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-160C/A polymorphism in the E-cadherin gene promoter and risk of hereditary, familial and sporadic prostate cancer.

https://arctichealth.org/en/permalink/ahliterature17926
Source
Int J Cancer. 2004 Apr 10;109(3):348-52
Publication Type
Article
Date
Apr-10-2004
Author
Jonsson B-A
Adami H-O
Hägglund M
Bergh A
Göransson I
Stattin P
Wiklund F
Grönberg H
Author Affiliation
Department of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden.
Source
Int J Cancer. 2004 Apr 10;109(3):348-52
Date
Apr-10-2004
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Cadherins - genetics
Case-Control Studies
Comparative Study
Gene Frequency
Genetic Predisposition to Disease
Genotype
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide
Promoter Regions (Genetics)
Prostate
Prostatic Neoplasms - epidemiology - genetics
Research Support, Non-U.S. Gov't
Risk factors
Sweden - epidemiology
Abstract
The E-cadherin (CDH1) gene has been associated with prostate carcinogenesis. The C/A polymorphism--160 base pairs relative to the transcription start site has been shown to decrease gene transcription. We analyzed the association between this polymorphism and the risk of sporadic, familial (2 close relatives) and hereditary (3 or more close relatives) prostate cancer. We combined data from 3 population-based epidemiologic studies in Sweden encompassing altogether 1,036 prostate cancer cases and 669 controls that were genotyped for the short nucleotide polymorphism. Odds ratios with 95% confidence intervals were estimated through unconditional logistic regression. We found no significant association between the A-allele and sporadic (OR = 1.0; 95% CI = 0.8-1.2) or familial (OR = 1.4; 95% CI = 0.9-2.2) prostate cancer. In contrast, risk of hereditary cancer was increased among heterozygote CA carriers (OR = 1.7; 95% CI = 1.0-2.7) and particularly among homozygote AA carriers (OR = 2.6; 95% CI = 1.4-4.9). Our data indicate that the -160 single nucleotide polymorphism in CDH1 is a low-penetrant prostate cancer susceptibility gene that might explain a proportion of familial and notably hereditary prostate cancer.
PubMed ID
14961571 View in PubMed
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Age specific risks of familial prostate carcinoma: a basis for screening recommendations in high risk populations.

https://arctichealth.org/en/permalink/ahliterature20908
Source
Cancer. 1999 Aug 1;86(3):477-83
Publication Type
Article
Date
Aug-1-1999
Author
H. Grönberg
F. Wiklund
J E Damber
Author Affiliation
Department of Oncology, Umeå University, Sweden.
Source
Cancer. 1999 Aug 1;86(3):477-83
Date
Aug-1-1999
Language
English
Publication Type
Article
Keywords
Age Distribution
Aged
Cohort Studies
Family Health
Genetic Predisposition to Disease
Humans
Male
Middle Aged
Nuclear Family
Prostatic Neoplasms - epidemiology - genetics
Registries - statistics & numerical data
Research Support, Non-U.S. Gov't
Sweden - epidemiology
Abstract
BACKGROUND: A positive family history is one of the strongest known risk factors for prostate carcinoma in addition to age and race. In this article, the authors present age specific risks for developing prostate carcinoma in families with an aggregation of prostate carcinoma. METHODS: Data from a population-based cohort study including 5706 sons of Swedish men who had been diagnosed with prostate carcinoma between 1959 and 1963 were used. The age specific incidence rates were calculated for different cohorts of prostate carcinoma families with respect to patient age at the time of prostate carcinoma diagnosis and the number of men affected. RESULTS: Both patient age at the time of prostate carcinoma diagnosis and the number of men affected in the families influenced the risk of developing prostate carcinoma significantly. Unaffected men in families with two or more cases of prostate carcinoma have a very high risk of developing prostate carcinoma at a young age. The cumulative risks in these families are 5%, 15%, and 30% by ages 60 years, 70 years, and 80 years, respectively, compared with only 0.45%, 3%, and 10%, respectively, at the same ages in the general population. CONCLUSIONS: The findings of the current study together with data from the literature support the case for the screening of high risk families. The authors also conclude that men with at least two close relatives with prostate carcinoma have a very high risk of developing prostate carcinoma before age 70 years. The authors recommend these men undergo testing for prostate specific antigen and a digital rectal examination annually between the ages 50 years 70 years, ages at which patients usually are offered curative treatment for localized tumors. Screening of individuals before age 50 years may be recommended in selected families with a history of prostate carcinoma of very early onset.
PubMed ID
10430256 View in PubMed
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ARLTS1 and prostate cancer risk--analysis of expression and regulation.

