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    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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  • 3
    Keywords: carcinoma ; SUSCEPTIBILITY ; BREAST ; germline mutations ; SKIN-CANCER ; MYCOSIS-FUNGOIDES ; CUTANEOUS MALIGNANT-MELANOMA ; SPECTRUM ; DYSPLASTIC NEVUS SYNDROME ; FAMMM SYNDROME
    Abstract: Using the Swedish Family-Cancer Database, we assessed the effect of a detailed family history of melanoma on risk for other tumors (other than melanoma). Among 248,011 individuals with a family history of melanoma, 43,931 other tumors were diagnosed from 1958 to 2010. Standardized incidence ratios (SIRs) were calculated for other tumors in patients who had a family history of melanoma, as compared with those without. A detailed family history of melanoma was investigated according to an increasing number of melanomas in either 1 or 〉= 2 first-degree relatives (FDRs). Associations were considered significant when there were at least two independently significant SIRs or a statistically significant trend of increasing SIRs with increasing number of melanomas in relatives. The applied criteria for significant associations were convincingly met by pancreatic, breast, prostate, and squamous cell skin tumors and ependymoma, although there was significant but not overwhelming evidence for thyroid, parathyroid, lung, and unknown primary tumors, meningioma, mycosis fungoides, and myeloid leukemia. To our knowledge, no studies have previously considered a detailed family history of melanoma and the use of internal validation to assess familial associations of melanoma with other tumors. We established associations for 12 other tumors, and the associations for myeloid leukemia, parathyroid, and unknown primary tumors are, to our knowledge, previously unreported.
    Type of Publication: Journal article published
    PubMed ID: 24192716
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  • 4
    Keywords: COMMON ; RISKS ; smoking ; DATABASE ; TOBACCO ; ENVIRONMENTAL-FACTORS ; ALCOHOL-DRINKING ; HUMAN CARCINOGENS
    Abstract: The population attributable fraction (PAF) defines the proportion of a disease that would be prevented if the exposure to a particular risk factor was avoided. Familial risk is a known risk factor for many cancers, but an unbiased estimation of the PAF for familial risk requires a large study population to include rare cancers. PAFs and their corresponding standardized incidence ratios (SIRs) were calculated for familial relative risk among first-degree relatives (FDRs) and second-degree relatives (SDRs) diagnosed with the same (concordant) invasive or in situ cancers. Calculations were based on the Swedish Family-Cancer Database considering 8,148,737 individuals. To assess environmental effects, PAFs were also calculated for concordant cancers among spouses. Almost all cancers showed a significant familial risk. The highest PAFs were found for the common cancers of the prostate (13.94%), breast (7.46%) and colorectum (6.78%) among the FDRs. In the FDRs, the overall PAF for any concordant cancer was 4.20%, but in the SDRs, it was only 0.34%. The overall PAFs for in situ cancers were 0.86% and 0.56% for the FDRs and SDRs, respectively. The overall independent familial PAF was 5.96% for the invasive and in situ cancers in the FDRs and SDRs. The cancers between spouses yielded an overall PAF of 0.14%. For esophageal cancer, the risk among spouses was higher than the familial risk. Our study shows that the overall familial PAF of 5.96%, although underestimated for sex-specific cancers, ranks as the third most common population burden after tobacco smoking and unhealthy diet.
    Type of Publication: Journal article published
    PubMed ID: 24590453
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  • 5
    Keywords: SURVIVAL ; MORTALITY ; POPULATION ; RISK ; mechanisms ; MULTIPLE-MYELOMA ; DISORDERS ; CANCER INCIDENCE
    Abstract: Increased risk of Hodgkin lymphoma (HL) associated with personal history of several autoimmune diseases (ADs), such as rheumatoid arthritis, systemic lupus erythematosus, sarcoidosis, and immune thrombocytopenic purpura, are known. Whether there are other HL-related ADs and whether the increased risk of HL after ADs holds across sex, age, year of diagnosis, or HL histological subtype is unclear. We systematically analyzed the risk of HL in 878 161 Swedish patients diagnosed with 33 different ADs in 1964-2010. During similar to 10-year follow-up of ADs patients, 371 incident HL cases were diagnosed. Significantly increased overall standardized incidence ratio (SIR) for HL after ADs was 2.0 (95% confidence interval: 1.8-2.2); AD-specific SIRs: autoimmune hemolytic anemia 19.9 (7.2-43.6), sarcoidosis 10.3 (7.8-13.4), systemic lupus erythematosus 8.4 (5.2-12.9), immune thrombocytopenic purpura 7.0 (3.2-13.3), polyarteritis nodosa 6.6 (1.2-19.5), polymyositis/dermatomyositis 6.3 (2.0-14.9), Behcet's disease 5.6 (2.7-10.3), Sjogren's syndrome 5.0 (2.1-9.8), rheumatoid arthritis 3.2 (2.6-3.9), polymyalgia rheumatica 2.2 (1.4-3.5), and psoriasis 1.9 (1.3-2.6). Men with AD had slightly higher risk of HL (2.4, 2.0-2.7) compared with women (1.8, 1.5-2.0). Only 23% of ADs were diagnosed before age 35 years and the overall SIR for HL diagnosis before age 35 [1.4, (1.0-1.8)] was lower than that in older ages [35 a parts per thousand currency sign age 〈 50: 2.1 (1.6-2.7); age a parts per thousand yen 50: 2.2 (2.0-2.5)], except for sarcoidosis [age 〈 35: 19.3 (10.5-32.5); 35 a parts per thousand currency sign age 〈 50: 10.4 (5.7-17.5); age a parts per thousand yen 50: 8.4 (5.6-12.1)]. Risks of all classical HLs significantly increased after ADs: lymphocyte depletion 3.7 (1.5-7.6), lymphocyte-rich 3.7 (2.3-5.9), mixed cellularity 2.4 (1.8-3.2), and nodular sclerosis 1.7 (1.3-2.1). Several, but not all ADs (11/33), had a positive association with all classical histological subtypes of HL. Higher risks of classical HL after polyarteritis nodosa, polymyositis/dermatomyositis, Behcet's disease, Sjogren's syndrome, polymyalgia rheumatica, and psoriasis were novel findings of this study.
