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Absolute and relative risk of cardiovascular disease in men with prostate cancer: results from the Population-Based PCBaSe Sweden.

https://arctichealth.org/en/permalink/ahliterature96622
Source
J Clin Oncol. 2010 Jul 20;28(21):3448-56
Publication Type
Article
Date
Jul-20-2010
Author
Mieke Van Hemelrijck
Hans Garmo
Lars Holmberg
Erik Ingelsson
Ola Bratt
Anna Bill-Axelson
Mats Lambe
Pär Stattin
Jan Adolfsson
Author Affiliation
King's College London, London, United Kingdom. mieke.vanhemelrijck@kcl.ac.uk
Source
J Clin Oncol. 2010 Jul 20;28(21):3448-56
Date
Jul-20-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Androgen Antagonists - adverse effects
Cardiovascular Diseases - etiology
Gonadotropin-Releasing Hormone - adverse effects - analogs & derivatives - therapeutic use
Humans
Male
Middle Aged
Prostatic Neoplasms - complications - drug therapy
Risk
Abstract
PURPOSE: Cardiovascular disease (CVD) is a potential adverse effect of endocrine treatment (ET) for prostate cancer (PC). We investigated absolute and relative CVD risk in 76,600 patients with PC undergoing ET, curative treatment, or surveillance. METHODS: PCBaSe Sweden is based on the National Prostate Cancer Register, which covers more than 96% of PC cases. Standardized incidence ratios (SIRs) and standardized mortality ratios (SMRs) of ischemic heart disease (IHD), acute myocardial infarction (MI), arrhythmia, heart failure, and stroke were calculated to compare observed and expected (using total Swedish population) numbers of CVD, taking into account age, calendar time, and previous CVD. RESULTS: Between 1997 and 2007, 30,642 patients with PC received primary ET, 26,432 curative treatment, and 19,527 surveillance. SIRs for CVD were elevated in all men with the highest for those undergoing ET, independent of circulatory disease history (SIR MI for men without circulatory disease history: 1.40 [95% CI, 1.31 to 1.49], 1.15 [95% CI, 1.01 to 1.31], and 1.20 [95% CI, 1.11 to 1.30] for men undergoing ET, curative treatment, and surveillance, respectively). Absolute risk differences (ARD) showed that two (arrhythmia) to eight (IHD) extra cases of CVD would occur per 1,000 person-years. SMRs showed similar patterns, with ARD of zero (arrhythmia) to three (IHD) per 1,000 person-years. CONCLUSION: Increased relative risks of nonfatal and fatal CVD were found among all men with PC, especially those treated with ET. Because ET is currently the only effective treatment for metastatic disease and the ARDs were rather small, our findings indicate that CVD risk should be considered when prescribing ET but should not constitute a contraindication when the expected gain is tangible.
PubMed ID
20567006 View in PubMed
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Accuracy of prostate biopsies for predicting Gleason score in radical prostatectomy specimens: nationwide trends 2000-2012.

https://arctichealth.org/en/permalink/ahliterature282854
Source
BJU Int. 2017 Jan;119(1):50-56
Publication Type
Article
Date
Jan-2017
Author
Daniela Danneman
Linda Drevin
Brett Delahunt
Hemamali Samaratunga
David Robinson
Ola Bratt
Stacy Loeb
Pär Stattin
Lars Egevad
Source
BJU Int. 2017 Jan;119(1):50-56
Date
Jan-2017
Language
English
Publication Type
Article
Keywords
Aged
Biopsy, Needle
Humans
Male
Neoplasm Grading - trends
Predictive value of tests
Prostate - pathology
Prostatectomy - methods
Prostatic Neoplasms - pathology - surgery
Reproducibility of Results
Sweden
Time Factors
Abstract
To investigate how well the Gleason score in diagnostic needle biopsies predicted the Gleason score in a subsequent radical prostatectomy (RP) specimen before and after the 2005 International Society of Urological Pathology (ISUP) revision of Gleason grading, and if the recently proposed ISUP grades 1-5 (corresponding to Gleason scores 6, 3 + 4, 4 + 3, 8 and 9-10) better predict the RP grade.
All prostate cancers diagnosed in Sweden are reported to the National Prostate Cancer Register (NPCR). We analysed the Gleason scores and ISUP grades from the diagnostic biopsies and the RP specimens in 15 598 men in the NPCR who: were diagnosed between 2000 and 2012 with clinical stage T1-2 M0/X prostate cancer on needle biopsy; were aged =70 years; had serum PSA concentration of
PubMed ID
26918298 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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Androgen Deprivation Therapies and Changes in Comorbidity: A Comparison of Gonadotropin-releasing Hormone Agonists and Antiandrogen Monotherapy as Primary Therapy in Men with High-risk Prostate Cancer.