https://arctichealth.org/en/permalink/ahliterature108076
Source
PLoS One. 2013;8(8):e72040
Publication Type
Article
Date
2013
Author
Sanna Siltanen
Daniel Fischer
Tommi Rantapero
Virpi Laitinen
John Patrick Mpindi
Olli Kallioniemi
Tiina Wahlfors
Johanna Schleutker
Author Affiliation
Institute of Biomedical Technology/BioMediTech, University of Tampere and Fimlab Laboratories, Tampere, Finland.
Source
PLoS One. 2013;8(8):e72040
Date
2013
Language
English
Publication Type
Article
Keywords
ADP-Ribosylation Factors - genetics
Aged
Case-Control Studies
Finland - epidemiology
Gene Expression Profiling
Gene Expression Regulation, Neoplastic
Genetic Association Studies
Genetic Predisposition to Disease
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide
Prostatic Neoplasms - epidemiology - genetics - metabolism
Quantitative Trait Loci
Risk factors
Abstract
Prostate cancer (PCa) is a heterogeneous trait for which several susceptibility loci have been implicated by genome-wide linkage and association studies. The genomic region 13q14 is frequently deleted in tumour tissues of both sporadic and familial PCa patients and is consequently recognised as a possible locus of tumour suppressor gene(s). Deletions of this region have been found in many other cancers. Recently, we showed that homozygous carriers for the T442C variant of the ARLTS1 gene (ADP-ribosylation factor-like tumour suppressor protein 1 or ARL11, located at 13q14) are associated with an increased risk for both unselected and familial PCa. Furthermore, the variant T442C was observed in greater frequency among malignant tissue samples, PCa cell lines and xenografts, supporting its role in PCa tumourigenesis. In this study, 84 PCa cases and 15 controls were analysed for ARLTS1 expression status in blood-derived RNA. A statistically significant (p?=?0.0037) decrease of ARLTS1 expression in PCa cases was detected. Regulation of ARLTS1 expression was analysed with eQTL (expression quantitative trait loci) methods. Altogether fourteen significant cis-eQTLs affecting the ARLTS1 expression level were found. In addition, epistatic interactions of ARLTS1 genomic variants with genes involved in immune system processes were predicted with the MDR program. In conclusion, this study further supports the role of ARLTS1 as a tumour suppressor gene and reveals that the expression is regulated through variants localised in regulatory regions.
Notes
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PubMed ID
23940804 View in PubMed
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Association of frequent consumption of fatty fish with prostate cancer risk is modified by COX-2 polymorphism.

https://arctichealth.org/en/permalink/ahliterature80057
Source
Int J Cancer. 2007 Jan 15;120(2):398-405
Publication Type
Article
Date
Jan-15-2007
Author
Hedelin Maria
Chang Ellen T
Wiklund Fredrik
Bellocco Rino
Klint Asa
Adolfsson Jan
Shahedi Katarina
Xu Jianfeng
Adami Hans-Olov
Grönberg Henrik
Bälter Katarina Augustsson
Author Affiliation
Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden. maria.hedelin@ki.se
Source
Int J Cancer. 2007 Jan 15;120(2):398-405
Date
Jan-15-2007
Language
English
Publication Type
Article
Keywords
Aged
Animals
Cyclooxygenase 2 - genetics
Diet
Fatty Acids, Omega-3 - administration & dosage
Fish Oils - administration & dosage
Fish Products
Humans
Male
Membrane Proteins - genetics
Polymorphism, Single Nucleotide
Prostatic Neoplasms - epidemiology - genetics
Risk
Salmon
Sweden - epidemiology
Abstract
Dietary intake of marine fatty acids from fish may protect against prostate cancer development. We studied this association and whether it is modified by genetic variation in cyclooxygenase (COX)-2, a key enzyme in fatty acid metabolism and inflammation. We assessed dietary intake of fish among 1,499 incident prostate cancer cases and 1,130 population controls in Sweden. Five single nucleotide polymorphisms (SNPs) were identified and genotyped in available blood samples for 1,378 cases and 782 controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by multivariate logistic regression. Multiplicative and additive interactions between fish intake and COX-2 SNPs on prostate cancer risk were evaluated. Eating fatty fish (e.g., salmon-type fish) once or more per week, compared to never, was associated with reduced risk of prostate cancer (OR: 0.57, 95% CI: 0.43-0.76). The OR comparing the highest to the lowest quartile of marine fatty acids intake was 0.70 (95% CI: 0.51-0.97). We found a significant interaction (p
PubMed ID
17066444 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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CHEK2 variants associate with hereditary prostate cancer.

