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  • 1
    Keywords: CANCER ; carcinoma ; neoplasms ; DIAGNOSIS ; FOLLOW-UP ; COHORT ; EPIDEMIOLOGY ; incidence ; POPULATION ; RISK ; RISKS ; SITE ; PATIENT ; prognosis ; RISK-FACTORS ; treatment ; LINKAGE ; DESIGN ; NUMBER ; AGE ; risk factors ; CANCER-PATIENTS ; CANCER PATIENTS ; TRENDS ; REGISTRY ; cancer registries ; PRIMARY TUMORS ; SWITZERLAND ; INTERVAL ; PRIMARY NEOPLASMS ; second primary cancers ; cancer registry ; pooled analysis ; RISK-FACTOR ; CANCERS ; REGISTRIES ; population-based ; PRIMARY MALIGNANCIES ; second primary cancer
    Abstract: Context: Increasing incidence and improved prognosis of thyroid cancer have led to concern about the development of second primary cancers, especially after radioiodine treatment. Thyroid cancer can also arise as a second primary neoplasm after other cancers. Objective: The objective of the study was to assess the risk of second primary cancer after thyroid cancer and vice versa. Design: This was a multinational record linkage study. Setting: The study was conducted at 13 population-based cancer registries in Europe, Canada, Australia, and Singapore. Patients or Other Participants: A cohort of 39,002 people (356,035 person-yr of follow-up) with primary thyroid cancer were followed up for SPN for up to 25 yr, and 1,990 cases of thyroid cancer were diagnosed after another primary cancer. Main Outcome Measures: To assess any possible excess of second primary neoplasms after thyroid cancer, the observed numbers of neoplasms were compared with expected numbers derived from age-, the cancer registries, yielding standardized incidence ratios (SIRs). The SIR of second primary thyroid cancer after various types of cancer was also calculated. Results: During the observation period, there were 2821 second primary cancers (all sites combined) after initial diagnosis of thyroid cancer, SIR of 1.31 ( 95% confidence interval 1.26 - 1.36) with significantly elevated risks for many specific cancers. Significantly elevated risks of second primary thyroid cancer were also seen after many types of cancer. Conclusion: Pooled data from 13 cancer registries show a 30% increased risk of second primary cancer after thyroid cancer and increased risks of thyroid cancer after various primary cancers. Although bias (detection, surveillance, misclassification) and chance may contribute to some of these observations, it seems likely that shared risk factors and treatment effects are implicated in many. When following up patients who have been treated for primary thyroid cancer, clinicians should maintain a high index of suspicion for second primary cancers
    Type of Publication: Journal article published
    PubMed ID: 16478820
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  • 2
    Keywords: CANCER ; Germany ; DISEASE ; DISEASES ; incidence ; RISK ; RISKS ; GENES ; GENOME ; METABOLISM ; TUMORS ; FAMILY ; NO ; DESIGN ; familial risk ; RELATIVES ; CLUES ; clustering ; RE ; sibling risk ; SIBLINGS ; FAMILIES ; heritability ; USA ; population-based ; SCANS ; outcome ; PITUITARY-ADENOMAS ; RATIO ; SCAN ; SWEDISH ; AUTOIMMUNE ; genome scan ; ANTERIOR
    Abstract: Context: Familial clustering of a disease is an indicator of a possible heritable cause. In the era of genome scans, the consideration of data on heritability should be important in the assessment of the likely success of the scans. Object: The objective of the study was to carry out a family study on nonthyroid endocrine diseases to search familial clustering of these diseases beyond the known syndromes. Design and Setting: The Swedish Multigeneration Register on 0- to 72-yr-old subjects was linked to the Hospital Discharge Register from years 1964 to 2004. Main Outcome Measure: Standardized incidence ratios were calculated for offspring of affected parents and siblings by comparing with those whose relatives had no hospitalization for nonthyroid endocrine diseases. Results: A total of 11,948 hospitalized cases and 443 familial cases were identified. The familial standardized incidence ratios were increased for parathyroid, pituitary, and adrenal hyperfunctions and hypofunctions, some findings consistent with known syndromes, most clearly that for adrenal cortical hypofunction showing recessive inheritance described for autoimmune polyendocrine syndrome 1. The sibling risks were very high for many diseases, but some of these affecting young individual may be due to bias caused by selective hospitalization. A high sibling risk observed for anterior pituitary hypofunction may represent a yet-unknown recessive syndrome. Conclusions: To our knowledge this is a first population-based study on nonthyroid endocrine diseases. The results call for further studies to sort out the challengingly high sibling risk for many individual nonthyroid endocrine diseases, whether they aredueto bias or possible recessive effects. (J Clin Endocrinol Metab 93: 4755-4758, 2008)
