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Age-and sex-specific seasonal variation of venous thromboembolism in patients with and without family history: a nationwide family study in Sweden.

https://arctichealth.org/en/permalink/ahliterature107143
Source
Thromb Haemost. 2013 Dec;110(6):1164-71
Publication Type
Article
Date
Dec-2013
Author
Bengt Zöller
Xinjun Li
Henrik Ohlsson
Jan Sundquist
Kristina Sundquist
Author Affiliation
Dr. Bengt Zöller, Center for Primary Health Care Research, CRC, Building 28, Floor 11, Jan Waldenströms gata 35, Skåne University Hospital, S-205 02 Malmö, Sweden, Tel.: +46 70 6691476, Fax: +46 40 391370, E-mail: bengt.zoller@med.lu.se 
Source
Thromb Haemost. 2013 Dec;110(6):1164-71
Date
Dec-2013
Language
English
Publication Type
Article
Keywords
Adolescent
Age Factors
Aged
Aged, 80 and over
Child
Child, Preschool
Disease Progression
Family
Female
Genetic Predisposition to Disease
Humans
Incidence
Infant
Male
Middle Aged
Pedigree
Risk
Seasons
Sex Factors
Sweden
Venous Thromboembolism - epidemiology - genetics
Young Adult
Abstract
Seasonal variation in venous thromboembolism (VTE) risk in individuals with familial predisposition to VTE has not been explored. This nationwide study aimed to determine whether there are age- and sex-specific seasonal differences in risk of hospitalisation of VTE among individuals with and without a family history of VTE. The Swedish Multi-Generation Register was linked to Hospital Discharge Register data for the period 1964-2010. Seasonal variation in first VTE events in 1987-2010 for individuals with and without a family history of VTE (siblings or parents) was determined by several independent methods. Stratified analyses were performed according to age, sex, and VTE subtype (pulmonary embolism [PE] or deep venous thrombosis [DVT]). Seasonal variation in VTE incidence, mostly with a peak during the winter, was observed in both sexes in individuals with and without family history with overall peak-to-low ratios (PLRs) of 1.15 and 1.21, respectively. The peak day was December 25 and February 1 for those with and without a family history of VTE, respectively. Seasonal variation was strongest among individuals aged >50 years. Among individuals aged 0-25 years with a family history, the peak for VTE was in July (PLR = 1.20). Significant seasonal variation was observed for PE and DVT with the exception of DVT among those with a family history (PLR = 1.01). In conclusion, our data support the presence of a modest seasonal variation of VTE among individuals with and without a family history of VTE. However, young age and family history may modify and attenuate the effect of season on VTE.
PubMed ID
24048360 View in PubMed
Less detail

Age at diagnosis and age at death in familial prostate cancer.

https://arctichealth.org/en/permalink/ahliterature98697
Source
Oncologist. 2009 Dec;14(12):1209-17
Publication Type
Article
Date
Dec-2009
Author
Andreas Brandt
Justo Lorenzo Bermejo
Jan Sundquist
Kari Hemminki
Author Affiliation
Division of Molecular Genetic Epidemiology, German Cancer Research Centre, Im Neuenheimer Feld 580, D-69120 Heidelberg, Germany. andreas.brandt@dkfz.de
Source
Oncologist. 2009 Dec;14(12):1209-17
Date
Dec-2009
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Family Health
Genetic Predisposition to Disease
Humans
Incidence
Male
Middle Aged
Prostatic Neoplasms - diagnosis - genetics - mortality
Risk factors
Sweden - epidemiology
Abstract
OBJECTIVES: A family history of prostate cancer is associated with a higher risk for prostate cancer to first-degree relatives. If greater surveillance of men at familial risk is considered to be useful, population-based estimates of the differences in the age at diagnosis between familial and sporadic prostate cancer cases are needed. METHODS: The men in the nationwide Swedish Family-Cancer Database were classified according to the number and type of affected first-degree relatives (father or brother) and according to the relative's age at diagnosis. The cumulative incidence of prostate cancer and cumulative prostate cancer-specific mortality were estimated using a stratified Cox model. RESULTS: The cumulative incidence was highest for men with multiple affected first-degree relatives, and it was higher for brothers than for sons of prostate cancer patients. The age to reach the same cumulative incidence as the general population at age 55 years decreased with decreasing age at diagnosis of the relative, ranging from 48.7 years (father diagnosed before 60 years of age) to 53.7 years (father diagnosed after 82 years of age). Prostate cancer-specific mortality was also related to the number and type of affected relatives but there was no clear evidence for a dependency on the age at diagnosis of the relative. CONCLUSIONS: Men with a father or a brother affected by prostate cancer are diagnosed and die at earlier ages than men without a family history of prostate cancer. This study should encourage further analysis in order to assess the risks and benefits of screening for prostate cancer in men at higher risk.
PubMed ID
19939895 View in PubMed
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Age, period and cohort trends in drug abuse hospitalizations within the total Swedish population (1975-2010).

