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Hans-Olov Adami

Publications and source records attributed to Hans-Olov Adami.

At least 55 records · Page 3Linked to original sources
PubMed2005

Radical prostatectomy versus watchful waiting in early prostate cancer.

BACKGROUND: In 2002, we reported the initial results of a trial comparing radical prostatectomy with watchful waiting in the management of early prostate cancer. After three more years of follow-up, we report estimated 10-year results. METHODS: From October 1989 through February 1999, 695 men with early prostate cancer (mean age, 64.7 years) were randomly assigned to radical prostatectomy (347 men) or watchful waiting (348 men). The follow-up was complete through 2003, with blinded evaluation of the causes of death. The primary end point was death due to prostate cancer; the secondary end points were death from any cause, metastasis, and local progression. RESULTS: During a median of 8.2 years of follow-up, 83 men in the surgery group and 106 men in the watchful-waiting group died (P=0.04). In 30 of the 347 men assigned to surgery (8.6 percent) and 50 of the 348 men assigned to watchful waiting (14.4 percent), death was due to prostate cancer. The difference in the cumulative incidence of death due to prostate cancer increased from 2.0 percentage points after 5 years to 5.3 percentage points after 10 years, for a relative risk of 0.56 (95 percent confidence interval, 0.36 to 0.88; P=0.01 by Gray's test). For distant metastasis, the corresponding increase was from 1.7 to 10.2 percentage points, for a relative risk in the surgery group of 0.60 (95 percent confidence interval, 0.42 to 0.86; P=0.004 by Gray's test), and for local progression, the increase was from 19.1 to 25.1 percentage points, for a relative risk of 0.33 (95 percent confidence interval, 0.25 to 0.44; P<0.001 by Gray's test). CONCLUSIONS: Radical prostatectomy reduces disease-specific mortality, overall mortality, and the risks of metastasis and local progression. The absolute reduction in the risk of death after 10 years is small, but the reductions in the risks of metastasis and local tumor progression are substantial.

Aged↗
PubMed2005

Sequence variants in Toll-like receptor gene cluster (TLR6-TLR1-TLR10) and prostate cancer risk.

BACKGROUND: Chronic inflammation plays an important role in several human cancers and may be involved in the etiology of prostate cancer. Toll-like receptors (TLRs) are important in the innate immune response to pathogens and in cross-talk between innate immunity and adaptive immunity. Our previous finding of an association of TLR4 gene sequence variants and prostate cancer risk provides evidence for a role of TLRs in prostate cancer. In this study, we investigated whether sequence variants in the TLR6-TLR1-TLR10 gene cluster, residing within a 54-kb region on 4p14, were associated with prostate cancer risk. METHODS: We selected 32 single-nucleotide polymorphisms (SNPs) covering these three genes and genotyped these SNPs in 96 control subjects from the Cancer Prostate in Sweden (CAPS) population-based prostate cancer case-control study. Five distinct haplotype blocks were inferred at this region, and we identified 17 haplotype-tagging SNPs (htSNPs) that could uniquely describe >95% of the haplotypes. These 17 htSNPs were then genotyped in the entire CAPS study population (1383 case subjects and 780 control subjects). Odds ratios of prostate cancer for the carriers of a variant allele versus those with the wild-type allele were estimated using unconditional logistic regression. RESULTS: The allele frequencies of 11 of the 17 SNPs were statistically significantly different between case and control subjects (P = .04-.001), with odds ratios for variant allele carriers (homozygous or heterozygous) compared with wild-type allele carriers ranging from 1.20 (95% confidence interval [CI] = 1.00 to 1.43) to 1.38 (95% CI = 1.12 to 1.70). Phylogenetic tree analyses of common haplotypes identified a clade of two evolutionarily related haplotypes that are statistically significantly associated with prostate cancer risk. These two haplotypes contain all the risk alleles of these 11 associated SNPs. CONCLUSION: The observed multiple associated SNPs at the TLR6-TLR1-TLR10 gene cluster were dependent and suggest the presence of a founder prostate cancer risk variant on this haplotype background. The TLR6-TLR1-TLR10 gene cluster may play a role in prostate cancer risk, although further functional studies are needed to pinpoint the disease-associated variants in this gene cluster.

