Skip header and navigation

Refine By

44 records – page 1 of 5.

Age at immigration and duration of stay in relation to risk for testicular cancer among Finnish immigrants in Sweden.

https://arctichealth.org/en/permalink/ahliterature18240
Source
J Natl Cancer Inst. 2003 Aug 20;95(16):1238-40
Publication Type
Article
Date
Aug-20-2003
Author
Anders Ekbom
Lorenzo Richiardi
Olof Akre
Scott M Montgomery
Pär Sparén
Author Affiliation
Clinical Epidemiology Unit, Department of Medicine, Karolinska Hospital, Stockholm, Sweden. Anders.Ekbom@medks.ki.se
Source
J Natl Cancer Inst. 2003 Aug 20;95(16):1238-40
Date
Aug-20-2003
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Aged
Cohort Studies
Dysgerminoma - epidemiology
Emigration and Immigration
Finland - ethnology
Humans
Incidence
Male
Middle Aged
Risk assessment
Risk factors
Seminoma - epidemiology
Sweden - epidemiology
Testicular Neoplasms - epidemiology - ethnology - etiology
Time Factors
Abstract
Although the incidence of testicular cancer is increasing, substantial differences in incidence between countries and populations exist. These differences cannot be explained solely by genetic differences, but environmental exposures, particularly early exposures, have been implicated in the etiology of testicular cancer. To assess whether early exposures contribute to the incidence of testicular cancer, we identified 93 172 Finnish men who immigrated to Sweden between 1969 and 1996 and followed them for the occurrence of testicular cancer. The risk of testicular cancer was lower for Finnish immigrants to Sweden than for the Swedish general population (standardized incidence ratio [SIR] = 0.34, 95% confidence interval [CI] = 0.21 to 0.53). The reduced risk was associated with both seminomas and non-seminomas. Neither age at immigration nor duration of stay in Sweden had any impact on the reduced risk. Although the type of environmental exposures remains unknown, the results strongly indicate that early exposures are major determinants for testicular cancer.
PubMed ID
12928349 View in PubMed
Less detail

Birth order, sibship size, and risk for germ-cell testicular cancer.

https://arctichealth.org/en/permalink/ahliterature17758
Source
Epidemiology. 2004 May;15(3):323-9
Publication Type
Article
Date
May-2004
Author
Lorenzo Richiardi
Olof Akre
Mats Lambe
Fredrik Granath
Scott M Montgomery
Anders Ekbom
Author Affiliation
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Lorenzo.richiardi@meb.ki.se
Source
Epidemiology. 2004 May;15(3):323-9
Date
May-2004
Language
English
Publication Type
Article
Keywords
Adult
Birth Order
Case-Control Studies
Confidence Intervals
Germinoma - diagnosis - epidemiology
Humans
Infant, Newborn
Male
Maternal Age
Middle Aged
Odds Ratio
Paternal Age
Prevalence
Registries
Research Support, Non-U.S. Gov't
Risk assessment
Siblings
Socioeconomic Factors
Sweden - epidemiology
Testicular Neoplasms - diagnosis - epidemiology
Time Factors
Abstract
BACKGROUND: Several studies have reported an inverse association between birth order and testicular cancer risk, but estimates vary greatly and the biologic mechanism underlying the association is not established. METHODS: We have evaluated the effect of birth order, sibship size, and the combined effect of these 2 variables in relation to risk for testicular cancer in a large, nested case-control study. Specifically, we compared 3051 patients with germ-cell testicular cancer (diagnosed between 1958 and 1998 and identified through the Swedish Cancer Registry) with 9007 population control subjects. Using record linkage with the Multi-Generation Register and the Census, we obtained information on number, order, and sex of the subjects' siblings, parental age, and paternal socioeconomic status. RESULTS: Both birth order and sibship size had an inverse and monotonically decreasing association with testicular cancer risk after adjusting for parental age, paternal socioeconomic status, and twin status. The associations were modified by subjects' cohort of birth and were not present among those born after 1959. The odds ratio for having at least 3 siblings, compared with none, was 0.63 (95% confidence interval = 0.53-0.75) among subjects born before 1960. Stratified analyses showed that birth order and number of younger siblings had a similar inverse association with the risk for testicular cancer. CONCLUSIONS: Sibship size, and not only birth order, is associated with testicular cancer risk. This suggests a higher prevalence of parental subfertility among patients with testicular cancer.
PubMed ID
15097013 View in PubMed
Less detail