https://arctichealth.org/en/permalink/ahliterature105832
Source
Drug Alcohol Depend. 2014 Jan 1;134:355-61
Publication Type
Article
Date
Jan-1-2014
Author
Giuseppe N Giordano
Henrik Ohlsson
Kenneth S Kendler
Marilyn A Winkleby
Kristina Sundquist
Jan Sundquist
Author Affiliation
Center for Primary Health Care Research, Lund University, Jan Waldenströmsgata 35, CRC, building 28, floor 11, entrance 72, Malmö University Hospital, Malmö, S-205 02, Sweden. Electronic address: giuseppe_nicola.giordano@med.lu.se.
Source
Drug Alcohol Depend. 2014 Jan 1;134:355-61
Date
Jan-1-2014
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Cohort Studies
Female
Hospitalization - trends
Humans
Male
Middle Aged
Population Surveillance - methods
Substance-Related Disorders - diagnosis - epidemiology - therapy
Sweden - epidemiology
Time Factors
Young Adult
Abstract
The societal consequences of drug abuse (DA) are severe and well documented, the World Health Organization recommending tracking of population trends for effective policy responses in treatment of DA and delivery of health care services. However, to correctly identify possible sources of DA change, one must first disentangle three different time-related influences on the need for treatment due to DA: age effects, period effects and cohort effects.
We constructed our main Swedish national DA database (spanning four decades) by linking healthcare data from the Swedish Hospital Discharge Register to individuals, which included hospitalisations in Sweden for 1975-2010. All hospitalized DA cases were identified by ICD codes. Our Swedish national sample consisted of 3078,129 men and 2921,816 women. We employed a cross-classified multilevel logistic regression model to disentangle any net age, period and cohort effects on DA hospitalization rates.
We found distinct net age, period and cohort effects, each influencing the predicted probability of hospitalisation for DA in men and women. Peak age for DA in both sexes was 33-35 years; net period effects showed an increase in hospitalisation for DA from 1996 to 2001; and in birth cohorts 1968-1974, we saw a considerable reduction (around 75%) in predicted probability of hospitalisation for DA.
The use of hospital admissions could be regarded as a proxy of the population's health service use for DA. Our results may thus constitute a basis for effective prevention planning, treatment and other appropriate policy responses.
PubMed ID
24300899 View in PubMed
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Age-time risk patterns of solid cancers in 60 901 non-Hodgkin lymphoma survivors from Finland, Norway and Sweden.

https://arctichealth.org/en/permalink/ahliterature102725
Source
Br J Haematol. 2014 Mar;164(5):675-83
Publication Type
Article
Date
Mar-2014
Author
Justo Lorenzo Bermejo
Eero Pukkala
Tom B Johannesen
Jan Sundquist
Kari Hemminki
Source
Br J Haematol. 2014 Mar;164(5):675-83
Date
Mar-2014
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Aged
Aged, 80 and over
Female
Finland - epidemiology
Follow-Up Studies
Humans
Incidence
Lymphoma, Non-Hodgkin - epidemiology - therapy
Male
Middle Aged
Neoplasms, Second Primary - epidemiology - etiology
Norway - epidemiology
Registries
Risk Assessment - methods
Sweden - epidemiology
Time Factors
Abstract
Survival after non-Hodgkin lymphoma (NHL) has increased thanks to improved treatment but NHL survivors have an increased risk of second neoplasms. The assessment of cancer risk patterns after NHL may help to quantify the late side-effects of therapy. Poisson regression was used to estimate relative risks (RRs) and absolute incidence rates for nine solid tumours based on a nationwide cohort of 60 901 NHL survivors from Finland, Norway and Sweden. Patients were diagnosed between 1980 and 2006 and developed 6815 s neoplasms. NHL patients showed an increased risk of each of the nine investigated cancer sites: prostate and pancreas (both RRs 1·28), breast (1·37), colorectum (1·48), urinary bladder (1·52), stomach and lung (both RRs 1·87), skin (melanoma 2·27) and kidney (2·56). The RRs showed a U-shaped relationship with time after NHL for all nine-second cancer types. NHL diagnosis early in life was a risk factor for the development of second cancers with the exception of melanoma, but a risk excess was even observed in patients diagnosed with NHL at age 80+ years. The present study provides accurate estimates on the adverse late effects of NHL therapy, which should guide the establishment of cancer prevention strategies in NHL survivors.
PubMed ID
24528128 View in PubMed
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Alcohol consumption has a protective effect against hematological malignancies: a population-based study in Sweden including 420,489 individuals with alcohol use disorders.

