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Changes in plasma C-reactive protein and hemostatic factors prior to and after a first myocardial infarction with a median follow-up time of 8 years.

https://arctichealth.org/en/permalink/ahliterature89367
Source
Blood Coagul Fibrinolysis. 2009 Jul;20(5):340-6
Publication Type
Article
Date
Jul-2009
Author
Thøgersen Anna M
Nilsson Torbjörn K
Weinehall Lars
Boman Kurt
Eliasson Mats
Hallmans Göran
Jansson Jan-Håkan
Author Affiliation
Department of Public Health and Clinical Medicine, Umeå University Hospital, Umeå, Sweden. anmat@rn.dk
Source
Blood Coagul Fibrinolysis. 2009 Jul;20(5):340-6
Date
Jul-2009
Language
English
Publication Type
Article
Abstract
The objective of this study was to determine whether a first myocardial infarction leads to increased plasma levels of hemostatic factors and high sensitive C-reactive protein (hs-CRP) and whether the association between theses biomarkers and myocardial infarction was greater at follow-up compared with baseline. Of more than 36,000 persons screened in northern Sweden, 78 developed a first myocardial infarction (on average 18 months after sampling) in a population-based, prospective, nested patient-referent study. Fifty of these had participated in a follow-up health survey (on average 8 and a half years between surveys) and were sex-matched and age-matched with 56 referents. The mean increases in hs-CRP, tissue plasminogen activator (tPA) mass, plasminogen activator inhibitor-1 mass, and tPA/plasminogen activator inhibitor-1 complex concentration and von Willebrand factor among patients and referents were comparable during follow-up. Conditional logistic regression indicated that hs-CRP was not significantly associated with first myocardial infarction in a univariate analysis, whereas high plasma levels of tPA and creatinine were significantly associated with outcome at baseline and follow-up. tPA/plasminogen activator inhibitor-1 complex was not superior to tPA as a risk marker in this study. A first myocardial infarction did not in this study induce significantly different changes in plasma levels of hs-CRP and hemostatic factors among patients compared with referents during follow-up.
PubMed ID
19357504 View in PubMed
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Circulating enterolactone and risk of endometrial cancer.

https://arctichealth.org/en/permalink/ahliterature80965
Source
Int J Cancer. 2006 Nov 15;119(10):2376-81
Publication Type
Article
Date
Nov-15-2006
Author
Zeleniuch-Jacquotte Anne
Lundin Eva
Micheli Andrea
Koenig Karen L
Lenner Per
Muti Paola
Shore Roy E
Johansson Ingegerd
Krogh Vittorio
Lukanova Annekatrin
Stattin Pär
Afanasyeva Yelena
Rinaldi Sabina
Arslan Alan A
Kaaks Rudolf
Berrino Franco
Hallmans Göran
Toniolo Paolo
Adlercreutz Herman
Author Affiliation
Department of Environmental Medicine, New York University School of Medicine, New York, NY 10016-3240, USA. anne.jacquotte@med.nyu.edu
Source
Int J Cancer. 2006 Nov 15;119(10):2376-81
Date
Nov-15-2006
Language
English
Publication Type
Article
Keywords
4-Butyrolactone - analogs & derivatives - blood
Adult
Aged
Case-Control Studies
Endometrial Neoplasms - blood
Female
Humans
Italy
Lignans - blood
Middle Aged
New York
Odds Ratio
Prospective Studies
Risk assessment
Risk factors
Sweden
Tumor Markers, Biological - blood
Abstract
It has been suggested that phytoestrogens protect against hormone-dependent cancers. Lignans are the main class of phytoestrogens in Western diets. We conducted a prospective study of endometrial cancer and circulating levels of the main human lignan, enterolactone. The design was a case-control study nested within 3 prospective cohort studies, in New York, Sweden and Italy. Serum or plasma samples had been collected at enrollment and stored at -80 degrees C. A total of 153 cases, diagnosed a median of 5.3 years after blood donation, and 271 matched controls were included. No difference in circulating enterolactone was observed between cases (median, 19.2 nmol/L) and controls (18.5 nmol/L). Adjusting for body mass index, the odds ratio for the top tertile of enterolactone, as compared to the lowest was 1.2 (95% CI, 0.7-2.0; p for trend = 0.53). Lack of association was observed in both pre- and postmenopausal women. No correlation was observed between enterolactone and circulating estrogens or SHBG in healthy postmenopausal women. These results do not support a protective role of circulating lignans, in the range of levels observed, against endometrial cancer.
PubMed ID
16929490 View in PubMed
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Circulating vitamin d and risk of epithelial ovarian cancer.