    Type of Publication: Journal article published
    PubMed ID: 18827002
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  • 3
    Keywords: RISK ; GENETIC POLYMORPHISMS ; ASSOCIATION ; POLYMORPHISMS ; nutrition ; ESTROGEN ; PREMENOPAUSAL WOMEN ; MULTIETHNIC COHORT ; ANDROGEN ; SEX-HORMONES ; SHBG GENE
    Abstract: Context: Sex steroids play a central role in breast cancer development. Objective: This study aimed to relate polymorphic variants in 36 candidate genes in the sex steroid pathway to serum concentrations of sex steroid hormones and SHBG. Design: Data on 700 genetic polymorphisms were combined with existing hormone assays and data on breast cancer incidence, within the European Prospective Investigation into Cancer and Nutrition (EPIC) and the Nurses' Health Study (NHS) cohorts; significant findings were reanalyzed in the Multiethnic Cohort (MEC). Setting and Participants: We analyzed data from a pooled sample of 3852 pre- and postmenopausal Caucasian women from EPIC and NHS and 454 postmenopausal women from MEC. Main Outcome Measures: Outcome measures were SHBG, testosterone, dehydroepiandrosterone (DHEAS), androstenedione, estrone (E1), and estradiol (E2) as well as breast cancer risk. Results: Globally significant associations were found among pre- and postmenopausal women combined between levels of SHBG and the SHBG gene and between DHEAS and the FSHR and AKR1C3 genes. Among postmenopausal women, serum E1 and E2 were significantly associated with the genes CYP19 and FSHR, and E1 was associated with ESR1. None of the variants related to serum hormone levels showed any significant association with breast cancer risk. Conclusions: We confirmed associations between serum levels of SHBG and the SHBG gene and of E1 and E2 and the CYP19 and ESR1 genes. Novel associations were observed between FSHR and DHEAS, E1, and E2 and between AKR1C3 and DHEAS.
    Type of Publication: Journal article published
    PubMed ID: 21177793
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  • 4
    Keywords: carcinoma ; POLYMORPHISMS ; BREAST-CANCER ; POPULATIONS ; TUMOR-SUPPRESSOR ; susceptibility loci ; COMMON VARIANTS ; FOXD3 ; RNA HELICASES ; FOXE1
    Abstract: Context: Genome-wide association studies (GWASs) on differentiated thyroid cancer (DTC) have identified robust associations with single nucleotide polymorphisms (SNPs) at 9q22.33 (FOXE1), 14q13.3 (NKX2-1), and 2q35 (DIRC3). Our recently published GWAS suggested additional susceptibility loci specific for the high-incidence Italian population. Objective: The purpose of this study was to identify novel Italian-specific DTC risk variants based on our GWAS and to test them further in low-incidence populations. Design: We investigated 45 SNPs selected from our GWAS first in an Italian population. SNPs that showed suggestive evidence of association were investigated in the Polish and Spanish cohorts. Results: The combined analysis of the GWAS and the Italian replication study (2260 case patients and 2218 control subjects) provided strong evidence of association with rs10136427 near BATF (odds ratio [ OR] = 1.40, P = 4.35 x 10(-7)) and rs7267944 near DHX35 (OR = 1.39, P = 2.13 x 10(-8)). A possible role in DTC susceptibility in the Italian populations was also found for rs13184587 (ARSB) (P = 8.54 x 10(-6)) and rs1220597 (SPATA13) (P = 3.25 x 10(-6)). Only the associations between rs10136427 and rs7267944 and DTC risk were replicated in the Polish and the Spanish populations with little evidence of population heterogeneity (GWAS and all replications combined, OR = 1.30, P = 9.30 x 10(-7) and OR = 1.32, P = 1.34 x 10(-8), respectively). In silico analyses provided new insights into the possible functional consequences of the SNPs that showed the strongest association with DTC. Conclusions: Our findings provide evidence for novel DTC susceptibility variants. Further studies are warranted to identify the specific genetic variants responsible for the observed associations and to functionally validate our in silico predictions.