Case-Control Studies↗
PubMed2005

Body mass index and risk of malignant lymphoma in Scandinavian men and women.

BACKGROUND: The incidence of non-Hodgkin lymphoma and prevalence of obesity are increasing globally. A suggested positive association between obesity and risk of non-Hodgkin lymphoma has prompted us to investigate the relationship between body mass index (BMI) and risk of malignant lymphoma subtypes in a population-based case-control study. METHODS: Telephone interviews were conducted with 3055 case patients with non-Hodgkin lymphoma and 618 case patients with Hodgkin lymphoma diagnosed between October 1, 1999, and August 30, 2002, and 3187 population-based control subjects. The interviews assessed current height, normal adult weight, and other possible risk factors. Multivariable odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for risk of lymphoma were estimated by unconditional logistic regression. All statistical tests were two-sided. RESULTS: BMI was not associated with risk of overall non-Hodgkin lymphoma or of Hodgkin lymphoma (for example, comparing the highly obese group [BMI > or =35.0 kg/m2] with the normal-weight group [BMI = 18.5-24.9 kg/m2], OR for risk of non-Hodgkin lymphoma = 0.9, 95% CI = 0.6 to 1.3; P(trend) across all categories of BMI = .27). BMI was also not associated with risk of any non-Hodgkin lymphoma subtype evaluated, although there was some evidence of a positive association with risk of diffuse large B-cell lymphoma (for example, comparing the highly obese group with the normal-weight group, OR for diffuse large B-cell lymphoma = 1.5, 95% CI = 0.9 to 2.4; P(trend) =.05). CONCLUSIONS: Excess weight does not appear to be associated with an increased risk of malignant lymphoma in general, or with a risk of most major lymphoma subtypes. Hence, the growing incidence of obesity is unlikely to be an important contributor to the increasing incidence of non-Hodgkin lymphoma worldwide.

Adult↗
PubMed2005

Ultraviolet radiation exposure and risk of malignant lymphomas.

BACKGROUND: The incidence of malignant lymphomas has been increasing rapidly, but the causes of these malignancies remain poorly understood. One hypothesis holds that exposure to ultraviolet (UV) radiation increases lymphoma risk. We tested this hypothesis in a population-based case-control study in Denmark and Sweden. METHODS: A total of 3740 patients diagnosed between October 1, 1999, and August 30, 2002, with incident malignant lymphomas, including non-Hodgkin lymphoma, chronic lymphocytic leukemia, and Hodgkin lymphoma, and 3187 population controls provided detailed information on history of UV exposure and skin cancer and information on other possible risk factors for lymphomas. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated by logistic regression. Statistical tests were two-sided. RESULTS: Multivariable-adjusted analyses revealed consistent, statistically significant negative associations between various measures of UV light exposure and risk of non-Hodgkin lymphoma. A high frequency of sun bathing and sunburns at age 20 years and 5-10 years before the interview and sun vacations abroad were associated with 30%-40% reduced risks of non-Hodgkin lymphoma (e.g., for sunbathing four times a week or more at age 20 versus never sunbathing, OR = 0.7, 95% CI = 0.6 to 0.9; for two or more sunburns a year at age 20 versus no sunburns, OR = 0.6, 95% CI = 0.5 to 0.8). These inverse associations increased in strength with increasing levels of exposure (all P(trend)< or =.01). Similar, albeit weaker, associations were observed for Hodgkin lymphoma. There were no clear differences among non-Hodgkin lymphoma subtypes, although associations were stronger for B-cell than for T-cell lymphomas. A history of skin cancer was associated with a doubling in risks of both non-Hodgkin and Hodgkin lymphoma. CONCLUSIONS: A history of high UV exposure was associated with reduced risk of non-Hodgkin lymphoma. The positive association between skin cancer and malignant lymphomas is, therefore, unlikely to be mediated by UV exposure.

Adult↗
PubMed2005

Profound changes in breast cancer incidence may reflect changes into a Westernized lifestyle: a comparative population-based study in Singapore and Sweden.