https://arctichealth.org/en/permalink/ahliterature302621
Source
Eur Urol. 2019 04; 75(4):676-683
Publication Type
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Date
04-2019
Author
Kerri Beckmann
Hans Garmo
Jan Adolfsson
Cecilia Bosco
Eva Johansson
David Robinson
Lars Holmberg
Par Stattin
Mieke Van Hemelrijck
Author Affiliation
Australian Centre for Precision Health, University of South Australia, Adelaide, Australia; Translational Oncology & Urology Research (TOUR), School of Cancer and Pharmaceutical Sciences, King's College London, London, UK. Electronic address: Kerri.beckmann@kcl.ac.uk.
Source
Eur Urol. 2019 04; 75(4):676-683
Date
04-2019
Language
English
Publication Type
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Aged
Aged, 80 and over
Androgen Antagonists - adverse effects - therapeutic use
Antineoplastic Agents, Hormonal - adverse effects - therapeutic use
Comorbidity
Databases, Factual
Gonadotropin-Releasing Hormone - agonists
Humans
Male
Prostatic Neoplasms - drug therapy - mortality - pathology
Registries
Risk assessment
Risk factors
Sweden - epidemiology
Time Factors
Treatment Outcome
Abstract
Some studies suggest that gonadotropin-releasing hormone (GnRH) agonists are associated with higher risk of adverse events than antiandrogens (AAs) monotherapy. However, it has been unclear whether this is due to indication bias.
To investigate rates of change in comorbidity for men on GnRH agonists versus AA monotherapy in a population-based register study.
Men with advanced nonmetastatic prostate cancer (PCa) who received primary AA (n=2078) or GnRH agonists (n=4878) and age- and area-matched PCa-free men were selected from Prostate Cancer Database Sweden 3.0. Increases in comorbidity were measured using the Charlson Comorbidity Index (CCI), from 5yr before through to 5yr after starting androgen deprivation therapy (ADT).
Multivariable linear regression was used to determine differences in excess rate of CCI change before and after ADT initiation. Risk of any incremental change in CCI following ADT was assessed using multivariable Cox regression analyses.
Men on GnRH agonists experienced a greater difference in excess rate of CCI change after starting ADT than men on AA monotherapy (5.6% per yr, p
PubMed ID
30497883 View in PubMed
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Association between baseline serum glucose, triglycerides and total cholesterol, and prostate cancer risk categories.

https://arctichealth.org/en/permalink/ahliterature279405
Source
Cancer Med. 2016 06;5(6):1307-18
Publication Type
Article
Date
06-2016
Author
Rhonda Arthur
Henrik Møller
Hans Garmo
Lars Holmberg
Pår Stattin
Håkan Malmstrom
Mats Lambe
Niklas Hammar
Göran Walldius
David Robinson
Ingmar Jungner
Mieke Van Hemelrijck
Source
Cancer Med. 2016 06;5(6):1307-18
Date
06-2016
Language
English
Publication Type
Article
Keywords
Aged
Blood glucose
Cholesterol - blood
Comorbidity
Humans
Male
Middle Aged
Neoplasm Grading
Neoplasm Staging
Population Surveillance
Prostatic Neoplasms - blood - epidemiology - pathology
Registries
Risk
Sweden - epidemiology
Triglycerides - blood
Abstract
Lifestyle-related risk factors such as hyperglycemia and dyslipidemia have been associated with several cancers. However, studies exploring their link with prostate cancer (PCa) clinicopathological characteristics are sparse and inconclusive. Here, we investigated the associations between serum metabolic markers and PCa clinicopathological characteristics. The study comprised 14,294 men from the Swedish Apolipoprotein MOrtality RISk (AMORIS) cohort who were diagnosed with PCa between 1996 and 2011. Univariate and multivariable logistic regression were used to investigate the relation between glucose, triglycerides and total cholesterol and PCa risk categories, PSA, Gleason score, and T-stage. Mean age at time of PCa diagnosis was 69 years. Men with glucose levels >6.9 mmol/L tend to have PSA20 µg/L compared to PSA 4.0-9.9 µg/L. Hypertriglyceridemia was also positively associated with PSA>20 µg/L. Hyperglycemic men had a greater odds of intermediate- and high-grade PCa and advanced stage or metastatic PCa. Similarly, hypertriglyceridemia was positively associated with high-grade PCa. There was also a trend toward an increased odds of intermediate risk localized PCa and advanced stage PCa among men with hypertriglyceridemia. Total cholesterol did not have any statistically significant association with any of the outcomes studied. Our findings suggest that high serum levels of glucose and triglycerides may influence PCa aggressiveness and severity. Further investigation on the role of markers of glucose and lipid metabolism in influencing PCa aggressiveness and severity is needed as this may help define important targets for intervention.
PubMed ID
26923095 View in PubMed
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Association of Radical Local Treatment with Mortality in Men with Very High-risk Prostate Cancer: A Semiecologic, Nationwide, Population-based Study.

