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Adjuvant chemotherapy in colorectal cancer: a joint analysis of randomised trials by the Nordic Gastrointestinal Tumour Adjuvant Therapy Group.

https://arctichealth.org/en/permalink/ahliterature16598
Source
Acta Oncol. 2005;44(8):904-12
Publication Type
Article
Date
2005
Author
Bengt Glimelius
Olav Dahl
Björn Cedermark
Anders Jakobsen
Søren M Bentzen
Hans Starkhammar
Henrik Grönberg
Ragnar Hultborn
Maria Albertsson
Lars Påhlman
Kjell-Magne Tveit
Author Affiliation
Department of Oncology, Radiology and Clinical Immunology, University Hospital, Uppsala, Sweden. bengt.glimelius@onkologi.uu.se
Source
Acta Oncol. 2005;44(8):904-12
Date
2005
Language
English
Publication Type
Article
Abstract
Due to uncertainties regarding clinically meaningful gains from adjuvant chemotherapy after colorectal cancer surgery, several Nordic Groups in the early 1990s initiated randomised trials to prove or reject such gains. This report gives the joint analyses after a minimum 5-year follow-up. Between October 1991 and December 1997, 2 224 patients under 76 years of age with colorectal cancer stages II and III were randomised to surgery alone (n = 1 121) or adjuvant chemotherapy (n = 1 103) which varied between trials (5FU/levamisole for 12 months, n = 444; 5FU/leucovorin for 4-5 months according to either a modified Mayo Clinic schedule (n = 262) or the Nordic schedule (n = 397). Some centres also randomised patients treated with 5FU/leucovorin to+/-levamisole). A total of 812 patients had colon cancer stage II, 708 colon cancer stage III, 323 rectal cancer stage II and 368 rectal cancer stage III. All analyses were according to intention-to-treat. No statistically significant difference in overall survival, stratified for country or region, could be found in any group of patients according to stage or site. In colon cancer stage III, an absolute difference of 7% (p = 0.15), favouring chemotherapy, was seen. The present analyses corroborate a small but clinically meaningful survival gain from adjuvant chemotherapy in colon cancer stage III, but not in the other presentations.
PubMed ID
16332600 View in PubMed
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Alcohol drinking and risk of localized versus advanced and sporadic versus familial prostate cancer in Sweden.

https://arctichealth.org/en/permalink/ahliterature9200
Source
Cancer Causes Control. 2005 Apr;16(3):275-84
Publication Type
Article
Date
Apr-2005
Author
Ellen T Chang
Maria Hedelin
Hans-Olov Adami
Henrik Grönberg
Katarina A Bälter
Author Affiliation
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. ellen.chang@meb.ki.se
Source
Cancer Causes Control. 2005 Apr;16(3):275-84
Date
Apr-2005
Language
English
Publication Type
Article
Keywords
Aged
Alcohol Drinking - adverse effects
Case-Control Studies
Humans
Incidence
Male
Middle Aged
Neoplasm Staging
Prostatic Neoplasms - epidemiology - etiology - genetics
Research Support, Non-U.S. Gov't
Risk factors
Sweden - epidemiology
Abstract
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.
PubMed ID
15947879 View in PubMed
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Alcohol influence on acrylamide to glycidamide metabolism assessed with hemoglobin-adducts and questionnaire data.