Breast cancer incidence in Sweden has always been approximately twice as high as in Singapore. In recent years, this difference is limited to postmenopausal women. The aim of this study was to explore the reasons behind these differences through the use of age-period-cohort modeling. This population-based study included all breast cancer cases reported to the Swedish and the Singapore cancer registries from 1968 to 1997, with a total of 135,581 Swedish and 10,716 Singaporean women. Poisson regression using age-period and age-cohort models was used to determine the effects of age at diagnosis, calendar period and birth cohort. Incidence rate ratios were used to summarize these effects. An age-cohort model provided the best fit to the data in both countries, indicating that changes over lifetime, rather than recent differences in medical surveillance, might account for the observed differences in these 2 populations. The changes over birth cohort were much greater among Singaporean women. The relative effect of age was very similar in the 2 countries. Analyses show that age and cohort effects may explain the differences in trends of female breast cancer incidence between Sweden and Singapore. The larger cohort effect seen in Singaporean women may be attributed to more rapid changes in reproduction and lifestyle patterns than that of Swedish women during the period studied. The incidence of breast cancer in postmenopausal women in Singapore will probably continue to rise in the coming decades to match the current Swedish rates.

Adult↗
PubMed2005

The role of epidemiology in understanding the relationship between dietary acrylamide and cancer risk in humans.

Since April 2002, when the Swedish National Food Administration first reported its finding of elevated levels of the substance acrylamide in commonly consumed foods (Swedish National Food Administration, 2002), there has been considerable debate about the health effects of dietary exposure to acrylamide. In particular, researchers have speculated on whether the amount of acrylamide consumed through the typical diet could increase the risk of cancer in humans. In this paper, we review the epidemiological data to date examining dietary acrylamide in relation to cancer risk. We highlight the strengths and limitations of using epidemiology to address this public health question. Finally, we provide an overview of future directions of epidemiological research on the health effects of dietary acrylamide.

Acrylamides↗
PubMed2005

Alcohol drinking and risk of localized versus advanced and sporadic versus familial prostate cancer in Sweden.

BACKGROUND: It is unknown whether the association of alcohol consumption with prostate cancer risk varies between localized and advanced cases, or between sporadic and familial cases. METHODS: We assessed recent alcohol drinking in a population-based case--control study of Swedish men, including 1499 cases and 1130 controls. Drinking status and average volume, frequency, and type of alcohol consumed were evaluated. Unconditional logistic regression was performed to estimate the odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for associations between alcohol consumption and prostate cancer risk. RESULTS: Prostate cancer cases were more likely than controls to be current or former, rather than never, drinkers. However, there was no association between recent total alcohol, beer, wine, and liquor consumption and risk of overall prostate cancer, nor advanced, sporadic, or familial prostate cancer. The OR for risk of overall disease among men who drank more than 135 g of total alcohol per week versus non-drinkers was 1.2 (95% CI: 0.9, 1.5), p(trend)=0.12. There was a marginal positive association between alcohol intake and risk of localized disease. CONCLUSIONS: We detected no association between recent alcohol consumption and risk of advanced, sporadic, or familial prostate cancer, and a borderline positive association with localized disease.

Aged↗
PubMed2005

Body mass index and mortality in a prospectively studied cohort of Scandinavian women: the women's lifestyle and health cohort study.

Overweight and obesity increase the risk of numerous chronic diseases, including several forms of cancer. However, the association between excess body weight and all-cause mortality among young and middle-aged women is incompletely known, and the impact of menopausal status on the association has hardly been investigated. We studied prospectively a cohort comprising a population sample of 102,446 women from Norway and Sweden aged 30-50 years when they answered an extensive questionnaire in 1991/1992. During follow-up through year 2000, 1187 women in the cohort died. We used Cox proportional hazard models to estimate multivariate Hazard rate ratios (HRR) with 95% confidence intervals (CI) of death in relation to body mass index (BMI, weight (kg)/height (m(2))) at start of follow-up. Both in age-adjusted models and in models adjusting for several variables (including smoking and physical activity) mortality increased with increasing BMI among premenopausal women, whereas a U-shaped relationship was seen among the postmenopausal women. Among premenopausal women obesity (BMI 30.0) doubled the mortality (HRR = 2.2, 95% CI: 1.7-3.0) when compared to women of normal weight (BMI 18.5-24.9), whilst the association was modest after menopause. Although we had limited power to analyze women who were underweight (BMI<18.5), an excess mortality of about 50% was seen among postmenopausal women. No excess risk was found for underweight premenopausal women. The data indicate that the rapidly growing prevalence of obesity in many Western countries will substantially increase premature deaths among young women.