https://arctichealth.org/en/permalink/ahliterature262809
Source
Neoplasia. 2014 Mar;16(3):229-34, 234.e1
Publication Type
Article
Date
Mar-2014
Author
Jianguang Ji
Jan Sundquist
Kristina Sundquist
Source
Neoplasia. 2014 Mar;16(3):229-34, 234.e1
Date
Mar-2014
Language
English
Publication Type
Article
Keywords
Adult
Aged
Alcohol drinking - epidemiology
Alcoholism - epidemiology
Female
Follow-Up Studies
Hematologic Neoplasms - epidemiology - etiology
Humans
Leukemia - epidemiology - etiology
Lymphoma, Non-Hodgkin - epidemiology - etiology
Male
Middle Aged
Multiple Myeloma - epidemiology - etiology
Odds Ratio
Registries
Risk factors
Siblings
Sweden - epidemiology
Young Adult
Abstract
It has been suggested that alcohol consumption is associated with increased risk of a few solid cancers, although studies that examined the association with hematological malignancies have shown inconsistent results. In this study, we examined the risk of hematological malignancies among individuals who had alcohol use disorders (AUDs) in Sweden.
Individuals with AUDs were identified from the nationwide Swedish Hospital Discharge Register and Outpatient Register, the Crime Register, and the Prescription Drug Register, and they were linked to the Swedish Cancer Registry to calculate standardized incidence ratios (SIRs) of hematological malignancies, using those Swedes without AUDs as a reference. In addition, we used a quasi-experimental sibling design to investigate the odds ratios among sibling pairs who were discordant with AUDs.
A total of 420,489 individuals were identified with AUDs. After more than 15 million person-years of follow-up, a total of 1755 individuals developed hematological malignancies demonstrating a low risk, i.e., SIR = 0.60 (95% confidence interval = 0.57-0.63). People with AUDs had low risks for developing specific types of malignancies. The lowest risk (0.51) was for leukemia, followed by myeloma (0.52), non-Hodgkin lymphoma (0.65), and Hodgkin disease (0.71). The risk was lower among AUDs identified at an older age. The low risks of hematological malignancies were also noted using sibling analysis.
Our data suggest that alcohol consumption has a protective effect against hematological malignancies. However, further studies are needed to identity the underlying mechanisms of the protective effect of alcohol consumption against hematological malignancies.
Notes
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PubMed ID
24783999 View in PubMed
Less detail

Alcohol use disorder and divorce: evidence for a genetic correlation in a population-based Swedish sample.