https://arctichealth.org/en/permalink/ahliterature291221
Source
Eur Urol. 2017 07; 72(1):125-134
Publication Type
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Date
07-2017
Author
Pär Stattin
Fredrik Sandin
Frederik Birkebæk Thomsen
Hans Garmo
David Robinson
Ingela Franck Lissbrant
Håkan Jonsson
Ola Bratt
Author Affiliation
Department of Surgical Sciences, Uppsala University, Uppsala, Sweden; Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University Hospital, Umeå, Sweden. Electronic address: par.stattin@umu.se.
Source
Eur Urol. 2017 07; 72(1):125-134
Date
07-2017
Language
English
Publication Type
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Aged
Androgen Antagonists - adverse effects - therapeutic use
Antineoplastic Agents, Hormonal - adverse effects - therapeutic use
Databases, Factual
Humans
Kallikreins - blood
Male
Middle Aged
Neoplasm Grading
Neoplasm Staging
Prostate-Specific Antigen - blood
Prostatectomy - adverse effects - mortality
Prostatic Neoplasms - blood - mortality - pathology - therapy
Radiotherapy - mortality
Radiotherapy Dosage
Risk assessment
Risk factors
Sweden - epidemiology
Time Factors
Treatment Outcome
Abstract
Current guidelines recommend androgen deprivation therapy only for men with very high-risk prostate cancer (PCa), but there is little evidence to support this stance.
To investigate the association between radical local treatment and mortality in men with very high-risk PCa.
Semiecologic study of men aged
Notes
CommentIn: Eur Urol. 2017 Apr;71(4):e113-e114 PMID 27717521
CommentIn: Eur Urol. 2017 Apr;71(4):e115-e116 PMID 27720538
PubMed ID
27481175 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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Blood glucose and risk of incident and fatal cancer in the metabolic syndrome and cancer project (me-can): analysis of six prospective cohorts.