https://arctichealth.org/en/permalink/ahliterature98517
Source
Food Chem Toxicol. 2010 Mar;48(3):820-4
Publication Type
Article
Date
Mar-2010
Author
Anna C Vikström
Kathryn M Wilson
Birgit Paulsson
Ioannis Athanassiadis
Henrik Grönberg
Hans-Olov Adami
Jan Adolfsson
Lorelei A Mucci
Katarina Bälter
Margareta Törnqvist
Author Affiliation
Department of Materials and Environmental Chemistry, Stockholm University, Stockholm, Sweden. anna.vikstrom@mk.su.se
Source
Food Chem Toxicol. 2010 Mar;48(3):820-4
Date
Mar-2010
Language
English
Publication Type
Article
Keywords
Acrylamides - metabolism
Adult
Alcohol Drinking - metabolism
Case-Control Studies
Central Nervous System Depressants - pharmacology
Epoxy Compounds - metabolism
Ethanol - pharmacology
Food Habits
Hemoglobins - metabolism
Humans
Male
Prostatic Neoplasms - epidemiology
Questionnaires
Smoking - adverse effects
Sweden - epidemiology
Abstract
Our purpose was to investigate whether alcohol (ethanol) consumption could have an influence on the metabolism of acrylamide to glycidamide in humans exposed to acrylamide through food. We studied a subsample from a population-based case-control study of prostate cancer in Sweden (CAPS). Questionnaire data for alcohol intake estimates was compared to the ratio of hemoglobin-adduct levels for acrylamide and glycidamide, used as a measure of individual differences in metabolism. Data from 161 non-smoking men were processed with regard to the influence of alcohol on the metabolism of acrylamide to glycidamide. A negative, linear trend of glycidamide-adduct to acrylamide-adduct-level ratios with increasing alcohol intake was observed and the strongest association (p-value for trend=0.02) was obtained in the group of men with the lowest adduct levels (47 pmol/g globin) when alcohol intake was stratified by acrylamide-adduct levels. The observed trend is likely due to a competitive effect between ethanol and acrylamide as both are substrates for cytochrome P450 2E1. Our results, strongly indicating that ethanol influence metabolism of acrylamide to glycidamide, partly explain earlier observations of only low to moderate associations between questionnaire data on dietary acrylamide intake and hemoglobin-adduct levels.
PubMed ID
20034532 View in PubMed
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Analysis of the macrophage scavenger receptor 1 gene in Swedish hereditary and sporadic prostate cancer.

https://arctichealth.org/en/permalink/ahliterature17838
Source
Prostate. 2004 May 1;59(2):132-40
Publication Type
Article
Date
May-1-2004
Author
Fredrik Lindmark
Björn-Anders Jonsson
Anders Bergh
Pär Stattin
S Lilly Zheng
Deborah A Meyers
Jianfeng Xu
Henrik Grönberg
Author Affiliation
Department of Radiation Sciences, Oncology, University of Umeå, Umeå, Sweden.
Source
Prostate. 2004 May 1;59(2):132-40
Date
May-1-2004
Language
English
Publication Type
Article
Keywords
Aged
Case-Control Studies
Cell Adhesion Molecules
Chromosomes, Human, Pair 8 - genetics
DNA - analysis
DNA Mutational Analysis
Genotype
Humans
Male
Middle Aged
Pedigree
Polymerase Chain Reaction
Polymorphism, Genetic
Prostatic Neoplasms - genetics
Receptors, Immunologic - genetics
Receptors, Scavenger
Research Support, Non-U.S. Gov't
Risk factors
Scavenger Receptors, Class A
Sweden
Abstract
BACKGROUND: The macrophage scavenger receptor 1 (MSR1) gene on chromosome 8p22 was recently reported as a candidate gene for hereditary prostate cancer (HPC). Here, we further elucidate the role of MSR1 in both Swedish families with HPC and in a cohort of unselected prostate cancer. METHODS: DNA samples from 83 Swedish HPC families and 215 unselected population based cases of prostate cancer as well as 425 age-matched controls were genotyped. RESULTS: A total of 18 variants were identified, including 2 exonic, 7 intronic changes, and 9 changes in the 5'- or 3'-uncoding region. Of the two exonic changes, one previously reported truncation mutation was identified, a R293X nonsense mutation. This mutation was found in 2 of the 83 (2.4%) HPC families. The R293X mutation was found more frequently in men with PC (4.9%) than in unaffected men (2.7%), consistent with previous published results, however our results were not significant (P = 0.16). To additionally test for potential association of common sequence variants and increased risk for the disease, five common polymorphisms (PRO3, INDEL1, IVS5-57, P275A, INDEL7) were genotyped in the group of 215 prostate cancer cases and 425 age-matched controls. No association between any of the five common sequence variants and prostate cancer were found. CONCLUSION: Our results suggest that mutations in MSR1 gene might play a role in prostate cancer susceptibility, particularly the R293X mutation. This study warrants further investigations of the role of MSR1 in prostate cancer etiology.