Cannabis Use and Incidence of Testicular Cancer: A 42-Year Follow-up of Swedish Men between 1970 and 2011.

https://arctichealth.org/en/permalink/ahliterature292471
Source
Cancer Epidemiol Biomarkers Prev. 2017 Nov; 26(11):1644-1652
Publication Type
Journal Article
Date
Nov-2017
Author
Russell C Callaghan
Peter Allebeck
Olof Akre
Katherine A McGlynn
Anna Sidorchuk
Author Affiliation
Northern Medical Program, University of Northern British Columbia, Prince George, British Columbia, Canada. russ.callaghan@unbc.ca.
Source
Cancer Epidemiol Biomarkers Prev. 2017 Nov; 26(11):1644-1652
Date
Nov-2017
Language
English
Publication Type
Journal Article
Keywords
Aged
Cannabis - adverse effects
Follow-Up Studies
Humans
Incidence
Male
Marijuana Smoking - adverse effects - epidemiology - legislation & jurisprudence
Proportional Hazards Models
Registries - statistics & numerical data
Risk factors
Surveys and Questionnaires
Sweden - epidemiology
Testicular Neoplasms - epidemiology - etiology
Abstract
Background: Given current drug policy reforms to decriminalize or legalize cannabis in numerous countries worldwide, the current study assesses the relation between cannabis use and the development of testicular cancer.Methods: The study included a population-based sample (n = 49,343) of young men ages 18-21 years who underwent conscription assessment for Swedish military service in 1969-1970. The conscription process included a nonanonymous questionnaire eliciting information about drug use. Conscription information was linked to Swedish health and administrative registry data. Testicular cancers diagnosed between 1970 and 2011 were identified by International Classification of Diseases-7/8/9/10 testicular cancer codes in the Swedish National Patient Register, the Cancer Register, or the Cause of Death Register. Cox regression modeling was used to estimate the hazards associated with cannabis use and time to diagnosis of testicular cancer.Results: No evidence was found of a significant relation between lifetime "ever" cannabis use and the subsequent development of testicular cancer [n = 45,250; 119 testicular cancer cases; adjusted HR (aHR), 1.42; 95% confidence interval (CI), 0.83-2.45]. "Heavy" cannabis use (defined as usage of more than 50 times in lifetime, as measured at conscription) was associated with the incidence of testicular cancer (n = 45,250; 119 testicular cancer cases; aHR 2.57; 95% CI, 1.02-6.50).Conclusions: The current study provides additional evidence to the limited prior literature suggesting cannabis use may contribute to the development of testicular cancer.Impact: Emerging changes to cannabis drug policy should consider the potential role of cannabis use in the development of testicular cancer. Cancer Epidemiol Biomarkers Prev; 26(11); 1644-52. ©2017 AACR.
Notes
Cites: Cancer Epidemiol Biomarkers Prev. 2015 Jan;24(1):15-31 PMID 25587109
Cites: Acta Psychiatr Scand Suppl. 1976;264:1-312 PMID 1068631
Cites: BMC Cancer. 2015 Nov 11;15:897 PMID 26560314
Cites: Cancer Causes Control. 2013 Oct;24(10):1811-20 PMID 23846283
Cites: Nature. 1993 Sep 2;365(6441):61-5 PMID 7689702
Cites: Mol Pharmacol. 1988 Nov;34(5):605-13 PMID 2848184
Cites: Addiction. 2008 May;103(5):712-20 PMID 18412748
Cites: Biochem Biophys Res Commun. 2001 Jun 8;284(2):363-8 PMID 11394887
Cites: N Engl J Med. 1974 Apr 18;290(16):872-4 PMID 4816961
Cites: Am J Public Health. 2015 May;105(5):994-1000 PMID 25790384
Cites: Br Med J (Clin Res Ed). 1988 Apr 9;296(6628):1021-5 PMID 3130122
Cites: Nat Rev Urol. 2014 Mar;11(3):169-77 PMID 24535583
Cites: Nat Rev Endocrinol. 2011 Jan;7(1):43-53 PMID 21116298
Cites: World J Urol. 2015 May;33(5):623-31 PMID 25030752
Cites: Cancer. 2009 Mar 15;115(6):1215-23 PMID 19204904
Cites: Curr Opin Psychiatry. 2009 May;22(3):258-62 PMID 19293714
Cites: Toxicol Ind Health. 2010 Feb;26(1):11-23 PMID 19942653
Cites: Lancet. 2016 Apr 23;387(10029):1762-74 PMID 26651223
Cites: Int J Drug Policy. 2016 Mar;29:9-13 PMID 26895950
Cites: Cancer. 2011 Feb 15;117(4):848-53 PMID 20925043
Cites: Cancer. 2012 Nov 1;118(21):5374-83 PMID 22965656
Cites: NIDA Res Monogr. 1992;126:48-56 PMID 1491718
Cites: Andrology. 2015 Jan;3(1):13-8 PMID 25331158
Cites: Lancet. 1987 Dec 26;2(8574):1483-6 PMID 2892048
Cites: Addiction. 1999 Nov;94(11):1663-78 PMID 10892006
Cites: Subst Use Misuse. 2015 Jan;50(1):79-89 PMID 25268294
Cites: Am J Public Health. 2016 Jan;106(1):21-7 PMID 26562117
Cites: Addiction. 2008 Mar;103(3):439-49; discussion 450-1 PMID 18269364
Cites: Milbank Q. 2014 Jun;92(2):243-9 PMID 24890246
Cites: Eur J Epidemiol. 2009;24(11):659-67 PMID 19504049
PubMed ID
29093004 View in PubMed
Less detail