    Type of Publication: Journal article published
    PubMed ID: 24718892
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  • 6
    Keywords: BLADDER-CANCER ; DATABASE ; STRATEGIES ; END ; NORDIC COUNTRIES ; SWEDISH ; KIDNEY-CANCER
    Abstract: BACKGROUND: This study aimed at elucidating the effect of family history on the development of subsequent cancers in renal cell carcinoma (RCC) survivors and aimed at assessing whether the interactions between risks of subsequent cancers in RCC survivors and familial risk of subsequent cancer are additive or multiplicative interactions. METHODS: A population-based cohort (Swedish Family-Cancer Database) of 14,267 RCC patients diagnosed in 1990-2010 was followed for cancer incidence. Standardised incidence ratios (SIRs) were calculated for subsequent cancers in RCC survivors and in RCC survivors with a family history of subsequent cancer. Familial risk of subsequent cancer was calculated for individuals with family history of specific cancer, compared to those without. RESULTS: For subsequent hemangioblastoma (HB) in RCC survivors, drastically elevated risk was observed for the effect of family history of HB [SIR=777 (95% confidence interval (CI): 160-2270)] and of family history of RCC [378 (46-1367)]. Colorectal, lung, prostate and RCCs favoured additive interactions between risk of subsequent cancers in RCC survivors and familial risk, while endocrine glands, nervous system and urinary bladder cancers favoured multiplicative interactions. CONCLUSIONS: Risks of subsequent HB in RCC survivors were tremendously modified by family history of RCC or HB, which may resemble characteristics of von Hippel-Lindau syndrome and show the power of present approach to detect heritable cancer clusters. Additive or multiplicative interactions found for colorectal, lung, prostate, endocrine glands, nervous system, urinary bladder and RCCs might raise awareness among clinicians and RCC survivors with a family history of seven cancers about elevated risks of subsequent those cancers.
    Type of Publication: Journal article published
    PubMed ID: 24923229
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  • 7
    Keywords: MODEL ; POPULATION ; BREAST ; PROSTATE-CANCER ; PREDICTION ; BIOPSY ; SINGLE-NUCLEOTIDE POLYMORPHISMS ; EXTERNAL VALIDATION ; PREVENTION TRIAL ; COMMON GENETIC-VARIANTS
    Abstract: PURPOSE: Detailed family history offers an inexpensive alternative to genetic profiling for individual risk assessment. The objective here was to update the Prostate Cancer Prevention Trial Risk Calculator (PCPTRC) to include detailed family history. MATERIALS AND METHODS: Data comprised 55168 prostate cancer cases and 638218 controls from the Swedish Family-Cancer Database who were 〉/= 55 years of age in 1999, had at least one male first-degree relative (FDR) 〉/= 40 years and one female FDR 〉/= 30 years. Likelihood ratios (LR) were computed as the ratio of risk of observing a specific family history pattern in a prostate cancer case compared to control and used to update the PCPTRC. RESULTS: Having at least one relative with prostate cancer increased the risk of prostate cancer. The LR was 1.63 for one FDR 〉/= 60 at diagnosis (10.1% of cancer cases, 6.2% of controls), 2.47 if the relative was 〈 60 years (1.5% versus 0.6%, respectively), 3.46 for 〉/= 2 relatives 〉/= 60 years (1.2% versus 0.3%), and 5.68 for 〉/= 2 relatives 〈 60 years (0.05% versus 0.009%). Among men with no diagnosed FDRs, the LR was 1.09 for one or more SDRs diagnosed with prostate cancer (12.7% versus 11.7%, respectively). Additional FDRs with breast cancer or FDRs or SDRs with prostate cancer compounded these risks. CONCLUSIONS: Detailed family history is an independent predictor of prostate cancer to the commonly-used risk factors and should be incorporated into decision-making regarding biopsy. Compared with costly other biomarkers, it is inexpensive and universally available.