    Type of Publication: Journal article published
    PubMed ID: 25029422
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  • 5
    Keywords: MORTALITY ; POPULATION ; CIGARETTE-SMOKING ; OSTEOPOROSIS ; ABSORPTION ; POSTMENOPAUSAL WOMEN ; ADULTS ; METAANALYSIS ; PUBLIC-HEALTH ; NHANES-III
    Abstract: Context: Data from physiological studies suggest smoking to have detrimental effects on calcium absorption, but large-scale investigations of this interaction and its importance with respect to bone health in humans are lacking. Objective: The objective of the study was to examine the potential smoking-associated effect heterogeneity in the relationship of dietary calcium intake with bone mineral density in the general population. Design: This was an observational, cross-sectional study. Participants: A total of 14 116 participants of the Third National Health and Nutrition Examination Survey, including 6882 never, 3532 former, and 3702 current smokers. The median age of the participants was 44 years, and 52% were female. Main Outcome Measure: Bone mineral density at the femoral neck as determined by dual-energy x-ray absorptiometry was measured. Results: In multiple linear regression adjusting for age, sex, race/ethnicity, and education, the association of calcium intake with bone mineral density was characterized by suggestive overall positive trends in all three smoking behavior categories. Detailed dose-response analyses by restricted cubic spline modeling revealed more pronounced nonlinearity among former smokers, but the interaction of smoking with calcium intake on bone mineral density did not reach statistical significance in any of these models. The dose-response curves became even more homogenous across smoking behavior strata after additional adjustment for body mass index and physical activity. Conclusion: Even though the present results cannot rule out that smoking-associated differences in calcium absorption exist, they do suggest that smoking behavior does not have any relevant impact on the beneficial effects of calcium intake on bone mineral density at the population level.
    Type of Publication: Journal article published
    PubMed ID: 25387257
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  • 6
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; tumor ; carcinoma ; Germany ; human ; RISK ; GENE ; GENES ; TUMORS ; PATIENT ; TISSUES ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; BREAST ; breast cancer ; BREAST-CANCER ; PROGRESSION ; DESIGN ; PROMOTER ; NUMBER ; AGE ; SNP ; PATHOGENESIS ; REGION ; REGIONS ; case-control studies ; case-control study ; RE ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; case control studies ; INTERVAL ; single-nucleotide ; GATA-3 ; GROWTH-HORMONE ; SYSTEMIC-LUPUS-ERYTHEMATOSUS/
    Abstract: Context: The contribution of prolactin (PRL) through its receptor (PRLR) to the pathogenesis and progression of human mammary tumors has received recent attention. Objective: We investigated whether genetic variation in the PRL and PRLR genes is associated with the risk of breast cancer ( BC). Design: We conducted a case-control study with a total of seven single nucleotide polymorphisms (SNPs). Setting: The study was conducted at an academic research laboratory and university clinics. Patients and Other Participants: A total of 441 German familial, unrelated BC cases and 552 controls matched by age, ethnicity, and geographical region participated in the study. Intervention(s): There were no interventions. Main Outcome Measures(s): SNP genotype and haplotype distributions and haplotype interactions were correlated with the risk of BC. Results: Two SNPs (rs1341239 and rs12210179) within the PRL promoter regions were significantly associated with increased risk in homozygotes for the variant alleles [ odds ratio ( OR), 1.67 and 95% confidence interval (CI), 1.11 - 2.50; and OR, 2.09 and 95% CI, 1.23 - 3.52, respectively]. The PRL haplotype containing the variant alleles of the promoter SNPs increased significantly the risk of BC ( OR 1.42, 95% CI 1.07 - 1.90). A PRLR haplotype was associated with a significant decrease in BC risk ( OR 0.69, 95% CI 0.54 - 0.89). An increasing number of PRL and PRLR risk haplotypes led to a significant trend of increasing risk for BC (chi(2) = 12.15; P = 0.007). Conclusions: Genetic variation in the PRL and PRLR genes was shown to influence BC risk. Additional studies are needed to further clarify the role of the PRL and PRLR genes in the risk of BC
    Type of Publication: Journal article published
    PubMed ID: 16434456
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  • 7
    Keywords: CANCER ; PROSTATE ; DISEASE ; DISEASES ; incidence ; POPULATION ; SAMPLE ; METABOLISM ; SERA ; hormone ; HEALTH ; DESIGN ; DIFFERENCE ; AGE ; MEN ; smoking ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; UNITED-STATES ; ALCOHOL ; BODY ; nutrition ; IMMUNOASSAYS ; ESTRADIOL ; SERUM ; BODIES ; ENDOCRINE ; WEIGHT ; ESTROGEN ; LEVEL ; SIZE ; USA ; CANCER INCIDENCE ; HORMONE LEVELS ; TESTOSTERONE ; STEROID-HORMONES ; prostate-specific antigen ; GENERAL-POPULATION ; BONE-MINERAL DENSITY ; AFRICAN-AMERICAN ; ANDROGEN CONCENTRATIONS ; BODY-COMPOSITION ; ENDOGENOUS SEX-HORMONES ; HORMONE-BINDING GLOBULIN
    Abstract: Context: Higher testosterone in black compared with white men has been postulated to explain their higher prostate cancer incidence. Previous studies comparing hormone levels by race might have been limited by size, restricted age variation, or lack of representation of the general population. Objective: Our objective was to compare serum testosterone, estradiol, and SHBG concentrations among non-Hispanic black, non-Hispanic white, and Mexican-American men. Participants, Design, and Setting: A total of 1413 men aged 20 + yr and who attended the morning examination session of the Third National Health and Nutrition Examination Survey (NHANES III) in 1988-1991 were included in this cross-sectional study. Measurement: Serum hormone concentrations were measured by electrochemiluminescence immunoassays. Results: After applying sampling weights and adjusting for age, percent body fat, alcohol, smoking, and activity, testosterone concentrations were not different between non-Hispanic blacks (n = 363; eometric mean, 5.29 ng/ml) and non-Hispanic whites (n = 674; 5.11 ng/ml; P 〉 0.05) but were higher in Mexican-Americans (n = 376; 5.48 ng/ml; P 〈 0.05). Non- Hispanic blacks ( 40.80 pg/ml) had a higher estradiol concentration than non-Hispanic whites (35.46 pg/ml; P 〈 0.01) and Mexican-Americans (34.11 pg/ml; P 〈 0.01). Non-hispanic blacks (36.49 nmol/liter) had a higher SHBG concentration than non-Hispanic whites (34.91 nmol/liter; P 〈 0.05) and Mexican-Americans (35.04 nmol/liter; P 〈 0.05). Conclusions: Contrary to the postulated racial difference, testosterone concentrations did not differ notably between black and white men. However, blacks had higher estradiol levels. Mexican-Americans had higher testosterone than whites but similar estradiol and SHBG concentrations. Given these findings, it may be equally if not more important to investigate estradiol as testosterone in relation to diseases with racial disparity
    Type of Publication: Journal article published
    PubMed ID: 17456570
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  • 8
  • 9
    Keywords: BREAST-CANCER ; PROSTATE-CANCER ; RENAL-CARCINOMA ; VITAMIN-D ; HORMONE-RELATED PROTEIN ; POLYCYTHEMIA-VERA ; ENDOCRINE NEOPLASIA TYPE-1 ; PRIMARY HYPERPARATHYROIDISM ; NATIONWIDE COHORT ; ADENOMA CELLS
