHODS AND FINDINGS: The Metabolic syndrome and Cancer project (Me-Can) includes cohorts from Norway, Austria, and Sweden; the current study included 274,126 men and 275,818 women. Mean age at baseline was 44.8 years and mean follow-up time was 10.4 years. Excluding the first year of follow-up, 18,621 men and 11,664 women were diagnosed with cancer, and 6,973 men and 3,088 women died of cancer. We used Cox regression models to calculate relative risk (RR) for glucose levels, and included adjustment for body mass index (BMI) and smoking status in the analyses. RRs were corrected for regression dilution ratio of glucose. RR (95% confidence interval) per 1 mmol/l increment of glucose for overall incident cancer was 1.05 (1.01-1.10) in men and 1.11 (1.05-1.16) in women, and corresponding RRs for fatal cancer were 1.15 (1.07-1.22) and 1.21 (1.11-1.33), respectively. Significant increases in risk among men were found for incident and fatal cancer of the liver, gallbladder, and respiratory tract, for incident thyroid cancer and multiple myeloma, and for fatal rectal cancer. In women, significant associations were found for incident and fatal cancer of the pancreas, for incident urinary bladder cancer, and for fatal cancer of the uterine corpus, cervix uteri, and stomach. CONCLUSIONS: Data from our study indicate that abnormal glucose metabolism, independent of BMI, is associated with an increased risk of cancer overall and at several cancer sites. Our data showed stronger associations among women than among men, and for fatal cancer compared to incident cancer. Please see later in the article for the Editors' Summary.
Brain tumour has few established determinants. We assessed to which extent risk of brain tumour was related to metabolic syndrome factors in adults.
In the Me-Can project, 580?000 individuals from Sweden, Austria, and Norway were followed for a median of 10 years after baseline measurement. Data on brain tumours were obtained from national cancer registries. The factors of metabolic syndrome (BMI, SBP and DBP, and blood levels of glucose, cholesterol, and triglycerides), separately and combined, were analysed in quintiles and for transformed z-scores (mean transformed to 0 and standard deviation to 1). Cox proportional hazards multivariate regression models were used, with corrections for measurement error.
During follow-up, 1312 primary brain tumours were diagnosed, predominantly meningioma (n?=?348) and high-grade glioma (n?=?436). For meningioma, the hazard ratio was increased for z-scores of SBP [hazard ratio?=?1.27 per unit standard deviation, 95% confidence interval (CI) 1.03-1.57], of DBP (hazard ratio?=?1.29, 95% CI 1.04-1.58), and of the combined metabolic syndrome score (hazard ratio?=?1.31, 95% CI 1.11-1.54). An increased risk of high-grade glioma was found for DBP (hazard ratio?=?1.23, 95% CI 1.01-1.50) and triglycerides (hazard ratio?=?1.35, 95% CI 1.05-1.72). For both meningioma and high-grade glioma, the risk was more than double in the fifth quintiles of DBP compared to the lowest quintile. For meningioma this risk was even larger for SBP.
Increased blood pressure was associated with risk of brain tumours, especially of meningiomas.
Observational studies have shown inconsistent results for the association between blood pressure and cancer risk. We investigated the association in 7 cohorts from Norway, Austria, and Sweden. In total, 577799 adults with a mean age of 44 years were followed for, on average, 12 years. Incident cancers were 22184 in men and 14744 in women, and cancer deaths were 8724 and 4525, respectively. Cox regression was used to calculate hazard ratios of cancer per 10-mmHg increments of midblood pressure, which corresponded with 0.7 SDs and, for example, an increment of systolic/diastolic blood pressure of 130/80 to 142/88 mmHg. All of the models used age as the time scale and were adjusted for possible confounders, including body mass index and smoking status. In men, midblood pressure was positively related to total incident cancer (hazard ratio per 10 mmHg increment: 1.07 [95% CI: 1.04-1.09]) and to cancer of the oropharynx, colon, rectum, lung, bladder, kidney, malignant melanoma, and nonmelanoma skin cancer. In women, midblood pressure was not related to total incident cancer but was positively related to cancer of the liver, pancreas, cervix, uterine corpus, and malignant melanoma. A positive association was also found for cancer mortality, with HRs per 10-mmHg increment of 1.12 (95% CI: 1.08-1.15) for men and 1.06 (95% CI: 1.02-1.11) for women. These results suggest a small increased cancer risk overall in men with elevated blood pressure level and a higher risk for cancer death in men and women.
The Norwegian Breast Cancer Screening Program started in 1996. To the authors' knowledge, this is the first report using individual-based data on invitation and participation to analyze breast cancer mortality among screened and nonscreened women in the program.
