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  • 1
    Keywords: CANCER ; human ; MODEL ; MODELS ; SUPPORT ; COHORT ; EPIDEMIOLOGY ; EXPOSURE ; RISK ; RISKS ; MARKER ; RISK-FACTORS ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; CARE ; HEALTH ; AGE ; WOMEN ; SWEDEN ; RISK FACTOR ; INDIVIDUALS ; CHILDREN ; SERUM ; REGRESSION ; HUMAN CHORIONIC-GONADOTROPIN ; preeclampsia ; PREGNANCY ; BIRTH ; USA ; INCREASED RISK ; RISK-FACTOR ; FETAL ; CONFIDENCE ; 2ND TRIMESTER ; HYPEREMESIS GRAVIDARUM ; MOTHER ; TRANSIENT INCREASE
    Abstract: Background: Human chorionic gonadotropin (hCG) is a pregnancy-specific hormone, proposed to be involved in the protective effect against breast cancer afforded to mothers who bear children. In comparison with normal pregnancies, Down syndrome pregnancies are characterized by further elevated hCG concentrations from late first trimester to the middle of the second trimester. This study aimed to compare the risk of breast cancer in women who gave birth to a child with Down syndrome (as a marker of elevated hCG exposure) with that of women who had only unaffected children. Methods: The study cohort included all mothers of live-born children in Norway and Sweden from 1967-1973 through 2004. During the study period, 54,063 women developed breast cancer; 5330 children with Down syndrome were born and 139 breast cancer cases were diagnosed in their mothers. We fitted Cox proportional hazards regression models to obtain relative risks of breast cancer, adjusted for risk factors for breast cancer, such as overall parity and age at births. Results: Mothers of Down syndrome children were at 23% increased risk to develop breast cancer (95% confidence interval = 4%-46%). The risk increase was limited to women who had a Down syndrome child after age 30, and seemed to be confined to women whose cancer was diagnosed before age 50. Conclusions: Study results do not support the hypothesis of a protective effect of elevated pregnancy hCG on maternal breast cancer. (Epidemiology 2009;20: 584-589)
    Type of Publication: Journal article published
    PubMed ID: 19451822
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  • 2
  • 3
    Keywords: CANCER ; BLOOD ; carcinoma ; COHORT ; cohort studies ; cohort study ; RISK ; ASSOCIATION ; HEALTH ; WOMEN ; OBESITY ; PROSPECTIVE COHORT ; COLORECTAL-CANCER ; SWEDEN ; CARCINOMAS ; body mass index ; REGRESSION ; ASSOCIATIONS ; WEIGHT ; BODY-SIZE ; GROWTH-FACTOR-I ; metabolic syndrome ; blood pressure ; SERUM-LEVELS ; prospective ; CORONARY HEART-DISEASE ; INCREASED RISK ; CANCERS ; CANCER-RISK ; CIRCULATING LEVELS ; C-PEPTIDE ; BODY-MASS ; endometrial neoplasms ; journals ; AGED NORWEGIAN MEN ; metabolic syndrome X
    Abstract: The authors examined the association between the metabolic syndrome and risk of incident endometnal and fatal uterine corpus cancer within a large prospective cohort study Approximately 290,000 women from Austria, Norway, and Sweden were enrolled during 1974-2005, with measurements of height, weight, systolic and diastolic blood pressure, and circulating levels of glucose, total cholesterol, and tnglycendes Relative risks were estimated using Cox proportional hazards regression. The metabolic syndrome was assessed as a composite z score, as the standardized sum of z scores for body mass index, blood pressure, glucose, cholesterol, and tnglycendes. A total of 917 endonnetnal carcinomas and 129 fatal cancers were identified Increased risks of incident endometnal carcinoma and fatal uterine corpus cancer were seen for the metabolic syndrome factors combined, as well as for individual factors (except for cholesterol) The relative risk of endometnal carcinoma for the metabolic syndrome was 1.37 (95% confidence interval 1 28, 1 46) per 1-unit increment of z score The positive associations between metabolic syndrome factors (both individually and combined) and endometrial carcinoma were confined to the heaviest women. The association between the metabolic syndrome and endometnal carcinoma risk seems to go beyond the risk conferred by obesity alone, particularly in women with a high body mass index