Adult↗
PubMed2005

Causality in cancer epidemiology.

In this review, issues of causality in epidemiologic research with emphasis on the aetiology of human cancer are considered. Principles of assessing causation in epidemiological studies of cancer are distinguished into those concerning an individual study, several studies and a particular person. Strengths and weaknesses of various approaches of documenting carcinogenicity in humans are examined and lists of major established causes of human cancer are presented. The review concludes with estimates of mortality from cancer around the world that can be attributed to specific factors under the light of the current scientific knowledge.

Bias↗
PubMed2005

Genetic implications of bilateral breast cancer: a population based cohort study.

BACKGROUND: Women with breast cancer are at high risk of bilateral breast cancer. We aimed to assess the incidence of bilateral breast cancer in relation to age and time since diagnosis of first cancer. METHODS: We analysed a population-based cohort of 123757 women with a first primary breast cancer diagnosed in Sweden from 1970 to 2000 for frequency of bilateral breast cancers and deaths by means of record linkage. Second primary breast cancers were categorised as synchronous bilateral breast cancers if diagnosed within 3 months of the first primary cancer or as metachronous if diagnosed more than 3 months after diagnosis of first primary cancer. FINDINGS: We identified 6550 women who had developed bilateral breast cancer. Age-incidence patterns of synchronous and unilateral breast cancer were similar, although the absolute rates of synchronous bilateral cancer were 50-100 times lower than those of unilateral cancer. A woman aged 80 years or older is at least twice as likely to be diagnosed with synchronous bilateral breast cancer than is a woman younger than 40 years. In the first 20 years after diagnosis of primary breast cancer, incidence of metachronous bilateral cancer decreased from about 800 per 10(5) person-years to 400 per 10(5) person-years in patients diagnosed with primary breast cancer before the age of 45 years, whereas incidence remained at 500-600 per 10(5) person-years in those age 45 years or older at diagnosis. After 30 years' follow-up, cumulative risk of metachronous bilateral breast cancer was about 15% irrespective of age at first primary breast cancer. INTERPRETATION: The higher than expected risk of synchronous bilateral breast cancer could be explained by non-genetic factors. By contrast, incidence of metachronous bilateral cancer fits neither a model of highly penetrant genes nor aggregation of environmental risk factors.

Adult↗
PubMed2005

Physical activity as a determinant of mortality in women.

BACKGROUND: There is substantial evidence that higher levels of activity reduce the risk of mortality, but several research questions remain about the protective effect of physical activity. We aimed to quantify the effect of physical activity on overall mortality in younger women and to assess the effect of past versus current activity. METHODS: During 1991-1992, we enrolled 99,099 women, age 30-49 years, from the entire country of Norway and one Swedish region, in a population-based cohort study. The women provided information on physical activity level at age 14 and 30 years and at enrollment, as well as information on other personal characteristics at enrollment. We achieved complete follow-up into 2003 using record linkages to nationwide registers. We used Cox proportional hazard models to calculate multivariate relative risks (RRs) of dying from any cause. RESULTS: During an average 11.4 years of follow-up, 1,313 women died. Risk of death decreased with increasing physical activity at enrollment (5 categories; P for trend<0.0001) and was reduced by half in the highest compared with the lowest category (RR=0.46; 95% confidence intervals=0.33-0.65). This protective effect was consistent across strata of age at entry, smoking, country, and education. After adjustment for physical activity at enrollment, activity at age 14 and 30 was not associated with mortality. CONCLUSIONS: Current physical activity substantially reduces mortality among women. This association is observed even with low levels of physical activity and is accentuated with increased physical activity.

Adult↗
PubMed2005

Dietary factors and risk of non-hodgkin lymphoma in men and women.