https://arctichealth.org/en/permalink/ahliterature182875
Source
Br J Cancer. 2003 Nov 17;89(10):1966-70
Publication Type
Article
Date
Nov-17-2003
Author
E H Seppälä
T. Ikonen
N. Mononen
V. Autio
A. Rökman
M P Matikainen
T L J Tammela
J. Schleutker
Author Affiliation
Laboratory of Cancer Genetics, Institute of Medical Technology, Lenkkeilijänkatu 8,University of Tampere and Tampere University Hospital, FIN-33014 University of Tampere, Finland.
Source
Br J Cancer. 2003 Nov 17;89(10):1966-70
Date
Nov-17-2003
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Checkpoint Kinase 2
DNA Mutational Analysis
DNA Replication
Epidemiologic Studies
Finland - epidemiology
Fungal Proteins
Genes, Tumor Suppressor
Genetic Predisposition to Disease
Humans
Male
Middle Aged
Odds Ratio
Pedigree
Prevalence
Prostatic Neoplasms - epidemiology - genetics - pathology
Protein-Serine-Threonine Kinases - genetics
Abstract
Recently, variants in CHEK2 gene were shown to associate with sporadic prostate cancer in the USA. In the present study from Finland, we found that the frequency of 1100delC, a truncating variant that abrogates the kinase activity, was significantly elevated among 120 patients with hereditary prostate cancer (HPC) (four out of 120 (3.3%); odds ratio 8.24; 95% confidence interval 1.49-45.54; P=0.02) compared to 480 population controls. Suggestive evidence of segregation between the 1100delC mutation and prostate cancer was seen in all positive families. In addition, I157T variant had significantly higher frequency among HPC patients (13 out of 120 (10.8%); odds ratio 2.12; 95% confidence interval 1.06-4.27; P=0.04) than the frequency 5.4% seen in the population controls. The results suggest that CHEK2 variants are low-penetrance prostate cancer predisposition alleles that contribute significantly to familial clustering of prostate cancer at the population level.
Notes
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PubMed ID
14612911 View in PubMed
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Common cancers share familial susceptibility: implications for cancer genetics and counselling.

https://arctichealth.org/en/permalink/ahliterature286911
Source
J Med Genet. 2017 Apr;54(4):248-253
Publication Type
Article
Date
Apr-2017
Author
Hongyao Yu
Christoph Frank
Jan Sundquist
Akseli Hemminki
Kari Hemminki
Source
J Med Genet. 2017 Apr;54(4):248-253
Date
Apr-2017
Language
English
Publication Type
Article
Keywords
Adult
Aged
Breast Neoplasms - epidemiology - genetics - pathology
Family
Female
Genetic Counseling
Genetic Predisposition to Disease
Humans
Male
Middle Aged
Prostatic Neoplasms - epidemiology - genetics - pathology
Risk factors
Sweden - epidemiology
Abstract
It has been proposed that cancer is more common in some families than in others, but the hypothesis lacks population level support. We use a novel approach by studying any cancers in large three-generation families and thus are able to find risks even though penetrance is low.
Individuals in the nation-wide Swedish Family-Cancer Database were organised in three generations and the relative risk (RR) of cancer was calculated to the persons in the third generation by the numbers of patients with cancer in generations 1, 2 and 3.
The RRs for any cancer in generation 3 increased by the numbers of affected relatives, reaching 1.61 when at least seven relatives were diagnosed. The median patient had two affected relatives, and 7.0% had five or more affected relatives with an RR of 1.46, which translated to an absolute risk of 21.5% compared with 14.7% in population by age 65 years. For prostate cancer, the RR was 2.85 with four or more affected family members with any cancer, and it increased to 14.42 with four or more concordant cancers in family members. RRs for prostate cancer were approximately equal (2.70 vs 2.85) if a man had one relative with prostate cancer or four or more relatives diagnosed with any cancer.
A strong family history of cancer, regardless of tumour type, increases cancer risk of family members and calls for mechanistic explanations. Our data provide tools for counselling of patients with cancer with both low and high familiar risks.
PubMed ID
27651446 View in PubMed
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Comparison of two methods for estimating absolute risk of prostate cancer based on single nucleotide polymorphisms and family history.