PubMed ID
15042613 View in PubMed
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Biochemical recurrence after robot-assisted radical prostatectomy in a European single-centre cohort with a minimum follow-up time of 5 years.

https://arctichealth.org/en/permalink/ahliterature124035
Source
Eur Urol. 2012 Nov;62(5):768-74
Publication Type
Article
Date
Nov-2012
Author
Prasanna Sooriakumaran
Leif Haendler
Tommy Nyberg
Henrik Gronberg
Andreas Nilsson
Stefan Carlsson
Abolfazl Hosseini
Christofer Adding
Martin Jonsson
Achilles Ploumidis
Lars Egevad
Gunnar Steineck
Peter Wiklund
Author Affiliation
Department of Urology, Karolinska University Hospital, Stockholm, Sweden.
Source
Eur Urol. 2012 Nov;62(5):768-74
Date
Nov-2012
Language
English
Publication Type
Article
Keywords
Aged
Confounding Factors (Epidemiology)
Disease-Free Survival
Follow-Up Studies
Hospitals, University
Humans
Kallikreins - blood
Kaplan-Meier Estimate
Male
Middle Aged
Multivariate Analysis
Neoplasm Grading
Neoplasm Staging
Proportional Hazards Models
Prostate-Specific Antigen - blood
Prostatectomy - adverse effects - methods - mortality
Prostatic Neoplasms - blood - mortality - pathology - surgery
Recurrence
Risk assessment
Risk factors
Robotics
Surgery, Computer-Assisted - adverse effects - mortality
Sweden
Time Factors
Treatment Outcome
Abstract
Robot-assisted radical prostatectomy (RARP) is an increasingly commonly used surgical treatment option for prostate cancer (PCa); however, its longer-term oncologic results remain uncertain.
To report biochemical recurrence-free survival (BRFS) outcomes for men who underwent RARP =5 yr ago at a single European centre.
A total of 944 patients underwent RARP as monotherapy for PCa from January 2002 to December 2006 at Karolinska University Hospital, Stockholm, Sweden. Standard clinicopathologic variables were recorded and entered into a secure, ethics-approved database made up of those men with registered domiciles in Stockholm. The median follow-up time was 6.3 yr (interquartile range: 5.6-7.2).
The outcome of this study was biochemical recurrence (BCR), defined as a confirmed prostate-specific antigen (PSA) of =0.2 ng/ml. Kaplan-Meier survival plots with log-rank tests, as well as Cox univariable and multivariable regression analyses, were used to determine BRFS estimates and determine predictors of PSA relapse, respectively.
The BRFS for the entire cohort at median follow-up was 84.8% (95% confidence interval [CI], 82.2-87.1); estimates at 5, 7, and 9 yr were 87.1% (95% CI, 84.8-89.2), 84.5% (95% CI, 81.8-86.8), and 82.6% (95% CI, 79.0-85.6), respectively. Nine and 19 patients died of PCa and other causes, respectively, giving end-of-follow-up Kaplan-Meier survival estimates of 98.0% (95% CI, 95.5-99.1) and 94.1% (95% CI, 90.4-96.4), respectively. Preoperative PSA >10, postoperative Gleason sum =4 + 3, pathologic T3 disease, positive surgical margin status, and lower surgeon volume were associated with increased risk of BCR on multivariable analysis. This study is limited by a lack of nodal status and tumour volume, which may have confounded our findings.
This case series from a single, high-volume, European centre demonstrates that RARP has satisfactory medium-term BRFS. Further follow-up is necessary to determine how this finding will translate into cancer-specific and overall survival outcomes.