BACKGROUND: The incidence of non-Hodgkin lymphoma (NHL) has increased worldwide in recent decades. Diet could influence NHL risk by modulating the immune system, although evidence is limited. We did a population-based case-control study to determine whether differences in diet were associated with NHL risk. METHODS: A total of 597 NHL cases and 467 population controls in Sweden completed a semiquantitative food frequency questionnaire evaluating their dietary habits 2 years before the interview. Unconditional logistic regression was used to estimate the odds ratios (OR) and corresponding 95% confidence intervals (95% CI) for associations between food intake and risk of NHL. RESULTS: High consumption of dairy products and fried red meat was associated with increased risk of NHL. The OR of NHL for individuals in the highest quartile compared with the lowest quartile of dairy intake was 1.5 (95% CI, 1.1-2.2; P(trend) = 0.003). The OR for the highest versus lowest quartile of fried red meat intake was 1.5 (95% CI, 1.0-2.1; P(trend) = 0.02). In contrast, high consumption of fruits and vegetables was associated with reduced risk of NHL, particularly follicular lymphoma, among women but not men. Compared with the lowest quartile of vegetable intake, the OR of follicular lymphoma among women in the highest quartile of vegetable intake was 0.3 (95% CI, 0.1-0.7; P(trend) = 0.002). CONCLUSIONS: The positive associations of NHL risk with dairy products and fried red meat and the inverse association with fruits and vegetables suggest that diet affects NHL risk and could explain the increase of some histopathogic subtypes.

Case-Control Studies↗
PubMed2005

Decreased alpha-methylacyl CoA racemase expression in localized prostate cancer is associated with an increased rate of biochemical recurrence and cancer-specific death.

Alpha-methylacyl CoA racemase (AMACR) is overexpressed in prostate cancer relative to benign prostatic tissue. AMACR expression is highest in localized prostate cancer and decreases in metastatic prostate cancer. Herein, we explored the use of AMACR as a biomarker for aggressive prostate cancer. AMACR protein expression was determined by immunohistochemistry using an image analysis system on two localized prostate cancer cohorts consisting of 204 men treated by radical prostatectomy and 188 men followed expectantly. The end points for the cohorts were time to prostate-specific antigen (PSA) failure (i.e., elevation >0.2 ng/mL) and time to prostate cancer death in the watchful waiting cohort. Using a regression tree method, optimal AMACR protein expression cut-points were determined to best differentiate prostate cancer outcome in each of the cohorts separately. Cox proportional hazard models were then employed to examine the effect of the AMACR cut-point on prostate cancer outcome, and adjusted for clinical variables. Lower AMACR tissue expression was associated with worse prostate cancer outcome, independent of clinical variables (hazard ratio, 3.7 for PSA failure; P = 0.018; hazard ratio, 4.1 for prostate cancer death, P = 0.0006). Among those with both low AMACR expression and high Gleason score, the risk of prostate cancer death was 18-fold higher (P = 0.006). The AMACR cut-point developed using prostate cancer-specific death as the end point predicted PSA failures independent of Gleason score, PSA, and margin status. This is the first study to show that AMACR expression is significantly associated with prostate cancer progression and suggests that not all surrogate end points may be optimal to define biomarkers of aggressive prostate cancer.

Biomarkers, Tumor↗
PubMed2005

Cigarette smoking and risk of non-Hodgkin's lymphoma--a population-based case-control study.