https://arctichealth.org/en/permalink/ahliterature94350
Source
J Oncol. 2009;2009:672492
Publication Type
Article
Date
2009
Author
Arslan Alan A
Clendenen Tess V
Koenig Karen L
Hultdin Johan
Enquist Kerstin
Agren Asa
Lukanova Annekatrin
Sjodin Hubert
Zeleniuch-Jacquotte Anne
Shore Roy E
Hallmans Göran
Toniolo Paolo
Lundin Eva
Author Affiliation
Department of Environmental Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.
Source
J Oncol. 2009;2009:672492
Date
2009
Language
English
Publication Type
Article
Abstract
We conducted a nested case-control study within two prospective cohorts, the New York University Women's Health Study and the Northern Sweden Health and Disease Study, to examine the association between prediagnostic circulating levels of 25-hydroxy vitamin D (25(OH)D) and the risk of subsequent invasive epithelial ovarian cancer (EOC). The 25(OH)D levels were measured in serum or plasma from 170 incident cases of EOC and 373 matched controls. Overall, circulating 25(OH)D levels were not associated with the risk of EOC in combined cohort analysis: adjusted OR for the top tertile versus the reference tertile, 1.09 (95% CI, 0.59-2.01). In addition, there was no evidence of an interaction effect between VDR SNP genotype or haplotype and circulating 25(OH)D levels in relation to ovarian cancer risk, although more complex gene-environment interactions may exist.
PubMed ID
19727412 View in PubMed
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C-reactive protein and ovarian cancer: a prospective study nested in three cohorts (Sweden, USA, Italy).

https://arctichealth.org/en/permalink/ahliterature89594
Source
Cancer Causes Control. 2009 Sep;20(7):1151-9
Publication Type
Article
Date
Sep-2009
Author
Lundin Eva
Dossus Laure
Clendenen Tess
Krogh Vittorio
Grankvist Kjell
Wulff Marianne
Sieri Sabina
Arslan Alan A
Lenner Per
Berrino Franco
Hallmans Goran
Zeleniuch-Jacquotte Anne
Toniolo Paolo
Lukanova Annekatrin
Author Affiliation
Department of Medical Biosciences, Umeå University, Umeå, Sweden.
Source
Cancer Causes Control. 2009 Sep;20(7):1151-9
Date
Sep-2009
Language
English
Publication Type
Article
Abstract
OBJECTIVES: Inflammatory processes may influence the risk of epithelial ovarian cancer, but available epidemiological evidence is limited and indirect. Circulating C-reactive protein (CRP), a sensitive marker of inflammation, may serve as a direct biological marker of an underlying association. METHODS: The association between ovarian cancer risk and pre-diagnostic circulating CRP was tested in a case-control study nested within three prospective cohorts from Sweden, USA, and Italy. The study included 237 cases and 427 individually matched controls. CRP was measured in stored blood samples by high-sensitivity immunoturbidimetric assay. Odds ratios (OR) and 95% confidence intervals (CI) were calculated by conditional logistic regression. RESULTS: Overall, CRP was not related to risk of ovarian cancer. However, a marked increase in risk was observed for CRP concentrations >10 mg/l: OR (95% CI) 4.4 (1.8-10.9), which remained significant after limiting analyses to cases diagnosed more than two or five years after blood donation (OR 3.0 (1.2-8.0) and 3.6 (1.0-13.2), respectively). Risk of mucinous tumors increased with high CRP, but the number of cases in this analysis was small. CONCLUSION: Study results offer additional support to the concept that chronic inflammation plays a role in epithelial ovarian cancer.
PubMed ID
19301134 View in PubMed
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The effects of commuting activity and occupational and leisure time physical activity on risk of myocardial infarction.