    Type of Publication: Journal article published
    PubMed ID: 20219764
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  • 4
    Keywords: brain ; CANCER ; Germany ; GENERATION ; SYSTEM ; COHORT ; EPIDEMIOLOGY ; incidence ; RISK ; SITE ; GENE ; GENES ; PATIENT ; FAMILY ; ASSOCIATION ; IDENTIFICATION ; NUMBER ; etiology ; COUNTRIES ; SWEDEN ; familial risk ; CHILDREN ; RELATIVES ; ONCOLOGY ; SIBLINGS ; BRAIN-TUMORS ; GLIOMA ; brain tumour ; methods ; ONSET ; CANCERS ; population-based ; FAMILIAL RISKS ; brain tumours ; tumours ; Genetic ; peripheral nerve tumour ; spinal tumour
    Abstract: BACKGROUND: Familial nervous system cancers are rare and limited data on familial aspects are available particularly on site-specific tumours. METHODS: Data from five Nordic countries were used to analyse familial risks of nervous system tumours. Standardised incidence ratios (SIRs) were calculated for offspring of affected relatives compared with offspring of non-affected relatives. RESULTS: The total number of patients with nervous system tumour was 63 307, of whom 32 347 belonged to the offspring generation. Of 851 familial patients (2.6%) in the offspring generation, 42 (4.7%) belonged to the families of a parent and at least two siblings affected. The SIR of brain tumours was 1.7 in offspring of affected parents; it was 2.0 in siblings and 9.4 in families with a parent and sibling affected. For spinal tumours, the SIRs were much higher for offspring of early onset tumours, 14.0 for offspring of affected parents and 22.7 for siblings. The SIRs for peripheral nerve tumours were 16.3 in offspring of affected parents, 27.7 in siblings and 943.9 in multiplex families. CONCLUSION: The results of this population-based study on medically diagnosed tumours show site-, proband-and age-specific risks for familial tumours, with implications for clinical genetic counselling and identification of the underlying genes. British Journal of Cancer (2010) 102, 1786-1790. doi: 10.1038/sj.bjc.6605708 www.bjcancer.com Published online 25 May 2010 (C) 2010 Cancer Research UK
    Type of Publication: Journal article published
    PubMed ID: 20502456
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  • 5
    Keywords: cohort study ; EPIDEMIOLOGY ; HEPATOCELLULAR-CARCINOMA ; hepatocellular carcinoma ; UNITED-STATES ; DIABETES-MELLITUS ; ALCOHOL-CONSUMPTION ; INCIDENCE RATES ; VIRUS-INFECTION ; metabolic syndrome ; US ADULTS ; REGRESSION DILUTION ; INTERNATIONAL TRENDS ; intrahepatic cholangiocarcinoma ; TOTAL SERUM-CHOLESTEROL
    Abstract: Initial studies have indicated diabetes and obesity to be risk factors for hepatocellular carcinoma; but the association between other metabolic risk factors and primary liver cancer (PLC) has not been investigated. The metabolic syndrome and cancer project (Me-Can) includes cohorts from Norway, Austria and Sweden with data on 578,700 subjects. We used Cox proportional hazard models to calculate relative risks (RRs) of PLC by body mass index (BMI), blood pressure and plasma levels of glucose, cholesterol and triglycerides as continuous standardized variables (z-score with mean = 0 and standard deviation (SD) = 1) and their standardized sum of metabolic syndrome (MetS) z-score. RRs were corrected for random error in measurements. During an average follow-up of 12.0 years (SD = 7.8), 266 PLCs were diagnosed among cohort members. RR of liver cancer per unit increment of z-score adjusted for age, smoking status and BMI and stratified by birth year, sex and sub-cohorts, was for BMI 1.39 (95% confidence interval (CI) 1.24-1.58), mid blood pressure 2.08 (0.95-4.73), blood glucose 2.13 (1.55-2.94) cholesterol 0.62 (0.51-0.76) and serum triglycerides 0.85 (0.65-1.10). The RR per one unit increment of the MetS z-score was 1.35 (1.12-1.61). BMI, glucose and a composite MetS score were positively and cholesterol negatively associated with risk of liver cancer.