https://arctichealth.org/en/permalink/ahliterature98549
Source
PLoS Med. 2009 Dec;6(12):e1000201
Publication Type
Article
Date
Dec-2009
Author
Tanja Stocks
Kilian Rapp
Tone Bjørge
Jonas Manjer
Hanno Ulmer
Randi Selmer
Annekatrin Lukanova
Dorthe Johansen
Hans Concin
Steinar Tretli
Göran Hallmans
Håkan Jonsson
Pär Stattin
Author Affiliation
Department of Surgical and Perioperative sciences, Urology and Andrology, Umeå University, Umeå, Sweden. tanja.stocks@urologi.umu.se
Source
PLoS Med. 2009 Dec;6(12):e1000201
Date
Dec-2009
Language
English
Publication Type
Article
Keywords
Adult
Blood Glucose - analysis
Body mass index
Cohort Studies
Europe - epidemiology
Female
Follow-Up Studies
Humans
Male
Metabolic Syndrome X - blood - epidemiology
Middle Aged
Neoplasms - blood - epidemiology
Prospective Studies
Risk assessment
Abstract
BACKGROUND: Prospective studies have indicated that elevated blood glucose levels may be linked with increased cancer risk, but the strength of the association is unclear. We examined the association between blood glucose and cancer risk in a prospective study of six European cohorts. METHODS AND FINDINGS: The Metabolic syndrome and Cancer project (Me-Can) includes cohorts from Norway, Austria, and Sweden; the current study included 274,126 men and 275,818 women. Mean age at baseline was 44.8 years and mean follow-up time was 10.4 years. Excluding the first year of follow-up, 18,621 men and 11,664 women were diagnosed with cancer, and 6,973 men and 3,088 women died of cancer. We used Cox regression models to calculate relative risk (RR) for glucose levels, and included adjustment for body mass index (BMI) and smoking status in the analyses. RRs were corrected for regression dilution ratio of glucose. RR (95% confidence interval) per 1 mmol/l increment of glucose for overall incident cancer was 1.05 (1.01-1.10) in men and 1.11 (1.05-1.16) in women, and corresponding RRs for fatal cancer were 1.15 (1.07-1.22) and 1.21 (1.11-1.33), respectively. Significant increases in risk among men were found for incident and fatal cancer of the liver, gallbladder, and respiratory tract, for incident thyroid cancer and multiple myeloma, and for fatal rectal cancer. In women, significant associations were found for incident and fatal cancer of the pancreas, for incident urinary bladder cancer, and for fatal cancer of the uterine corpus, cervix uteri, and stomach. CONCLUSIONS: Data from our study indicate that abnormal glucose metabolism, independent of BMI, is associated with an increased risk of cancer overall and at several cancer sites. Our data showed stronger associations among women than among men, and for fatal cancer compared to incident cancer. Please see later in the article for the Editors' Summary.
PubMed ID
20027213 View in PubMed
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Blood pressure and other metabolic syndrome factors and risk of brain tumour in the large population-based Me-Can cohort study.

https://arctichealth.org/en/permalink/ahliterature128682
Source
J Hypertens. 2012 Feb;30(2):290-6
Publication Type
Article
Date
Feb-2012
Author
Michael Edlinger
Susanne Strohmaier
Håkan Jonsson
Tone Bjørge
Jonas Manjer
Wegene T Borena
Christel Häggström
Anders Engeland
Steinar Tretli
Hans Concin
Gabriele Nagel
Randi Selmer
Dorthe Johansen
Tanja Stocks
Göran Hallmans
Pär Stattin
Hanno Ulmer
Author Affiliation
Department of Medical Statistics, Informatics and Health Economics, Medical University Innsbruck, Innsbruck, Austria.
Source
J Hypertens. 2012 Feb;30(2):290-6
Date
Feb-2012
Language
English
Publication Type
Article
Keywords
Adult
Austria - epidemiology
Blood pressure
Brain Neoplasms - epidemiology - physiopathology
Cohort Studies
Female
Humans
Male
Metabolic Syndrome X - physiopathology
Middle Aged
Norway - epidemiology
Sweden - epidemiology
Abstract
Brain tumour has few established determinants. We assessed to which extent risk of brain tumour was related to metabolic syndrome factors in adults.
In the Me-Can project, 580?000 individuals from Sweden, Austria, and Norway were followed for a median of 10 years after baseline measurement. Data on brain tumours were obtained from national cancer registries. The factors of metabolic syndrome (BMI, SBP and DBP, and blood levels of glucose, cholesterol, and triglycerides), separately and combined, were analysed in quintiles and for transformed z-scores (mean transformed to 0 and standard deviation to 1). Cox proportional hazards multivariate regression models were used, with corrections for measurement error.
During follow-up, 1312 primary brain tumours were diagnosed, predominantly meningioma (n?=?348) and high-grade glioma (n?=?436). For meningioma, the hazard ratio was increased for z-scores of SBP [hazard ratio?=?1.27 per unit standard deviation, 95% confidence interval (CI) 1.03-1.57], of DBP (hazard ratio?=?1.29, 95% CI 1.04-1.58), and of the combined metabolic syndrome score (hazard ratio?=?1.31, 95% CI 1.11-1.54). An increased risk of high-grade glioma was found for DBP (hazard ratio?=?1.23, 95% CI 1.01-1.50) and triglycerides (hazard ratio?=?1.35, 95% CI 1.05-1.72). For both meningioma and high-grade glioma, the risk was more than double in the fifth quintiles of DBP compared to the lowest quintile. For meningioma this risk was even larger for SBP.
Increased blood pressure was associated with risk of brain tumours, especially of meningiomas.
PubMed ID
22179083 View in PubMed
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147 records – page 1 of 15.