Causes of death in men with localized prostate cancer: a nationwide, population-based study.

https://arctichealth.org/en/permalink/ahliterature274154
Source
BJU Int. 2016 Mar;117(3):507-14
Publication Type
Article
Date
Mar-2016
Author
Mieke Van Hemelrijck
Yasin Folkvaljon
Jan Adolfsson
Olof Akre
Lars Holmberg
Hans Garmo
Pär Stattin
Source
BJU Int. 2016 Mar;117(3):507-14
Date
Mar-2016
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Case-Control Studies
Cause of Death
Humans
Male
Middle Aged
Prostatic Neoplasms - mortality
Risk factors
Sweden - epidemiology
Abstract
To detail the distribution of causes of death from localized prostate cancer (PCa).
The database PCBase Sweden links the Swedish National Prostate Cancer Register with other nationwide population-based healthcare registers. We selected all 57 187 men diagnosed with localized PCa between 1997 and 2009 and their 114 374 PCa-free control subjects, matched according to age and county of residence. Mortality was calculated using competing risk regression analyses, taking into account PCa risk category, age and Charlson comorbidity index (CCI).
In men with low-risk PCa, all-cause mortality was lower compared with that in corresponding PCa-free men: 10-year all-cause mortality was 18% for men diagnosed at age 70 years, with a CCI score of 0, and 21% among corresponding control subjects. Of these cases, 31% died from cardiovascular disease (CVD) compared with 37% of the corresponding control subjects. For men with low-risk PCa, 10-year PCa-mortality was 0.4, 1 and 3% when diagnosed at age 50, 60 and 70 years, respectively. PCa was the third most common cause of death (18%), after CVD (31%) and other cancers (30%). By contrast, PCa was the most common cause of death in men with intermediate- and high-risk localized PCa.
Men with low-risk PCa had lower all-cause mortality than PCa-free men because of lower CVD mortality, driven by early detection selection; however, for men with intermediate- or high-risk disease, the rate of PCa death was substantial, irrespective of CCI score, and this was even more pronounced for those diagnosed at age 50 or 60 years.
Notes
Cites: J Natl Compr Canc Netw. 2010 Feb;8(2):162-20020141676
Cites: J Natl Cancer Inst. 2010 Jul 7;102(13):950-820562373
Cites: J Urol. 2010 Oct;184(4):1322-720723940
Cites: J Urol. 2011 Mar;185(3):833-921239002
Cites: Scand J Urol Nephrol. 2011 Sep;45(4):226-3221463227
Cites: Eur J Cancer. 2012 Jan;48(1):75-8421852113
Cites: Ann Oncol. 2012 May;23(5):1325-3421965474
Cites: Stat Methods Med Res. 2012 Jun;21(3):257-7221216803
Cites: Int J Cancer. 2011 Oct 15;129(8):1881-821154740
Cites: J Urol. 2012 Sep;188(3):798-80122819416