Notes
Comment In: Eur Urol. 2012 Nov;62(5):775-6; discussion 777-822790290
PubMed ID
22633365 View in PubMed
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Birth characteristics and risk of prostate cancer: the contribution of genetic factors.

https://arctichealth.org/en/permalink/ahliterature149056
Source
Cancer Epidemiol Biomarkers Prev. 2009 Sep;18(9):2422-6
Publication Type
Article
Date
Sep-2009
Author
Sven Cnattingius
Frida Lundberg
Sven Sandin
Henrik Grönberg
Anastasia Iliadou
Author Affiliation
Department of Medicine, Karolinska Institutet at Karolinska University Hospital Solna, Stockholm, Sweden. sven.cnattingius@ki.se
Source
Cancer Epidemiol Biomarkers Prev. 2009 Sep;18(9):2422-6
Date
Sep-2009
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Birth Weight - genetics
Cohort Studies
Genetic Predisposition to Disease
Humans
Incidence
Male
Middle Aged
Proportional Hazards Models
Prospective Studies
Prostatic Neoplasms - epidemiology - genetics
Risk factors
Socioeconomic Factors
Sweden - epidemiology
Twins, Dizygotic
Twins, Monozygotic
Abstract
Prostate cancer has a strong hereditary component, but it has been proposed that hormonal influences in utero may contribute to offspring risk. We investigated the associations between birth characteristics and the risk of prostate cancer in twins, and whether possible associations could be confounded by familial factors, such as shared environment and common genes.
All like-sexed male twins in the Swedish Twin Registry, born from 1926 to 1958 and alive in 1973, were eligible. Data were obtained from birth records, and 11,420 male twins with reliable birth weight data were included in the final study population. Hazard ratios with 95% confidence intervals (CI) from Cox regression models were used to estimate associations between birth characteristics and risk of prostate cancer. Paired analysis was done to account for potential confounding by familial factors.
Compared with twins with a birth weight of 2,500 to 2,999 g, the hazard ratio (95% CI) for twins with a higher birth weight (>or=3,000 g) corresponded to 1.22 (0.94-1.57). In analyses within twin pairs, in which both twins had a birth weight of >or=2,500 g, a 500 g increase in birth weight was associated with an increased risk of prostate cancer within dizygotic twin pairs (odds ratio, 1.41; 95% CI, 1.02-1.57), but not within monozygotic twin pairs (odds ratio, 1.06; 95% CI, 0.61-1.84).
High birth weight is associated with an increased risk of prostate cancer. The difference in risk within dizygotic and monozygotic twin pairs may be due to genetic factors playing an important role in this association.
PubMed ID
19690187 View in PubMed
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Blood biomarker levels to aid discovery of cancer-related single-nucleotide polymorphisms: kallikreins and prostate cancer.