BACKGROUND: Epidemiologic evidence of an association between tobacco smoking and non-Hodgkin's lymphoma has been conflicting. This may reflect that non-Hodgkin's lymphoma comprises several distinct disease entities with different etiologies, as some studies have indicated an association between smoking and follicular lymphoma. OBJECTIVE: To investigate the association between cigarette smoking and non-Hodgkin's lymphoma risk, overall and by subtype. METHODS: As part of a nationwide Danish-Swedish population-based case-control study, we interviewed 3,055 incident non-Hodgkin's lymphoma patients and 3,187 population controls. All lymphomas were uniformly classified according to the WHO classification. We used unconditional logistic regression to estimate adjusted odds ratios (OR) and 95% confidence intervals (95% CI) for the association between cigarette smoking and risk of non-Hodgkin's lymphoma. RESULTS: Cigarette smoking was not associated with the risk of non-Hodgkin's lymphoma overall (OR, 0.97; 95% CI, 0.87-1.08) nor with the major subgroups such as diffuse large B-cell lymphoma (OR, 0.94; 95% CI, 0.79-1.10), chronic lymphocytic leukemia (OR, 0.86; 95% CI, 0.72-1.02), or follicular lymphoma (OR, 1.03; 95% CI, 0.85-1.24). Female smokers were at a marginally increased risk of follicular lymphoma (OR, 1.41; 95% CI, 1.04-1.92). Men who had ever smoked had a significantly increased risk of T-cell lymphoma (OR, 1.67; 95% CI, 1.11-2.51). No dose-response association with cigarette smoking could be established for any lymphoma subgroup. CONCLUSION: We found little evidence of an association between cigarette smoking and non-Hodgkin's lymphoma risk overall. Although increased risks of follicular lymphoma in female smokers and of T-cell lymphoma in male smokers were suggested, no dose-response relationship was observed, leaving limited support for causality.

Adolescent↗
PubMed2005

The interaction of four genes in the inflammation pathway significantly predicts prostate cancer risk.

It is widely hypothesized that the interactions of multiple genes influence individual risk to prostate cancer. However, current efforts at identifying prostate cancer risk genes primarily rely on single-gene approaches. In an attempt to fill this gap, we carried out a study to explore the joint effect of multiple genes in the inflammation pathway on prostate cancer risk. We studied 20 genes in the Toll-like receptor signaling pathway as well as several cytokines. For each of these genes, we selected and genotyped haplotype-tagging single nucleotide polymorphisms (SNP) among 1,383 cases and 780 controls from the CAPS (CAncer Prostate in Sweden) study population. A total of 57 SNPs were included in the final analysis. A data mining method, multifactor dimensionality reduction, was used to explore the interaction effects of SNPs on prostate cancer risk. Interaction effects were assessed for all possible n SNP combinations, where n = 2, 3, or 4. For each n SNP combination, the model providing lowest prediction error among 100 cross-validations was chosen. The statistical significance levels of the best models in each n SNP combination were determined using permutation tests. A four-SNP interaction (one SNP each from IL-10, IL-1RN, TIRAP, and TLR5) had the lowest prediction error (43.28%, P = 0.019). Our ability to analyze a large number of SNPs in a large sample size is one of the first efforts in exploring the effect of high-order gene-gene interactions on prostate cancer risk, and this is an important contribution to this new and quickly evolving field.

Case-Control Studies↗
PubMed2005

Physical activity in different periods of life and the risk of breast cancer: the Norwegian-Swedish Women's Lifestyle and Health cohort study.

BACKGROUND: Physical activity has been found to be associated with decreased risk of breast cancer in postmenopausal women in the majority of epidemiologic studies, but the association is inconsistent in premenopausal women. METHODS: We studied the effect of physical activity at various ages on the incidence of breast cancer in 99,504 women from 30 to 49 years of age at enrollment in the Women's Lifestyle and Health Study, a prospective population-based cohort study in Norway and Sweden. Physical activity level on an ordinal scale at age 14, age 30, and age at enrollment, participation in competitive sports, as well as information on other covariates was obtained using a self-administered questionnaire. Complete follow-up with data on incident invasive breast cancer and mortality was collected by linkage to national registries. The relation between physical activity and time to breast cancer development was assessed using Cox proportional hazard models, controlling for potential confounders. RESULTS: During an average 9.1 years of follow-up, there were 1,166 incident breast cancer cases. The mean age of the women was 41 years at enrollment, and the mean age at breast cancer diagnosis was 48 years. Compared to inactive women, women with higher levels of physical activity at enrollment had a similar risk of incident breast cancer (adjusted relative risk, 1.24 for vigorous activity compared with no activity; 95% CI, 0.85-1.82). Physical activity at age 30 or at age 14 also did not afford any significant protection from breast cancer, nor did a consistently high level of activity from younger ages to enrollment. CONCLUSIONS: We did not find evidence of a protective effect of physical activity on breast cancer risk in this group of primarily premenopausal women.

Adult↗