https://arctichealth.org/en/permalink/ahliterature97602
Source
Cancer Epidemiol Biomarkers Prev. 2010 Apr;19(4):1083-8
Publication Type
Article
Date
Apr-2010
Author
Fang-Chi Hsu
Jielin Sun
Yi Zhu
Seong-Tae Kim
Tao Jin
Zheng Zhang
Fredrik Wiklund
A Karim Kader
S Lilly Zheng
William Isaacs
Henrik Grönberg
Jianfeng Xu
Author Affiliation
Center for Cancer Genomics, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA.
Source
Cancer Epidemiol Biomarkers Prev. 2010 Apr;19(4):1083-8
Date
Apr-2010
Language
English
Publication Type
Article
Keywords
Aged
Area Under Curve
Epidemiologic Methods
Genetic Predisposition to Disease
Genome-Wide Association Study
Humans
Male
Middle Aged
Odds Ratio
Pedigree
Polymorphism, Single Nucleotide
Prostatic Neoplasms - epidemiology - genetics
ROC Curve
Risk factors
Abstract
Disease risk-associated single nucleotide polymorphisms (SNP) identified from genome-wide association studies have the potential to be used for disease risk prediction. An important feature of these risk-associated SNPs is their weak individual effect but stronger cumulative effect on disease risk. Several approaches are commonly used to model the combined effect in risk prediction, but their performance is unclear. We compared two methods to model the combined effect of 14 prostate cancer risk-associated SNPs and family history for the estimation of absolute risk for prostate cancer in a population-based case-control study in Sweden (2,899 cases and 1,722 controls). Method 1 weighs each risk allele equally using a simple method of counting the number of risk alleles, whereas method 2 weighs each risk SNP differently based on its odds ratio. We found considerable differences between the two methods. Absolute risk estimates from method 1 were generally higher than those of method 2, especially among men at higher risk. The difference in the overall discriminative performance, measured by area under the curve of the receiver operating characteristic, was small between method 1 (0.614) and method 2 (0.618), P = 0.20. However, the performance of these two methods in identifying high-risk individuals (2- or 3-fold higher than average risk), measured by positive predictive values, was higher for method 2 than for method 1. These results suggest that method 2 is superior to method 1 in estimating absolute risk if the purpose of risk prediction is to identify high-risk individuals.
PubMed ID
20332264 View in PubMed
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A comprehensive association study for genes in inflammation pathway provides support for their roles in prostate cancer risk in the CAPS study.