    Abstract: Context: There are limited reliable epidemiological data concerning whether individuals with benign/malignant parathyroid tumor are at an elevated risk of developing nonendocrine malignancies or vice versa. Objective: The objective of the study was to quantify these risks, especially risk of parathyroid tumors after other cancers. Design: This was a population-based retrospective cohort study. Participants: Participants included the Swedish Family-Cancer Database (1958-2008; 11,697,301 individuals; 1,128,735 survivors of first primary cancers including 12,037 patients with parathyroid adenoma and 83 parathyroid adenocarcinoma). Main Outcome Measure: Standardized incidence ratios (SIR) were adjusted for age; sex; period; residential area; socioeconomic status; and history of hospitalization for obesity, alcoholism, or chronic obstructive pulmonary disease. Results: Nonendocrine cancer sites with significantly increased risk after parathyroid adenoma were small intestine (SIR 2.3), blood (polycythemia vera 2.0), kidney (1.8), nervous system (1.6), skin (melanoma 1.4), and breast(women 1.2). Risk of parathyroid adenoma significantly increased after polycythemia vera (3.9) and malignancy in small intestine (3.5), kidney (2.8), nervous system (2.0), prostate (1.5), skin (melanoma 1.5), bladder (1.4), and breast (women 1.2). Twelve cases of parathyroid adenocarcinoma showed significantly higher risk after other tumors (2.4), especially after thyroid cancer (46.6) and parathyroid adenoma (27.3) but not vice versa in 11 cancer survivors. Conclusions: Parathyroid adenoma can be a risk factor for parathyroid adenocarcinoma; polycythemia vera; melanoma; and small intestine, kidney, nervous system and breast cancers. Further studies are suggested to find underlying mechanisms for these elevated risks, especially for increased risk of parathyroid tumor in patients with melanoma polycythemia vera, or malignancy in small intestine, kidney, nervous system, bladder, prostate, or breast.
    Type of Publication: Journal article published
    PubMed ID: 21525164
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  • 10
    Keywords: carcinoma ; EPIDEMIOLOGY ; GENE ; DISRUPTION ; SELECTION ; LOCUS ; EUROPEAN POPULATIONS ; FAMILIAL RISKS ; COMMON VARIANTS ; CARD9
    Abstract: Context: Genome-wide association studies(GWASs) of differentiated thyroid cancer (DTC) have identified associations with polymorphisms at 2q35 (DIRC3), 8p12 (NRG1), 9q22.33 (FOXE1), and 14q13.2 (NKX2-1). However, most of the inherited genetic risk factors of DTC remain to be discovered. Objective: Our objective was to identify additional common DTC susceptibility loci. Design: We conducted a GWAS in a high-incidence Italian population of 690 cases and 497 controls and followed up the most significant polymorphisms in 2 additional Italian series and in 3 low-incidence populations totaling 2958 cases and 3727 controls. Results: After excluding the most robust previously identified locus (9q22.33), the strongest association was shown by rs6759952, confirming the recently published association in DIRC3 (odds ratio [OR] = 1.21, P = 6.4 x 10(-10), GWAS and all replications combined). Additionally, in the combined analysis of the Italian series, suggestive associations were attained with rs10238549 and rs7800391 in IMMP2L (OR = 1.27, P = 4.1 x 10(-6); and OR = 1.25, P = 5.7 x 10(-6)), rs7617304 in RARRES1 (OR = 1.25, P = 4.6 x 10(-5)) and rs10781500 in SNAPC4/CARD9 (OR = 1.23, P = 3.5 x 10(-5)). Conclusions: Our findings provide additional insights into the genetic and biological basis of inherited genetic susceptibility to DTC. Additional studies are needed to determine the role of the identified polymorphisms in the development of DTC and their possible use in the clinical practice.
    Type of Publication: Journal article published
    PubMed ID: 23894154
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