    Type of Publication: Journal article published
    PubMed ID: 21805476
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  • 6
    Keywords: FOLLOW-UP ; COHORT ; MORTALITY ; BLOOD-PRESSURE ; DIABETES-MELLITUS ; METAANALYSIS ; BODY-MASS INDEX ; CUTANEOUS MALIGNANT-MELANOMA ; BASAL-CELL CARCINOMA ; REGRESSION DILUTION
    Abstract: Background Little is known about the associations of metabolic aberrations with malignant melanoma (MM) and nonmelanoma skin cancer (NMSC). Objectives To assess the associations between metabolic factors (both individually and combined) and the risk of skin cancer in the large prospective Metabolic Syndrome and Cancer Project (Me-Can). Methods During a mean follow-up of 12 years of the Me-Can cohort, 1728 (41% women) incident MM, 230 (23% women) fatal MM and 1145 (33% women) NMSC were identified. Most NMSC cases (76%) were squamous cell carcinoma (SCC) (873, 33% women). Hazard ratios (HRs) were estimated by Cox proportional hazards regression for quintiles and standardized z-scores (with a mean of 0 and SD of 1) of body mass index (BMI), blood pressure, glucose, cholesterol, triglycerides and for a combined metabolic syndrome score. Risk estimates were corrected for random error in the measurements. Results Blood pressure per unit increase of z-score was associated with an increased risk of incident MM cases in men and women [HR 1.17, 95% confidence interval (CI) 1.04-1.31 and HR 1.18, 95% CI 1.03-1.36, respectively] and fatal MM cases among women (HR 2.39, 95% CI 1.58-3.64). In men, all quintiles for BMI above the reference were associated with a higher risk of incident MM. In women, SCC NMSC risk increased across quintiles for glucose levels (P-trend 0.02) and there was a trend with triglyceride concentration (P-trend 0.09). Conclusion These findings suggest that mechanisms linked to blood pressure may be involved in the pathogenesis of MM. SCC NMSC in women could be related to glucose and lipid metabolism.
    Type of Publication: Journal article published
    PubMed ID: 22530854
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  • 7
    Keywords: carcinoma ; DISEASE ; TUMORS ; MUTATION ; FAMILY-HISTORY ; PAPILLARY ; COMMON VARIANTS ; GRIM-19
    Abstract: BACKGROUND: We aimed to estimate lifetime cumulative risk of thyroid cancer (CRTC) in first-degree relatives of patients with non-medullary thyroid cancers (NMTC), including papillary (PTC)/follicular/oxyphilic/anaplastic thyroid carcinoma, by histology and age at diagnosis in patients and their relatives. DESIGN: A population-based cohort of 63 495 first-degree relatives of 11 206 NMTC patients diagnosed in 1955-2009 in Nordic countries was followed for cancer incidence. Standardised incidence ratios (SIRs) were calculated using histology-specific, age-specific, sex-specific, period-specific and country-specific incidence rates as reference. RESULTS: The 0-84-year CRTC in female relatives of a patient with PTC was 2%, representing a threefold increase over the general population risk (SIR=2.9, 95% CI 2.4 to 3.4; Men: CRTC=1%, SIR=2.5, 95% CI 1.9 to 3.3). When there were 〉/=2 PTC patients diagnosed at age 〈60 years in a family, CRTC for female relatives was 10% (male 24%). Twins had a 23-fold increased risk of concordant PTC. Family history of follicular/oxyphilic/anaplastic carcinoma increased CRTC in relatives to about 1-2%. Although no familial case of concordant oxyphilic/anaplastic carcinoma was found, familial risks of discordant histology types of NMTC were interchangeably high for most of the types, for example, higher risk of PTC when a first-degree relative had follicular (SIR=3.0, 95%CI 1.7 to 4.9) or anaplastic (SIR=3.6, 95% CI 1.2 to 8.4) carcinoma. The earlier a patient was diagnosed with PTC in a family, the higher was the SIR in his/her younger relatives. There was a tendency towards concordant age at diagnosis of thyroid cancer among relatives of PTC patients. CONCLUSIONS: This study provides clinically relevant risk estimates for family members of NMTC patients.
    Type of Publication: Journal article published
    PubMed ID: 23585692
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  • 8
    Keywords: TUMORS ; familial risk ; TRENDS
    Abstract: Background: None of the population-based epidemiologic studies to date has had a large enough sample size to show the familial risk of testicular cancer (TC) by age at diagnosis for patients and their relatives or for rare histologic subtypes. Objective: To estimate absolute and relative risks of TC in relatives of TC patients by age at diagnosis in patients and their relatives and histological subtypes. Design, setting, and participants: In a joint population-based cohort study, 97 402 first-degree relatives of 21 254 TC patients who were diagnosed between1955 and 2010 in five European countries were followed for cancer incidence. Outcome measurements and statistical analysis: Standardized incidence ratios (SIRs) were estimated using histology-, age-, period-, and country-specific incidence rates as references. Lifetime cumulative risks were also calculated. Results and limitations: The lifetime cumulative risk of TC in brothers of a patient with TC was 2.3%, which represents a fourfold increase in risk (SIR 4.1, 95% confidence interval [CI] 3.6-4.6) compared to the general population. TC in a father increased the risk by up to twofold in his son (95% CI 1.7-2.4; lifetime risk 1.2%) and vice versa. When there were two or more TC patients diagnosed in a family, the lifetime TC risk for relatives was 10-11%. Depending on age at diagnosis, twins had a 9-74% lifetime risk of TC. Family history of most of the histologic subtypes of TC increased the risk of concordant and most discordant subtypes. There was a tendency toward concordant age at diagnosis of TC among relatives. Conclusions: This study provides clinically relevant age-specific cancer risk estimates for relatives of TC patients. Familial TC patients tended to develop TC at an age close to the age at diagnosis of TC among their relatives, which is a novel finding of this study. Patient summary: This joint European population study showed that sons and brothers of testicular cancer patients are at higher risk of developing this cancer at an age close to the age at diagnosis of their relatives.