https://arctichealth.org/en/permalink/ahliterature81026
Source
Prostate. 2006 Oct 1;66(14):1556-64
Publication Type
Article
Date
Oct-1-2006
Author
Zheng S Lilly
Liu Wennuan
Wiklund Fredrik
Dimitrov Latchezar
Bälter Katarina
Sun Jielin
Adami Hans-Olov
Johansson Jan-Erik
Sun Jishan
Chang Baoli
Loza Matthew
Turner Aubrey R
Bleecker Eugene R
Meyers Deborah A
Carpten John D
Duggan David
Isaacs William B
Xu Jianfeng
Grönberg Henrik
Author Affiliation
Center for Human Genomics, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.
Source
Prostate. 2006 Oct 1;66(14):1556-64
Date
Oct-1-2006
Language
English
Publication Type
Article
Keywords
Aged
Gene Expression Profiling
Gene Expression Regulation, Neoplastic - immunology
Genotype
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide
Prostatic Neoplasms - epidemiology - genetics - immunology
Prostatitis - epidemiology - genetics - immunology
Risk factors
Sweden - epidemiology
Abstract
BACKGROUND: Recently identified associations of prostate cancer risk with several genes involved in innate immunity support a role of inflammation in the etiology of prostate cancer. Considering inflammation is regulated by a complex system of gene products, we hypothesize sequence variants in many other genes of this pathway are associated with prostate cancer. METHODS: We evaluated 9,275 SNPs in 1,086 genes of the inflammation pathway using a MegAllele genotyping system among 200 familial cases and 200 unaffected controls selected from a large Swedish case-control population (CAPS). RESULTS: We found that significantly more than the expected numbers of SNPs were significant at a nominal P-value of 0.01, 0.05, and 0.1, providing overall support for our hypothesis. The excess was largest when using a more liberal nominal P-value (0.1); we observed 992 significant SNPs compared with the 854 significant SNPs expected by chance, and this difference was significant based on a permutation test (P = 0.0025). We also began the effort of differentiating true associated SNPs by selecting a small subset of significant SNPs (N = 26) and genotyped these in an independent sample of approximately 1,900 CAPS1 subjects. We were able to confirm 3 of these 26 SNPs. It is expected that many more true associated SNPs will be confirmed among the 992 significant SNPs identified in our pathway screen. CONCLUSIONS: Our study provides the first objective support for an association between prostate cancer and multiple modest-effect genes in inflammatory pathways.
PubMed ID
16921508 View in PubMed
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Confirmation of a positive association between prostate cancer risk and a locus at chromosome 8q24.

https://arctichealth.org/en/permalink/ahliterature78161
Source
Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):809-14
Publication Type
Article
Date
Apr-2007
Author
Suuriniemi Miia
Agalliu Ilir
Schaid Daniel J
Johanneson Bo
McDonnell Shannon K
Iwasaki Lori
Stanford Janet L
Ostrander Elaine A
Author Affiliation
Cancer Genetics Branch, National Human Genome Research Institute, NIH, Bethesda, MD 20892, USA.
Source
Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):809-14
Date
Apr-2007
Language
English
Publication Type
Article
Keywords
Adult
Alleles
Chi-Square Distribution
Chromosomes, Human, Pair 8
Genotype
Humans
Linkage Disequilibrium
Logistic Models
Male
Middle Aged
Polymorphism, Single Nucleotide
Population Surveillance
Prostatic Neoplasms - epidemiology - genetics
Variation (Genetics)
Washington - epidemiology
Abstract
BACKGROUND: Family-based linkage studies, association studies, and studies of tumors have highlighted human chromosome 8q as a genomic region of interest for prostate cancer susceptibility loci. Recently, a locus at 8q24, characterized by both a single nucleotide polymorphism (SNP) and a microsatellite marker, was shown to be associated with prostate cancer risk in Icelandic, Swedish, and U.S. samples. Although the data were provocative, the U.S. samples were not population based, which precludes assessment of the potential contribution of this locus to prostate cancer incidence in the United States. METHODS: We analyzed both markers in a population-based, case-control study of middle-aged men from King County, Washington. RESULTS: Overall, there was a significant positive association between the A allele of the SNP rs1447295 and prostate cancer risk [odds ratio, 1.4; 95% confidence interval (95% CI), 1.1-2.0] but no significant association with the microsatellite DG8S737. However, significant associations were observed for both markers in men with high Gleason scores. Adjusting for age, first-degree family history of prostate cancer, and prostate cancer screening history, the adjusted odds ratios were 1.4 (95% CI, 1.1-1.8) for the A allele of the SNP and 1.9 (95% CI, 1.2-2.8) for the -10 allele of the microsatellite. CONCLUSIONS: These data suggest that the locus on chromosome 8q24 harbors a genetic variant associated with prostate cancer and that the microsatellite marker is a stronger risk factor for aggressive prostate cancers defined by poorly differentiated tumor morphology.
PubMed ID
17416775 View in PubMed
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59 records – page 1 of 6.