https://arctichealth.org/en/permalink/ahliterature97191
Source
Cancer Prev Res (Phila Pa). 2010 May;3(5):611-9
Publication Type
Article
Date
May-2010
Author
Robert J Klein
Christer Halldén
Angel M Cronin
Alexander Ploner
Fredrik Wiklund
Anders S Bjartell
Pär Stattin
Jianfeng Xu
Peter T Scardino
Kenneth Offit
Andrew J Vickers
Henrik Grönberg
Hans Lilja
Author Affiliation
Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
Source
Cancer Prev Res (Phila Pa). 2010 May;3(5):611-9
Date
May-2010
Language
English
Publication Type
Article
Keywords
Area Under Curve
Case-Control Studies
Genetic Predisposition to Disease
Genotype
Humans
Kallikreins - genetics
Male
Polymerase Chain Reaction
Polymorphism, Single Nucleotide
Prostate-Specific Antigen - blood
Prostatic Neoplasms - blood - genetics
ROC Curve
Risk factors
Tumor Markers, Biological - analysis
Abstract
Polymorphisms associated with prostate cancer include those in three genes encoding major secretory products of the prostate: KLK2 (encoding kallikrein-related peptidase 2; hK2), KLK3 (encoding prostate-specific antigen; PSA), and MSMB (encoding beta-microseminoprotein). PSA and hK2, members of the kallikrein family, are elevated in sera of men with prostate cancer. In a comprehensive analysis that included sequencing of all coding, flanking, and 2 kb of putative promoter regions of all 15 kallikrein (KLK) genes spanning approximately 280 kb on chromosome 19q, we identified novel single-nucleotide polymorphisms (SNP) and genotyped 104 SNPs in 1,419 cancer cases and 736 controls in Cancer Prostate in Sweden 1, with independent replication in 1,267 cases and 901 controls in Cancer Prostate in Sweden 2. This verified prior associations of SNPs in KLK2 and in MSMB (but not in KLK3) with prostate cancer. Twelve SNPs in KLK2 and KLK3 were associated with levels of PSA forms or hK2 in plasma of control subjects. Based on our comprehensive approach, this is likely to represent all common KLK variants associated with these phenotypes. A T allele at rs198977 in KLK2 was associated with increased cancer risk and a striking decrease of hK2 levels in blood. We also found a strong interaction between rs198977 genotype and hK2 levels in blood in predicting cancer risk. Based on this strong association, we developed a model for predicting prostate cancer risk from standard biomarkers, rs198977 genotype, and rs198977 x hK2 interaction; this model had greater accuracy than did biomarkers alone (area under the receiver operating characteristic curve, 0.874 versus 0.866), providing proof in principle to clinical application for our findings.
PubMed ID
20424135 View in PubMed
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Body mass index and mortality in men with prostate cancer.

https://arctichealth.org/en/permalink/ahliterature265895
Source
Prostate. 2015 Aug 1;75(11):1129-36
Publication Type
Article
Date
Aug-1-2015
Author
Anna Cantarutti
Stephanie E Bonn
Hans-Olov Adami
Henrik Grönberg
Rino Bellocco
Katarina Bälter
Source
Prostate. 2015 Aug 1;75(11):1129-36
Date
Aug-1-2015
Language
English
Publication Type
Article
Keywords
Aged
Body mass index
Case-Control Studies
Comorbidity
Humans
Male
Middle Aged
Obesity - diagnosis - epidemiology
Proportional Hazards Models
Prostate - pathology
Prostatic Neoplasms - diagnosis - mortality
Risk factors
Sweden - epidemiology
Abstract
Body Mass index (BMI) has been shown to affect risk and mortality of several cancers. Prostate cancer and obesity are major public health concerns for middle-aged and older men. Previous studies of pre-diagnostic BMI have found an increased risk of prostate cancer mortality in obese patients.
To study the associations between BMI at time of prostate cancer diagnosis and prostate cancer specific and overall mortality.
BMI was analyzed both as a continuous variable and categorized into four groups based on the observed distribution in the cohort (BMI?
PubMed ID
25929695 View in PubMed
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Body mass index and weight change in men with prostate cancer: progression and mortality.

https://arctichealth.org/en/permalink/ahliterature261103
Source
Cancer Causes Control. 2014 Aug;25(8):933-43
Publication Type
Article
Date
Aug-2014
Author
Stephanie E Bonn
Fredrik Wiklund
Arvid Sjölander
Robert Szulkin
Pär Stattin
Erik Holmberg
Henrik Grönberg
Katarina Bälter
Source
Cancer Causes Control. 2014 Aug;25(8):933-43
Date
Aug-2014
Language
English
Publication Type
Article
Keywords
Aged
Body mass index
Disease Progression
Humans
Life Style
Male
Middle Aged
Obesity - epidemiology
Proportional Hazards Models
Prostatic Neoplasms - epidemiology - mortality - pathology
Sweden - epidemiology
Weight Gain
Weight Loss
Abstract
Body mass index (BMI) is a modifiable lifestyle factor that has been associated with an increased risk of fatal prostate cancer and biochemical recurrence. The main purpose of the present study was to investigate the association between the exposure BMI at the time of a prostate cancer diagnosis and weight change after diagnosis, and the outcomes of prostate cancer progression and mortality in a large cohort study.