    Type of Publication: Journal article published
    PubMed ID: 25913387
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  • 9
    Keywords: CANCER ; carcinoma ; COHORT ; EPIDEMIOLOGY ; RISK ; OBESITY ; HUMAN-PAPILLOMAVIRUS ; cholesterol ; METAANALYSIS ; VULVAR CANCER ; COMPLETENESS ; REGRESSION DILUTION ; COFACTORS ; MetS ; rare gynecological cancers
    Abstract: Background: Risk factors for rare gynecological cancers are largely unknown. Initial research has indicated that the metabolic syndrome (MetS) or individual components could play a role. Materials and methods: The Metabolic syndrome and Cancer project cohort includes 288 834 women. During an average follow-up of 11 years, 82 vulvar, 26 vaginal and 43 other rare gynecological cancers were identified. Hazard ratios (HRs) were estimated fitting Cox proportional hazards regression models for tertiles and standardized z-scores [with a mean of 0 and a standard deviation (SD) of 1] of body mass index (BMI), blood pressure, glucose, cholesterol, triglycerides and MetS. Risk estimates were corrected for random error in the measurement of metabolic factors. Results: The MetS was associated with increased risk of vulvar [HR 1.78, 95% confidence interval (CI) 1.30-2.41) and vaginal cancer (HR 1.87, 95% CI 1.07-3.25). Among separate MetS components, 1 SD increase in BMI was associated with overall risk (HR 1.43, 95% CI 1.23-1.66), vulvar (HR 1.36, 95% CI 1.11-1.69) and vaginal cancer (HR 1.79, 95% CI 1.30-2.46). Blood glucose and triglyceride concentrations were associated with increased risk of vulvar cancer (HR 1.98, 95% CI 1.10-3.58 and HR 2.09, 95% CI 1.39-3.15, respectively). Conclusion: The results from this first prospective study on rare gynecological cancers suggest that the MetS and its individual components may play a role in the development of these tumors
    Type of Publication: Journal article published
    PubMed ID: 20966183
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  • 10
    Keywords: CANCER ; GROWTH-FACTOR ; carcinoma ; COHORT ; EPIDEMIOLOGY ; RISK ; RISK-FACTORS ; score ; WOMEN ; OBESITY ; cervical cancer ; HUMAN-PAPILLOMAVIRUS ; SQUAMOUS-CELL CARCINOMA ; adenocarcinoma ; UTERINE CERVIX ; PROJECT ; metabolic syndrome ; COMPLETENESS ; REGRESSION DILUTION ; CONOR ; Squamous cell ; Metabolic factors
    Abstract: Background. Little is known about the association between metabolic risk factors and cervical cancer carcinogenesis. Material and methods. During mean follow-up of 11 years of the Me-Can cohort (N = 288,834) 425 invasive cervical cancer cases were diagnosed. Hazard ratios (HRs) were estimated by the use of Cox proportional hazards regression models for quintiles and standardized z-scores (with a mean of 0 and a SD of 1) of BMI, blood pressure, glucose, cholesterol, triglycerides and MetS score. Risk estimates were corrected for random error in the measurements. Results. BMI (per 1SD increment) was associated with 12%, increase of cervical cancer risk, blood pressure with 25% and triglycerides with 39%, respectively. In models including all metabolic factors, the associations for blood pressure and triglycerides persisted. The metabolic syndrome (MetS) score was associated with 26% increased corrected risk of cervical cancer. Triglycerides were stronger associated with squamous cell carcinoma (HR 1.48; 95% CI, 1.20-1.83) than with adenocarcinoma (0.92, 0.54-1.56). Among older women cholesterol (50-70 years 1.34; 1.00-1.81), triglycerides (50-70 years 1.49, 1.03-2.16 and 〉= 70 years 1.54, 1.09-2.19) and glucose (〉= 70 years 1.87, 1.13-3.11) were associated with increased cervical cancer risk. Conclusion. The presence of obesity, elevated blood pressure and triglycerides were associated with increased risk of cervical cancer.
    Type of Publication: Journal article published
    PubMed ID: 22330614
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