https://arctichealth.org/en/permalink/ahliterature290102
Source
Addiction. 2017 Apr; 112(4):586-593
Publication Type
Journal Article
Twin Study
Date
Apr-2017
Author
Jessica E Salvatore
Sara Larsson Lönn
Jan Sundquist
Paul Lichtenstein
Kristina Sundquist
Kenneth S Kendler
Author Affiliation
Department of Psychology, Virginia Commonwealth University, Richmond, VA, USA.
Source
Addiction. 2017 Apr; 112(4):586-593
Date
Apr-2017
Language
English
Publication Type
Journal Article
Twin Study
Keywords
Aged
Alcoholism - epidemiology - genetics
Divorce - statistics & numerical data
Environment
European Continental Ancestry Group - genetics
Female
Gene-Environment Interaction
Genetic Predisposition to Disease
Humans
Male
Middle Aged
Registries
Risk factors
Siblings
Sweden - epidemiology
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Abstract
We tested the association between alcohol use disorder (AUD) and divorce; estimated the genetic and environmental influences on divorce; estimated how much genetic and environmental influences accounted for covariance between AUD and divorce; and estimated latent genetic and environmental correlations between AUD and divorce. We tested sex differences in these effects.
We identified twin and sibling pairs with AUD and divorce information in Swedish national registers. We described the association between AUD and divorce using tetrachorics and used twin and sibling models to estimate genetic and environmental influences on divorce, on the covariance between AUD and divorce and the latent genetic and environmental correlations between AUD and divorce.
Sweden.
A total of 670?836 individuals (53% male) born 1940-1965.
Life-time measures of AUD and divorce.
AUD and divorce were related strongly (males: rtet  = +0.44, 95% CI = 0.43, 0.45; females rtet  = +0.37, 95% CI = 0.36, 0.38). Genetic factors accounted for a modest proportion of the variance in divorce (males: 21.3%, 95% CI = 7.6, 28.5; females: 31.0%, 95% CI = 18.8, 37.1). Genetic factors accounted for most of the covariance between AUD and divorce (males: 52.0%, 95% CI = 48.8, 67.9; females: 53.74%, 95% CI = 17.6, 54.5), followed by non-shared environmental factors (males: 45.0%, 95% CI = 37.5, 54.9; females: 41.6%, 95% CI = 40.3, 60.2). Shared environmental factors accounted for a negligible proportion of the covariance (males: 3.0%, 95% CI = -3.0, 13.5; females: 4.75%, 95% CI = 0.0, 6.6). The AUD-divorce genetic correlations were high (males: rA = +0.76, 95% CI = 0.53, 0.90; females +0.52, 95% CI = 0.24, 0.67). The non-shared environmental correlations were modest (males: rE = +0.32, 95% CI = 0.31, 0.40; females: +0.27, 95% CI = 0.27, 0.36).
Divorce and alcohol use disorder are correlated strongly in the Swedish population, and the heritability of divorce is consistent with previous studies. Covariation between AUD and divorce results from overlapping genetic and non-shared environmental factors. Latent genetic and non-shared environmental correlations for alcohol use disorder and divorce are high and moderate.
Notes
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PubMed ID
27981669 View in PubMed
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Alcohol Use Disorder and Mortality Across the Lifespan: A Longitudinal Cohort and Co-relative Analysis.

https://arctichealth.org/en/permalink/ahliterature282515
Source
JAMA Psychiatry. 2016 Jun 01;73(6):575-81
Publication Type
Article
Date
Jun-01-2016
Author
Kenneth S Kendler
Henrik Ohlsson
Jan Sundquist
Kristina Sundquist
Source
JAMA Psychiatry. 2016 Jun 01;73(6):575-81
Date
Jun-01-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Age of Onset
Aged
Alcoholism - genetics - mortality
Cause of Death
Cohort Studies
Diseases in Twins - genetics - mortality
Female
Genetic Predisposition to Disease - genetics
Humans
Longitudinal Studies
Male
Middle Aged
Proportional Hazards Models
Registries
Risk factors
Statistics as Topic
Sweden
Young Adult
Abstract
Excess alcohol consumption and alcohol use disorders (AUDs) are associated with substantially increased mortality. Efforts to reduce this toll require an understanding of their causes.
To clarify the degree to which the excess mortality associated with AUDs arises (1) from the predispositions of the person who develops AUD (and which would likely be shared by close relatives) and (2) as a direct result of AUD itself.
A prospective cohort and co-relative design study involving all individuals born in Sweden from 1940 to 1965 who had neither died nor migrated prior to 1973 or age 15 years (N?=?2?821?036). They were followed up from January 1, 1973, until December 31, 2010. Alcohol use disorder was assessed from medical, criminal, and pharmacy registries. Half-siblings, full-siblings, and monozygotic twin pairs discordant for AUD were obtained from the Multi-Generation and Twin Register.
Death obtained from the Swedish Death registry.
Our cohort (1?447?887 males and 1?373?149 females) included 131?895 males and 42?163 females registered with AUD. The mean (SD) age at first AUD registration was 39 (13.4) years. We ascertained 127?347 and 76?325 deaths in the male and female subsamples, respectively. Controlling for sex, educational status, and year of birth, the mortality hazard ratio associated with AUD was 5.83 (95% CI, 5.76-5.90) and varied-with an inverted U-shaped function-by age. Examining the AUD-mortality association in the general population and in relative pairs discordant for AUD exposure demonstrated substantial familial confounding in early to mid-adulthood: the AUD-associated mortality hazard ratio was much lower in discordant close relatives than in the general population. In middle to late adulthood, evidence for familial confounding decreased with increasing evidence for a direct effect of AUD on elevated mortality. In the oldest age group (65-70 years), the mortality hazard ratios were similar across the population and all relative pairs, suggesting that the excess mortality was largely a result of having AUD. Adding years since onset of AUD to the model showed that both increasing age and increasing years of duration of AUD contributed to the reduction of familial confounding in the association between AUD and elevated mortality.
Excess mortality associated with AUD arises both from the predispositions of the person who develops AUD and the direct result of having AUD. The effect of predisposition is more prominent early in the life course and in the early years of AUD. The direct effect of AUD becomes progressively more important later in life and with longer duration of AUD. These results have implications for interventions seeking to reduce the elevated AUD-associated mortality.
Notes
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PubMed ID
27097014 View in PubMed
Less detail