https://arctichealth.org/en/permalink/ahliterature79552
Source
Eur J Cardiovasc Prev Rehabil. 2006 Dec;13(6):924-30
Publication Type
Article
Date
Dec-2006
Author
Wennberg Patrik
Lindahl Bernt
Hallmans Göran
Messner Torbjörn
Weinehall Lars
Johansson Lars
Boman Kurt
Jansson Jan-Håkan
Author Affiliation
Bureå Health Centre, Bureå, Sweden. patrik.wennberg@medforskskelet.se
Source
Eur J Cardiovasc Prev Rehabil. 2006 Dec;13(6):924-30
Date
Dec-2006
Language
English
Publication Type
Article
Keywords
Chi-Square Distribution
Female
Humans
Leisure Activities
Logistic Models
Male
Middle Aged
Motor Activity
Myocardial Infarction - epidemiology
Occupations
Prospective Studies
Risk factors
Statistics, nonparametric
Sweden - epidemiology
Transportation
Abstract
BACKGROUND: Risk reduction of myocardial infarction has been shown for leisure time physical activity. The results of studies on occupational physical activity and risk of myocardial infarction are incongruous and studies on commuting activity are scarce. The aim of this study was to investigate how commuting activity, occupational physical activity and leisure time physical activity were associated with risk of future first myocardial infarction. DESIGN: We used a prospective incident case-referent study design nested in Västerbotten Intervention Program and the Northern Sweden MONICA study. METHODS: Commuting habits, occupational physical activity, leisure time physical activity and cardiovascular risk factors were assessed at baseline screening and compared in 583 cases (20% women) with a first myocardial infarction and 2098 matched referents. RESULTS: Regular car commuting was associated with increased risk of myocardial infarction versus commuting by bus, cycling or walking [odds ratio (OR) 1.74; 95% confidence interval (CI), 1.20-2.52] after multivariate adjustment. High versus low leisure time physical activity was associated with reduced risk of myocardial infarction (OR 0.69; 95% CI, 0.50-0.95) after adjustment for occupational physical activity and commuting activity, but the association was not statistically significant after further multivariate adjustment. After multivariate adjustment we observed a reduced risk for myocardial infarction in men with moderate (OR 0.70; 95% CI, 0.50-0.98) or high (OR 0.67; 95% CI, 0.42-1.08) versus low occupational physical activity. CONCLUSIONS: We found a clear association between car commuting and a first myocardial infarction and a corresponding inverse association with leisure time physical activity, while the impact of occupational physical activity on the risk of myocardial infarction was weaker.
PubMed ID
17143124 View in PubMed
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Endogenous steroid hormone levels in early pregnancy and risk of testicular cancer in the offspring: a nested case-referent study.

https://arctichealth.org/en/permalink/ahliterature89493
Source
Int J Cancer. 2009 Jun 15;124(12):2923-8
Publication Type
Article
Date
Jun-15-2009
Author
Holl Katsiaryna
Lundin Eva
Surcel Heljä-Marja
Grankvist Kjell
Koskela Pentti
Dillner Joakim
Hallmans Göran
Wadell Göran
Olafsdottir Gudridur H
Ogmundsdottir Helga M
Pukkala Eero
Lehtinen Matti
Stattin Pär
Lukanova Annekatrin
Author Affiliation
Department of Child and Adolescent Health, National Institute for Health and Welfare, Oulu, Finland. katsiaryna.holl@gmx.com
Source
Int J Cancer. 2009 Jun 15;124(12):2923-8
Date
Jun-15-2009
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Androstenedione - blood
Case-Control Studies
Child
Child, Preschool
Dehydroepiandrosterone Sulfate - blood
Estradiol - blood
Estrone - blood
Female
Gonadal Steroid Hormones - blood
Humans
Infant
Infant, Newborn
Male
Pregnancy
Prenatal Exposure Delayed Effects - epidemiology
Risk assessment
Risk factors
Sex Hormone-Binding Globulin - analysis
Testicular Neoplasms - epidemiology
Testosterone - blood
Young Adult
Abstract
According to the leading hypothesis on testicular cancer (TC) etiology exposure to a specific pattern of steroid hormones in utero, in particular, to high levels of estrogens and low levels of androgens is the major determinant of TC risk in the offspring. We performed a case-referent study nested within Finnish, Swedish and Icelandic maternity cohorts exploiting early pregnancy serum samples to evaluate the role of maternal endogenous steroid hormones with regard to the risk of TC. TC cases and referents were aged between 0 and 25 years. For each case-index mother pair, three or four matched referent-referent mother pairs were identified using national population registries. First trimester or early second trimester sera were retrieved from the index mothers of 73 TC cases and 286 matched referent mothers, and were tested for dehydroepiandrosterone sulfate (DHEAS), androstenedione, testosterone, estradiol, estrone, and sex hormone binding globulin (SHBG). Offspring of mothers with high DHEAS levels had a significantly decreased risk of TC (OR for highest vs. lowest DHEAS quartile, 0.18 (95% CI 0.06-0.58). In contrast, offspring of mothers with high androstenedione levels had an increased risk of TC (OR 4.1; 95% CI 1.2-12.0). High maternal total estradiol level also tended to be associated with an increased risk of TC in the offspring (OR 32; 95% CI 0.98-1,090). We report the first direct evidence that interplay of maternal steroid hormones in the early pregnancy is important in the etiology of TC in the offspring.
PubMed ID
19330837 View in PubMed
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Genetic polymorphism of chemokine receptors CCR2 and CCR5 in Swedish cervical cancer patients.