Cites: J Natl Cancer Inst. 2012 Sep 5;104(17):1335-4222835388
Cites: Cancer. 2012 Dec 15;118(24):6207-1622674346
Cites: Eur Urol. 2013 Jan;63(1):88-9622902040
Cites: Eur Urol. 2013 Mar;63(3):419-2523083803
Cites: Eur Urol. 2013 Mar;63(3):428-3523084329
Cites: Int J Cancer. 2013 Aug 15;133(4):937-4323354735
Cites: BJU Int. 2013 Jul;112(2):182-923795786
Cites: J Clin Oncol. 2014 Aug 10;32(23):2471-825002728
Cites: Scand J Urol. 2014 Oct;48(5):426-3524611795
Cites: JAMA. 2003 Mar 19;289(11):1414-2012636464
Cites: J Chronic Dis. 1987;40(5):373-833558716
Cites: Prostate Cancer Prostatic Dis. 2006;9(3):270-416770340
Cites: Scand J Urol Nephrol. 2007;41(6):456-7717934985
Cites: Scand J Urol Nephrol. 2008;42(4):352-718609293
Cites: JAMA. 2009 Sep 16;302(11):1202-919755699
Cites: Scand J Urol Nephrol. 2009;43(5):342-919921977
PubMed ID
25604807 View in PubMed
Less detail

Celiac disease is not a risk factor for infertility in men.

https://arctichealth.org/en/permalink/ahliterature136891
Source
Fertil Steril. 2011 Apr;95(5):1709-13.e1-3
Publication Type
Article
Date
Apr-2011
Author
Daniela Zugna
Lorenzo Richiardi
Olof Akre
Olof Stephansson
Jonas F Ludvigsson
Author Affiliation
Cancer Epidemiology Unit, Center for Experimental Research and Medical Studies and Center for Oncologic Prevention in Piedmont, University of Turin, Turin, Italy.
Source
Fertil Steril. 2011 Apr;95(5):1709-13.e1-3
Date
Apr-2011
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Birth rate
Case-Control Studies
Celiac Disease - complications - epidemiology
Child
Female
Humans
Infertility, Male - epidemiology - etiology
Male
Middle Aged
Parity
Pregnancy
Risk factors
Sweden - epidemiology
Young Adult
Abstract
To examine fertility in men with biopsy-verified celiac disease (CD) in light of research that suggests that men with CD have impaired sperm quality.
Using multinomial logistic regression and Cox regression, we estimated the fertility of the study group compared with that of 31,677 age-matched reference male controls.
Sweden.
Swedish nationwide population-based cohort of 7,121 men with CD (defined according to duodenal-jejunal biopsy data with [Marsh III] villous atrophy) ages 18-54 years at some point before the end of follow-up.
Number of children according to the Swedish Multi-Generation Register.
During follow-up, men with CD had 9,935 children compared with 42,245 among controls. Adjusting for age, calendar period, and parity and stratifying by education, the overall fertility hazard ratio in the men with biopsy-verified CD was 1.02 (95% confidence interval, 0.99-1.04).
This study found a normal fertility in men with diagnosed CD.
PubMed ID
21333987 View in PubMed
Less detail