Data from 4,376 men diagnosed with clinically localized prostate cancer between 1997 and 2002 were analyzed. BMI and weight change were self-reported in 2007. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated in complete-case analysis (n = 3,214) using Cox proportional hazards models.
Progression was experienced among 639 (14.6 %) of the study participants, and in total, 450 (10.3 %) deaths of any cause and 134 (3.1 %) prostate cancer-specific deaths were recorded during follow-up. Obese men had a 47 % increased rate of overall mortality compared to normal weight men (HR 1.47, 95 % CI 1.03-2.10). No statistically significant associations were found for BMI and prostate cancer progression or prostate cancer-specific mortality. A weight loss >5 % after diagnosis almost doubled the rate of overall mortality compared to maintaining a stable weight (HR 1.94, 95 % CI 1.41-2.66), while a weight gain >5 % was associated with an almost doubled increased rate of prostate cancer-specific mortality (HR 1.93, 95 % CI 1.18-3.16).
Being obese was associated with an increased rate of overall mortality, and gaining weight after a prostate cancer diagnosis was associated with an increased rate of prostate cancer-specific mortality.
PubMed ID
24810654 View in PubMed
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Causes of death in the Sami population of Sweden, 1961-2000.

https://arctichealth.org/en/permalink/ahliterature17183
Source
Int J Epidemiol. 2005 Jun;34(3):623-9
Publication Type
Article
Date
Jun-2005
Author
Sven Hassler
Robert Johansson
Per Sjölander
Henrik Grönberg
Lena Damber
Author Affiliation
Southern Lapland Research Department, Vilhelmina, Postgatan 7, SE-912 32 Vilhelmina, Sweden.
Source
Int J Epidemiol. 2005 Jun;34(3):623-9
Date
Jun-2005
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Distribution
Aged
Aged, 80 and over
Cardiovascular Diseases - mortality
Cause of Death
Child
Child, Preschool
Cohort Studies
Ethnic Groups
Female
Humans
Infant
Life expectancy
Male
Middle Aged
Neoplasms - mortality
Research Support, Non-U.S. Gov't
Respiratory Tract Diseases - mortality
Sex Distribution
Sweden - epidemiology - ethnology
Wounds and Injuries - mortality
Abstract
BACKGROUND: Indigenous people often have a pattern of mortality that is disadvantageous in comparison with the general population. The knowledge on causes of death among the Sami, the natives of northern Scandinavia, is limited. The aim of the present study was to compare gender and cause specific mortality patterns for reindeer herding Sami, non-herding Sami, and non-Sami between 1961 and 2000. METHODS: A Sami cohort was constructed departing from a group of index-Sami identified as either reindeer herding Sami or Sami eligible to vote for the Sami parliament. Relatives of index-Sami were identified in the National Kinship Register and added to the cohort. The cohort contained a total of 41 721 people (7482 reindeer herding Sami and 34 239 non-herding Sami). A demographically matched non-Sami reference population four times as large, was compiled in the same way. Relative mortality risks were analysed by calculating standardized mortality ratios (SMRs). RESULTS: The differences in overall mortality and life expectancy of the Sami, both reindeer herding and non-herding, compared with the reference population were relatively small. However, Sami men showed significantly lower SMR for cancers but higher for external causes of injury. For Sami women, significantly higher SMR was found for diseases of the circulatory system and diseases of the respiratory system. An increased risk of dying from subarachnoid haemorrhage was observed among both Sami men and women. CONCLUSIONS: The similarities in mortality patterns are probably a result of centuries of close interaction between the Sami and the non-Sami, while the observed differences might be due to lifestyle, psychosocial and/or genetic factors.
PubMed ID
15737965 View in PubMed
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54 records – page 1 of 6.