Alcohol use disorders are associated with venous thromboembolism.

https://arctichealth.org/en/permalink/ahliterature271195
Source
J Thromb Thrombolysis. 2015 Aug;40(2):167-73
Publication Type
Article
Date
Aug-2015
Author
Bengt Zöller
Jianguang Ji
Jan Sundquist
Kristina Sundquist
Source
J Thromb Thrombolysis. 2015 Aug;40(2):167-73
Date
Aug-2015
Language
English
Publication Type
Article
Keywords
Adult
Alcoholism - complications - epidemiology
Female
Humans
Male
Middle Aged
Registries
Risk factors
Sweden - epidemiology
Venous Thromboembolism - epidemiology - etiology
Abstract
Moderate alcohol consumption has been suggested to protect against venous thromboembolism (VTE). However, it is not known how alcohol abuse and its associated somatic complications affect the risk of VTE. The present study determined the risk of pulmonary embolism (PE) and deep vein thrombosis (DVT) of the lower extremities in patients with alcohol use disorders (AUDs) in Sweden. All inpatients with AUDs in 2002-2010 without a previous VTE event (72,024 patients) were matched to five controls without AUD and followed until the end of follow-up (December 31, 2010), death, emigration or a VTE event. Cox regression was used to determine adjusted hazard ratios (HRs) for VTE. AUD patients were further divided into those without alcohol-related somatic complications (AUD-) and those with alcohol-related somatic complications (AUD+, i.e., encephalopathy, epilepsy, polyneuropathy, myopathy, cardiomyopathy, gastritis, liver disease, acute pancreatitis, and chronic pancreatitis). The adjusted HR for VTE was significantly increased for both AUD- (HR 1.70, 95 % CI 1.55-1.87) and AUD+ (HR 1.73, 95 % CI 1.37-2.19) patients. The risk of DVT was increased in both AUD+ and AUD- patients (HR 1.62, 95 % CI 1.45-1.83 and HR 1.99, 95 % CI 1.53-2.59, respectively). However, the risk of PE was only significantly increased in AUD- patients (HR 1.87, 95 % 1.59-1.20) and not in AUD+ patients (HR 1.16, 95 % 0.70-1.91). In conclusion, the present study shows that AUD increases the risk of VTE, even in the absence of alcohol-related somatic complications. Our findings suggest that severe alcohol abuse increases the risk of VTE.
PubMed ID
25605687 View in PubMed
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An extended Swedish national adoption study of alcohol use disorder.