Comparative effectiveness of radical prostatectomy and radiotherapy in prostate cancer: observational study of mortality outcomes.

https://arctichealth.org/en/permalink/ahliterature104886
Source
BMJ. 2014;348:g1502
Publication Type
Article
Interactive/Multimedia
Date
2014
Author
Prasanna Sooriakumaran
Tommy Nyberg
Olof Akre
Leif Haendler
Inge Heus
Mats Olsson
Stefan Carlsson
Monique J Roobol
Gunnar Steineck
Peter Wiklund
Author Affiliation
Department of Urology, Karolinska University Hospital, Stockholm, Sweden.
Source
BMJ. 2014;348:g1502
Date
2014
Language
English
Publication Type
Article
Interactive/Multimedia
Keywords
Aged
Forecasting
Humans
Male
Middle Aged
Propensity Score
Prostatectomy - methods
Prostatic Neoplasms - mortality - radiotherapy - surgery
Retrospective Studies
Survival Rate - trends
Sweden - epidemiology
Treatment Outcome
Abstract
To compare the survival outcomes of patients treated with surgery or radiotherapy for prostate cancer.
Observational study.
Sweden, 1996-2010.
34,515 men primarily treated for prostate cancer with surgery (n=21,533) or radiotherapy (n=12,982). Patients were categorised by risk group (low, intermediate, high, and metastatic), age, and Charlson comorbidity score.
Cumulative incidence of mortality from prostate cancer and other causes. Competing risks regression hazard ratios for radiotherapy versus surgery were computed without adjustment and after propensity score and traditional (multivariable) adjustments, as well as after propensity score matching. Several sensitivity analyses were performed.
Prostate cancer mortality became a larger proportion of overall mortality as risk group increased for both the surgery and the radiotherapy cohorts. Among patients with non-metastatic prostate cancer the adjusted subdistribution hazard ratio for prostate cancer mortality favoured surgery (1.76, 95% confidence interval 1.49 to 2.08, for radiotherapy v prostatectomy), whereas there was no discernible difference in treatment effect among men with metastatic disease. Subgroup analyses indicated more clear benefits of surgery among younger and fitter men with intermediate and high risk disease. Sensitivity analyses confirmed the main findings.
This large observational study with follow-up to 15 years suggests that for most men with non-metastatic prostate cancer, surgery leads to better survival than does radiotherapy. Younger men and those with less comorbidity who have intermediate or high risk localised prostate cancer might have a greater benefit from surgery.
Notes
Cites: Eur Urol. 2014 Jan;65(1):124-3724207135
Cites: Int J Epidemiol. 2013 Aug;42(4):956-6722561842
Cites: J Clin Epidemiol. 2004 Jul;57(7):721-915358400
Cites: JAMA. 1998 Sep 16;280(11):969-749749478
Cites: Biometrics. 1998 Sep;54(3):948-639750244
Cites: JAMA. 1999 May 5;281(17):1591-710235151
Cites: Urology. 2007 Jun;69(6):1095-10117572194
Cites: Eur Urol. 2007 Oct;52(4):973-8217644245
Cites: Scand J Urol Nephrol. 2008;42(4):352-718609293
Cites: Scand J Urol Nephrol. 2009;43(5):342-919921977
Cites: J Natl Cancer Inst. 2010 Jan 6;102(1):39-4619996060
Cites: J Clin Oncol. 2010 Mar 20;28(9):1508-1320159826
Cites: J Natl Cancer Inst. 2010 Jul 7;102(13):950-820562373
Cites: Eur J Cancer. 2010 Nov;46(17):3095-10121047592
Cites: Cancer. 2010 Nov 15;116(22):5226-3420690197
Cites: J Natl Cancer Inst. 2010 Dec 1;102(23):1780-9320944078
Cites: J Urol. 2011 Mar;185(3):833-921239002
Cites: CA Cancer J Clin. 2011 Mar-Apr;61(2):69-9021296855
Cites: Eur Urol. 2011 Jan;59(1):88-9520965646
Cites: N Engl J Med. 2011 May 5;364(18):1708-1721542742
Cites: Cancer. 2011 Jul 1;117(13):2883-9121692049
Cites: J Natl Cancer Inst. 2011 Jul 20;103(14):1134; author reply 1134-521690487
Cites: JAMA. 2011 Dec 7;306(21):2359-6622147380
Cites: BJU Int. 2012 Feb;109 Suppl 1:22-922239226
Cites: Eur Urol. 2012 Apr;61(4):664-7522169079
Cites: Eur Urol. 2012 Apr;61(4):679-8522206800
Cites: J Urol. 2012 Apr;187(4):1259-6522335870
Cites: Eur Urol. 2012 Aug;62(2):204-922541389
Cites: N Engl J Med. 2012 Jul 19;367(3):203-1322808955
Cites: Int J Urol. 2012 Sep;19(9):836-44; author reply 844-522574746
Cites: BJU Int. 2013 Mar;111(3):381-822758210
Cites: Eur Urol. 2013 Sep;64(3):372-823506834
Cites: Int J Clin Oncol. 2013 Dec;18(6):1078-8423179638
Comment In: BMJ. 2014;348:g227124668778
Comment In: BMJ. 2014;348:g227324668697
Comment In: BMJ. 2014;348:g226624668796
Comment In: BMJ. 2014;348:g158024574475
Comment In: BMJ. 2014;348:g230524668764
PubMed ID
24574496 View in PubMed
Less detail