https://arctichealth.org/en/permalink/ahliterature79891
Source
Anticancer Res. 2006 Sep-Oct;26(5B):3669-74
Publication Type
Article
Author
Zheng Biying
Wiklund Fredrik
Gharizadeh Baback
Sadat Mehdi
Gambelunghe Giovanni
Hallmans Göran
Dillner Joakim
Wallin Keng-Ling
Ghaderi Mehran
Author Affiliation
Department of Molecular Medicine and Surgery, Karolinska Institute, Center for Molecular Medicine and Karolinska University Hospital Solna, Stockholm, Sweden.
Source
Anticancer Res. 2006 Sep-Oct;26(5B):3669-74
Language
English
Publication Type
Article
Keywords
Base Sequence
Case-Control Studies
DNA Primers
Female
Humans
Logistic Models
Papillomaviridae - isolation & purification
Polymorphism, Genetic
Receptors, CCR5 - genetics
Receptors, Chemokine - genetics
Sweden
Uterine Cervical Neoplasms - genetics - virology
Abstract
Chemokines are chemotactic cytokines that orchestrate leukocyte trafficking in tissues, thus, playing an important role in regulation of immunological processes. The aim of this study was to investigate the association of human papillomavirus (HPV) infection and cervical cancer with two DNA polymorphisms of the chemokine receptors CCR5-delta32 and CCR2-64I. The study material consisted of 50 cervical intraepithelial neoplasia (CIN) cases and 50 of age and sampling-date matched controls, 100 invasive cervix cancer cases and 100 of their corresponding matched disease-free controls. Pyrosequencing was employed to genotype the CCR2-64I polymorphism. CCR5-delta32 was genotyped using standard PCR fragment length analysis. The frequencies of CCR2 and CCR5 genotypes from 150 patients and 150 healthy controls were representative of the general population according to the Hardy-Weinberg equilibrium analysis. Risk association was computed with conditional logistic regression analysis. HPV-positive individuals with the rare CCR5deelta32/delta32 genotype have a risk of 4.58 (CI = 0.40-52.64, p-value = 0.045) compare to HPV negative group. The delta-32 mutation on the CCR locus is imperceptibly associated with increased risk of HPV infection. In total, cervical neoplasia was not associated with genetic polymorphism of CCR2 and CCR5.
PubMed ID
17094383 View in PubMed
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Genetic predisposition to long-term non-diabetic deteriorations in glucose homeostasis: ten-year follow-up of the GLACIER Study.