https://arctichealth.org/en/permalink/ahliterature263536
Source
JAMA Psychiatry. 2015 Mar;72(3):211-8
Publication Type
Article
Date
Mar-2015
Author
Kenneth S Kendler
Jianguang Ji
Alexis C Edwards
Henrik Ohlsson
Jan Sundquist
Kristina Sundquist
Source
JAMA Psychiatry. 2015 Mar;72(3):211-8
Date
Mar-2015
Language
English
Publication Type
Article
Keywords
Adoption
Adult
Alcohol-Related Disorders - epidemiology - etiology - genetics
Child
Environment
Female
Genetic Predisposition to Disease - epidemiology
Humans
Male
Middle Aged
Parents
Registries - statistics & numerical data
Risk factors
Siblings
Sweden - epidemiology
Young Adult
Abstract
Alcohol use disorder (AUD) runs strongly in families. It is unclear to what extent the cross-generational transmission of AUD results from genetic vs environmental factors.
To determine to what extent genetic and environmental factors contribute to the risk for AUD.
Follow-up in 8 public data registers of adoptees, their biological and adoptive relatives, and offspring and parents from stepfamilies and not-lived-with families in Sweden. In this cohort study, subtypes of AUD were assessed by latent class analysis. A total of 18,115 adoptees (born 1950-1993) and 171,989 and 107,696 offspring of not-lived-with parents and stepparents, respectively (born 1960-1993).
Alcohol use disorder recorded in medical, legal, or pharmacy registry records.
Alcohol use disorder in adoptees was significantly predicted by AUD in biological parents (odds ratio, 1.46; 95% CI, 1.29-1.66) and siblings (odds ratio, 1.94; 95% CI, 1.55-2.44) as well as adoptive parents (odds ratio, 1.40; 95% CI, 1.09-1.80). Genetic and environmental risk indices created from biological and adoptive relatives acted additively on adoptee AUD liability. Results from biological and adoptive relatives were replicated and extended from examinations of, respectively, not-lived-with parents and stepparents. Multivariate models in these families showed that AUD in offspring was significantly predicted by AUD, drug abuse, psychiatric illness, and crime in not-lived-with parents and by AUD, drug abuse, crime, and premature death in stepparents. Latent class analyses of adoptees and offspring of not-lived-with parents with AUDs revealed 3 AUD classes characterized by (1) female preponderance and high rates of psychiatric illness, (2) mild nonrecurrent symptoms, and (3) early-onset recurrence, drug abuse, and crime. These classes had distinct genetic signatures in the patterns of risk for various disorders in their not-lived-with parents and striking differences in the rates of recorded mood disorders.
Parent-offspring transmission of AUD results from both genetic and environmental factors. Genetic risk for AUD reflects both a specific liability to AUD and to other externalizing disorders. Environmental risk reflects features of both parental psychopathology and other aspects of the rearing environment. Alcohol use disorder is a heterogeneous syndrome and meaningful subtypes emerged from latent class analysis, which were validated by patterns of disorders in biological parents and specific psychiatric comorbidities. The general population contains informative family constellations that can complement more traditional adoption designs in clarifying the sources of parent-offspring resemblance.
Notes
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PubMed ID
25565339 View in PubMed
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Associated cancers in parents and offspring of polycythaemia vera and myelofibrosis patients.

https://arctichealth.org/en/permalink/ahliterature98896
Source
Br J Haematol. 2009 Nov;147(4):526-30
Publication Type
Article
Date
Nov-2009
Author
Kari Hemminki
Jan Sundquist
Justo L Bermejo
Author Affiliation
Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. k.hemminki@dkfz.de
Source
Br J Haematol. 2009 Nov;147(4):526-30
Date
Nov-2009
Language
English
Publication Type
Article
Keywords
Female
Genetic Predisposition to Disease
Humans
Male
Parents
Polycythemia Vera - epidemiology - genetics
Primary Myelofibrosis - epidemiology - genetics
Registries
Risk Assessment - methods
Siblings
Sweden - epidemiology
Abstract
Polycythaemia vera (PV) and primary myelofibrosis (MF) show concordant familial clustering but limited population level data are available on the aggregation of other discordant neoplasms in these families. We used the Swedish Family-Cancer Database to assess risks for VP and MF in families of cancer patients. A total of 3530 first PV and 1606 MF patients were identified, with high concordant familial risks. Several discordant familial associations were found for PV (acute myeloid leukaemia, Hodgkin disease, prostate and bladder cancers) or for MF (chronic lymphatic leukaemia, colorectal, kidney and cervical cancers) or for both (nervous system, eye and endocrine tumours).
PubMed ID
19754924 View in PubMed
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