Concordance of Non-Low-Risk Disease Among Pairs of Brothers With Prostate Cancer.

https://arctichealth.org/en/permalink/ahliterature302654
Source
J Clin Oncol. 2018 06 20; 36(18):1847-1852
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Twin Study
Date
06-20-2018
Author
Fredrik Jansson
Linda Drevin
Thomas Frisell
Pär Stattin
Ola Bratt
Olof Akre
Author Affiliation
Fredrik Jansson, Thomas Frisell, and Olof Akre, Karolinska Institute; Olof Akre, Karolinska University Hospital; Fredrik Jansson, Danderyd Hospital, Stockholm; Linda Drevin, Regional Cancer Centre, Uppsala/Örebro; Pär Stattin, Uppsala University Hospital, Uppsala; and Ola Bratt, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Source
J Clin Oncol. 2018 06 20; 36(18):1847-1852
Date
06-20-2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Twin Study
Keywords
Aged
Cohort Studies
Humans
Male
Middle Aged
Neoplasm Staging
Odds Ratio
Prostatic Neoplasms - epidemiology - genetics - pathology
Registries
Risk
Siblings
Sweden - epidemiology
Twins, Monozygotic - genetics
Abstract
Purpose Prostate cancer among first-degree relatives is a strong risk factor for diagnosis of prostate cancer, and the contribution of heritable factors in prostate cancer etiology is high. We investigated how the concordance of non-low-risk prostate cancer among brothers is affected by their genetic relation. Methods We identified 4,262 pairs of brothers with prostate cancer in the Prostate Cancer Database Sweden. Their cancers were categorized as low risk (Gleason score = 6; clinical stage T1-2, Nx/N0, Mx/M0; and prostate-specific antigen = 10 ng/mL) or non-low risk. The odds ratio (OR) for concordance of non-low-risk cancer was calculated with logistic regression for the different types of fraternity (monozygotic twins, dizygotic twins, full brothers, and half-brothers) Results Among monozygotic twins who both were diagnosed with prostate cancer, the OR for both brothers being in the non-low-risk category was 3.82 (95% CI, 0.99 to 16.72) after adjusting for age and year of diagnosis. Among full brothers, the corresponding adjusted OR was 1.21 (95% CI, 1.04 to 1.39). When the analysis was restricted to brothers who both were diagnosed within 4 years, the results were similar. Conclusion Non-low-risk prostate cancer has a heritable pattern suggesting shared genetic factors, with the highest concordance among monozygotic twins. Our results suggest that a man whose brother has been diagnosed with a non-low-risk prostate cancer is at a clinically relevant increased risk of developing an aggressive prostate cancer himself.
PubMed ID
29652556 View in PubMed
Less detail