Information on dates of invitation, attendance, breast cancer diagnosis, emigration, death, and cause of death was linked by using unique 11-digit personal identification numbers assigned all inhabitants of Norway at birth or immigration. In total, 699,628 women ages 50 to 69 years without prior a diagnosis of breast cancer were invited to the program from 1996 to 2009 and were followed for breast cancer through 2009 and death through 2010. Incidence-based breast cancer mortality rate ratios (MRRs) were compared between the screened and nonscreened cohorts using a Poisson regression model. The MRRs were adjusted for calendar period, attained age, years since inclusion in the cohorts, and self-selection bias.
The crude breast cancer mortality rate was 20.7 per 100,000 women-years for the screened cohort compared with 39.7 per 100,000 women-years for the nonscreened cohort, resulting in an MRR of 0.52 (95% confidence interval, 0.47-0.59). The mortality reduction associated with attendance in the program was 43% (MRR, 0.57; 95% confidence interval, 0.51-0.64) after adjusting for calendar period, attained age, years after inclusion in the cohort, and self-selection bias.
After 15 years of follow-up, a 43% reduction in mortality was observed among women who attended the national mammographic screening program in Norway.
Physical activity appears to be inversely related to cancer risk, although the evidence is convincing for colon cancer only. As physical activity levels are difficult to measure in the general population, we aimed to investigate how physical activity influences cancer risk using a cohort of Norwegian world class athletes.
The cohort includes 3,428 athletes. Individual questionnaires gave information about physical activity and lifestyle variables until attained age. To elucidate the level of cancer risk, groups of athletes were compared to the general population (external comparisons) and to each other (internal comparisons).
A slightly reduced risk of total cancer was observed in the cohort of athletes, but stronger effects were observed for subgroups. The risk reduction was most pronounced for lung cancer and for leukemia/lymphoma. In women, a threefold increased risk of thyroid cancer was observed.
This cohort of athletes seems to have a reduced risk of cancer. The beneficial association, however, is weak and may be attributed to healthy lifestyle as well as to physical activity. Prolonged strenuous exercise may also increase the risk of thyroid cancer in women.
Based on self-reported physical activity, there is epidemiologic evidence for a beneficial relation between physical activity and colon cancer in men, but findings for other cancers are inconclusive. Measured cardiorespiratory fitness (CRF) can provide knowledge about the cancer-preventive value of physical activity. We aimed to assess relationships between CRF and risk of site-specific cancers. A cohort of 1997 healthy Norwegian men, aged 40-59?years at inclusion in 1972-1975, was followed for cancer throughout 2012 using data from the Cancer Registry of Norway. CRF was measured by a maximal exercise bicycle test at inclusion. Relationships between CRF and site-specific cancers were estimated using Cox regression, adjusted for age, body mass index, and smoking. During follow-up, 898 cancer cases were diagnosed in 758 men. When comparing men in CRF tertile 1 with men in tertiles 2 and 3, respectively, we found decreased risk of proximal colon cancer in tertile 2 (HR: 0.30, 95% CI: 0.13-0.73) and decreased risk of cancers of lung (0.39 95% CI: 0.22-0.66), pancreas (0.32 95% CI: 0.10-1.00), and bladder (HR: 0.40 95% CI: 0.21-0.74) in tertile 3. Furthermore, a significant trend for lower risk by increasing CRF tertile was found for cancers of proximal colon, lung, and bladder (P-value for trend
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Few studies have taken risk of competing events into account when examining the relationship between cholesterol and prostate cancer incidence, and few studies have a follow-up over several decades. We aimed to use these approaches to examine the relationship between cholesterol and prostate cancer.
A cohort of 1997 healthy Norwegian men aged 40-59 years in 1972-75 was followed throughout 2012. Cancer data were extracted from the Cancer Registry of Norway. The association between cholesterol and prostate cancer incidence was assessed using competing risk regression analysis, with adjustment for potential confounders. Date and cause of death was obtained from the Cause of Death Registry of Norway.
The study cohort had a cancer risk similar to the general Norwegian population. Prostate cancer was registered in 213 men (11 %), including 62 (3 %) with advanced stage at diagnosis. For overall and advanced stage prostate cancer, the incidence was twice as high in the lowest quartile of cholesterol compared to the highest quartile. These associations remained significant after adjustment for age, smoking, physical fitness, BMI, and systolic blood pressure. Furthermore, high physical fitness and low BMI were associated with increased prostate cancer incidence. Sensitivity analyses excluding events during the first 20 years of observation revealed similar results.
Low cholesterol, as well as high physical fitness and low BMI, may be associated with increased risk of prostate cancer. These findings conflict with current prostate cancer prevention recommendations.
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