https://arctichealth.org/en/permalink/ahliterature99524
Source
Diabetes. 2010 Sep 24;
Publication Type
Article
Date
Sep-24-2010
Author
Renström Frida
Shungin Dmitry
Johansson Ingegerd
Florez Jose C
Hallmans Göran
Hu Frank B
Franks Paul W
Author Affiliation
Genetic Epidemiology & Clinical Research Group, Department of Public Health & Clinical Medicine, Section for Medicine, Umeå University Hospital, Umeå, Sweden.
Source
Diabetes. 2010 Sep 24;
Date
Sep-24-2010
Language
English
Publication Type
Article
Abstract
AbstractAims/hypothesis: To assess whether recently discovered genetic loci associated with hyperglycemia also predict long-term changes in glycemic traits. Methods: Sixteen fasting glucose-raising loci were genotyped in middle-aged adults from the GLACIER Study, a population-based prospective cohort study from Northern Sweden. Genotypes were tested for association with baseline fasting and 2-hr post-challenge glycemia (N=16,398), and with change in glycemic traits during a 10 year follow-up period (N=4,059). Results: Cross-sectional directionally consistent replication with fasting glucose concentrations was achieved for 12/16 variants; nine variants also associated with impaired fasting glucose (IFG) and seven were independently associated with 2-hr post-challenge glucose concentrations. In prospective analyses corrected for multiple testing, the effect alleles at four loci (GCK rs4607517, ADRA2A rs10885122, DGKB-TMEM195 rs2191349, G6PC2 rs560887) were statistically associated with worsening fasting glucose concentrations during 10-years follow-up. MTNR1B rs10830963, which was predictive of elevated fasting glucose concentrations in cross-sectional analyses, was associated with a protective effect on post-challenge glucose concentrations during follow-up; however, this was only when baseline fasting and 2-hr glucoses were adjusted for. An additive effect of multiple risk alleles on glycemic traits was observed: a weighted genetic risk score (80(th) vs. 20(th) centiles) was associated with a 0.16mmol/l (P=2.4×10(-6)) greater elevation in fasting glucose and a 64% (95% CI:33-201%) higher risk of developing IFG during 10-years follow-up. Conclusions: Our findings imply that genetic profiling might facilitate the early detection of persons who are genetically susceptible to deteriorating glucose control; studies of incident type 2 diabetes and discrete cardiovascular endpoints will help establish whether the magnitude of these changes is clinically relevant.
PubMed ID
20870969 View in PubMed
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Genetic variation in the SST gene and its receptors in relation to circulating levels of insulin-like growth factor-I, IGFBP3, and prostate cancer risk.

https://arctichealth.org/en/permalink/ahliterature89087
Source
Cancer Epidemiol Biomarkers Prev. 2009 May;18(5):1644-50
Publication Type
Article
Date
May-2009
Author
Johansson Mattias
McKay James D
Wiklund Fredrik
Rinaldi Sabina
Hallmans Göran
Bälter Katarina
Adami Hans-Olov
Grönberg Henrik
Stattin Pär
Kaaks Rudolf
Author Affiliation
International Agency For Research on Cancer, F-69372 Lyon Cedex 08, France.
Source
Cancer Epidemiol Biomarkers Prev. 2009 May;18(5):1644-50
Date
May-2009
Language
English
Publication Type
Article
Keywords
Case-Control Studies
Genetic Variation
Haplotypes
Humans
Insulin-Like Growth Factor Binding Proteins - metabolism
Insulin-Like Growth Factor I - metabolism
Male
Middle Aged
Polymorphism, Single Nucleotide
Prostatic Neoplasms - epidemiology - genetics - metabolism
Receptors, Somatostatin - genetics
Risk factors
Somatostatin - genetics
Sweden - epidemiology
Abstract
BACKGROUND: Somatostatin (SST) and its receptors (SSTR1-5) may have a role in prostate cancer by influencing the IGFI hormone axis or through direct effects on prostate epithelia. We have investigated if genetic variation in the SST and SSTR1-5 genes influences prostate cancer risk and/or circulating IGFI and IGFBP3 hormone levels. MATERIALS AND METHODS: We analyzed 28 haplotype tagging single nucleotide polymorphisms in the SST and SSTR1-5 genes in a case-control/genetic association study to investigate the association between genetic variation and prostate cancer risk. The study included 2863 cases and 1737 controls from the Cancer Prostate in Sweden (CAPS) study. To investigate the genetic influence on circulating hormone levels, plasma concentrations of IGFI and IGFBP3 were analyzed in 874 controls of the CAPS study and 550 male subjects from the Northern Sweden Health and Disease Cohort (NSHDC). RESULTS: No clear association between prostate cancer risk and genetic variation of the SST and SSTR1-5 genes was identified. The SSTR5 missense single nucleotide polymorphism rs4988483 was associated with circulating IGFI (P = 0.002) and IGFBP3 (P = 0.0003) hormone levels in CAPS controls, with a per allele decrease of approximately 11%. This decrease was replicated in NSHDC for circulating IGFBP3 (P = 0.01) but not for IGFI (P = 0.09). Combining CAPS and NSHDC subjects indicated evidence of association between rs4988483 and both IGFBP3 (P = 2 x 10(-5)) and IGFI (P = 0.0004) hormone levels. CONCLUSIONS: Our results suggest that genetic variation in the SSTR5 gene and, particularly, the rs4988483 single nucleotide polymorphism influence circulating IGFI and IGFBP3 hormone levels with no measurable effect on prostate cancer risk.
PubMed ID
19423539 View in PubMed
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38 records – page 1 of 4.