Congenital malformations and testicular germ cell tumors.

https://arctichealth.org/en/permalink/ahliterature114791
Source
Int J Cancer. 2013 Oct 15;133(8):1900-4
Publication Type
Article
Date
Oct-15-2013
Author
Britton Trabert
Daniela Zugna
Lorenzo Richiardi
Katherine A McGlynn
Olof Akre
Author Affiliation
Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA. britton.trabert@nih.gov
Source
Int J Cancer. 2013 Oct 15;133(8):1900-4
Date
Oct-15-2013
Language
English
Publication Type
Article
Keywords
Congenital Abnormalities - embryology - epidemiology
Cryptorchidism - complications - epidemiology
Female
Hernia, Inguinal - complications - epidemiology
Humans
Hypospadias - complications - epidemiology
Male
Neoplasms, Germ Cell and Embryonal - complications - epidemiology
Odds Ratio
Pregnancy
Prenatal Exposure Delayed Effects
Registries
Risk
Risk factors
Sweden - epidemiology
Testicular Neoplasms - complications - epidemiology
Testis - embryology
Abstract
Cryptorchidism is one of the few known risk factors for testicular germ cell tumors (TGCT). It has been postulated that other congenital malformations, in particular hypospadias, are also associated with increased risk; however, associations with birth defects have not been extensively studied. Using Swedish population-based registries we evaluated the relationship between birth defects and risk of TGCT. TGCT cases (n = 6,593) diagnosed between 15 and 65 years of age were identified from the Swedish Cancer Registry between 1964 and 2008. Five controls per case were randomly selected from the population register and matched on birth year and birth county. Congenital malformations were identified via linkage with the Hospital Discharge Register. Odds ratios (ORs) and 95% confidence intervals (CIs) for the association between each group of malformations and TGCT were estimated using conditional logistic regression. In addition to the expected association between cryptorchidism and TGCT risk [OR (95% CI): 3.18 (2.50-4.04)], hypospadias [2.41 (1.27-4.57)], inguinal hernia [1.37 (1.11-1.68)] and other genital malformations [2.19 (1.17-4.10)] were associated with an increased risk of TGCT. Mutual adjustment for cryptorchidism, hypospadias, inguinal hernia and other genital malformations did not appreciably change the associations (ORs: 3.16, 2.25, 1.30 and 1.90, respectively). The other (nongenital) malformations evaluated were not associated with TGCT. These data suggest that developmental urogenital abnormalities, specifically cryptorchidism, hypospadias and inguinal hernia, are associated with an increased risk of TGCT, further supporting the hypothesis that prenatal exposure(s) related to proper genital development are related to this tumor.
PubMed ID
23580254 View in PubMed
Less detail

Dihydrotestosterone levels and survival in screening-detected prostate cancer: a 15-yr follow-up study.

https://arctichealth.org/en/permalink/ahliterature163736
Source
Eur Urol. 2008 Jan;53(1):106-11
Publication Type
Article
Date
Jan-2008
Author
Anders Kjellman
Olof Akre
Ulf Norming
Magnus Törnblom
Ove Gustafsson
Author Affiliation
Department of Clinical Science, Intervention, and Technology, Karolinska Institutet, Stockholm, Sweden. anders.kjellman@karolinska.se
Source
Eur Urol. 2008 Jan;53(1):106-11
Date
Jan-2008
Language
English
Publication Type
Article
Keywords
Aged
Dihydrotestosterone - blood
Follow-Up Studies
Humans
Male
Mass Screening - methods
Middle Aged
Prostatic Neoplasms - blood - diagnosis - mortality
Radioimmunoassay
Risk factors
Survival Rate - trends
Sweden - epidemiology
Time Factors
Tumor Markers, Biological - blood
Abstract
It has been hypothesized that dihydrotestosterone (DHT), the main intracellular androgen in the prostate, affects prostatic tumour progression. In this study, we evaluated serum DHT levels at the time of prostate-cancer diagnosis in relation to survival.
Sixty-five screening-detected patients diagnosed in 1988-1989 were followed for 15 yr. DHT levels at the time of diagnosis were determined through radio-immuno assay. Subjects were followed up through the nationwide tax register. Medical records of all dead subjects were reviewed, and cause of death was established by an endpoint committee. Data were analyzed through Kaplan-Meier estimation and Cox proportional-hazards regression.
Seventeen of 41 deaths in the cohort during follow-up were attributed to prostate cancer. Patients with DHT above the median had a significant better prostate-cancer-specific survival than those with DHT below the median (log rank p=0.0075). In the univariate analyses, one unit increase in DHT was associated with a hazard ratio (HR) of 0.14 (95% CI=0.02-0.93). In the multivariate model, including prostate-specific antigen level, the association between DHT and prostate-cancer-specific survival was not significant (HR=0.18; 95% CI=0.02-1.6). DHT level below the median remained significantly associated with decreased survival in the multivariate model (HR=0.23; 95% CI=0.06-0.90). No association was found between DHT level and hazard of dying from causes other than prostate cancer.
Although the prognostic value of DHT levels at diagnosis remains unclear, these results provides evidence of an association between low DHT and decreased survival in prostate cancer patients.
PubMed ID
17482753 View in PubMed
Less detail

Effect of Comorbidity on Prostate Cancer-Specific Mortality: A Prospective Observational Study.

https://arctichealth.org/en/permalink/ahliterature286843
Source
J Clin Oncol. 2017 Nov 01;35(31):3566-3574
Publication Type
Article
Date
Nov-01-2017
Author
Prabhakar Rajan
Prasanna Sooriakumaran
Tommy Nyberg
Olof Akre
Stefan Carlsson
Lars Egevad
Gunnar Steineck
N Peter Wiklund
Source
J Clin Oncol. 2017 Nov 01;35(31):3566-3574
Date
Nov-01-2017
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Cohort Studies
Comorbidity
Humans
Kallikreins - blood
Male
Middle Aged
Proportional Hazards Models
Prostate-Specific Antigen - blood
Prostatic Neoplasms - blood - mortality - therapy
Sweden - epidemiology
Abstract
Purpose To determine the effect of comorbidity on prostate cancer (PCa)-specific mortality across treatment types. Patients and Methods These are the results of a population-based observational study in Sweden from 1998 to 2012 of 118,543 men who were diagnosed with PCa with a median follow-up of 8.3 years (interquartile range, 5.2 to 11.5 years) until death from PCa or other causes. Patients were categorized by patient characteristics (marital status, educational level) and tumor characteristics (serum prostate-specific antigen, tumor grade and clinical stage) and by treatment type (radical prostatectomy, radical radiotherapy, androgen deprivation therapy, and watchful waiting). Data were stratified by Charlson comorbidity index (0, 1, 2, or = 3). Mortality from PCa and other causes and after stabilized inverse probability weighting adjustments for clinical patient and tumor characteristics and treatment type was determined. Kaplan-Meier estimates and Cox proportional hazards regression models were used to calculate hazard ratios. Results In the complete unadjusted data set, we observed an effect of increased comorbidity on PCa-specific and other-cause mortality. After adjustments for patient and tumor characteristics, the effect of comorbidity on PCa-specific mortality was lost but maintained for other-cause mortality. After additional adjustment for treatment type, we again failed to observe an effect for comorbidity on PCa-specific mortality, although it was maintained for other-cause mortality. Conclusion This large observational study suggests that comorbidity affects other cause-mortality but not PCa-specific- mortality after accounting for patient and tumor characteristics and treatment type. Regardless of radical treatment type (radical prostatectomy or radical radiotherapy), increasing comorbidity does not seem to significantly affect the risk of dying from PCa. Consequently, differences in oncologic outcomes that were observed in population-based comparative effectiveness studies of PCa treatments may not be a result of the varying distribution of comorbidity among treatment groups.
PubMed ID
28930493 View in PubMed
Less detail

44 records – page 1 of 5.