    Type of Publication: Journal article published
    PubMed ID: 25242395
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  • 8
    Keywords: SURVIVAL ; SWEDEN ; cancer risk ; PREVALENCE ; asthma ; MALIGNANCY ; RHEUMATOID-ARTHRITIS ; AUTOIMMUNE-DISEASES ; hay fever ; METAANALYSIS ; HISTOLOGY ; allergic rhinitis ; SYMPTOMS ; standardized incidence ratio ; immune disturbance
    Abstract: Data on allergic conditions as risk or protective factors for cancer are controversial probably because most studies have used self-reported data on mixed groups of allergies in a case-control setting. We define cancer risks in medically diagnosed hay fever/allergic rhinitis patients in a nationwide cohort study. A total of 138,723 hay fever/allergic rhinitis patients were identified from three Swedish health care databases and standardized incidence ratios (SIRs) were calculated for subsequent cancers identified from the Swedish Cancer Registry. Overall cancer risk was not changed (SIR 1.03). For individual cancers, the highest SIR was observed for nasal cancer (SIR 2.63), followed by testicular (1.46) and endocrine tumors (1.42), and kidney (1.31), prostate (1.18) and breast (1.11) cancers. The results were consistent in the three sources of data and all SIRs were above unity, albeit mainly not statistically significant. The SIRs for nervous system tumors were above unity and of borderline significance. SIRs were decreased for esophageal (0.50), liver (0.62) and lung (0.78) cancers, and the three sources of data agreed in the direction of the effect. The increased risks for testicular, renal, prostate and endocrine cancers may be explained by immunological mechanisms. Excess risk for these cancer accounts for a significant population attributable fraction. Nervous system cancers showed a borderline increase and none of the histological types were significantly decreased, providing strong evidence against the published case-control studies, which have reported protective effects. The reasons for the reduced risks for esophageal, liver and lung cancer remain to be explained.
    Type of Publication: Journal article published
    PubMed ID: 24692097
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  • 9
    Keywords: DISEASE ; HISTORY ; CUTANEOUS MELANOMA ; CANCER DATABASE ; CDKN2A MUTATIONS ; SKIN-CANCER ; GENETIC EPIDEMIOLOGY ; PREDISPOSES ; POPULATION-BASED PREVALENCE ; MITF GERMLINE MUTATION
    Abstract: Background: We aimed at assessing familial risk of melanoma by considering a detailed family history of multiple primary (invasive/in situ) melanomas (MPM), stratified by histology and location. Methods: Among 65,429 melanoma patients diagnosed in 1958-2010 in the Swedish Family-Cancer Database, there were 4248 patients with familial melanoma. A detailed family history of MPM was investigated by number of melanomas in one first-degree relative (FDR) and in 〉= 2 FDRs. Familial melanoma risk was assessed by standardised incidence ratios (SIRs) comparing those with family history of melanoma to those without. Combining invasive/in situ melanoma was due to essentially identical familial risks. Results: For one affected FDR, familial risk increased from SIR = 2.2 (95% confidence interval (CI) = 2.2-2.3) for single melanoma to 16.3 (9.5-26.1) for 〉= 5 melanomas, while for 〉= 2 affected FDRs, the risk increased from 5.5 (4.8-6.2) for single melanoma to 23.9 (13.6-38.8) for 〉= 2 melanomas. Significantly higher familial risks for superficial spreading melanoma (SSM) [2.5 (2.3-2.6)] than lentigo maligna melanoma (LMM) [1.8 (1.6-2.1)], and for multiple parts [5.3 (3.1-8.4)] and trunk [2.6 (2.5-2.8)] than head/neck [2.0 (1.8-2.2)] were observed. Only at head/neck, significantly higher risk for SSM [2.4 (1.9-3.0)] than LMM [1.6 (1.4-1.8)] was noted. Conclusion: We found, for the first time, that familial risks were similar for two/three melanomas in one FDR or for a single melanoma in 〉= 2 FDRs and, higher familial risks for SSM than LMM occurred only at head/neck. This study provides new evidence for genetic counselling in melanoma, suggesting the need for considering not only the number of affected family members but also the diagnosis of MPM (even in situ) in relatives. (C) 2014 Elsevier Ltd. All rights reserved.
    Type of Publication: Journal article published
    PubMed ID: 25103454
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  • 10
    Keywords: SURVIVAL ; MORTALITY ; SUSCEPTIBILITY ; MALIGNANCIES ; SWEDEN ; MULTIPLE-MYELOMA ; DISORDERS ; CANCER INCIDENCE ; FAMILIAL RISKS ; HOSPITALIZATIONS
    Abstract: Background: The cumulative risk of non-Hodgkin lymphoma (NHL) in Sweden by age 80 years has increased to 1.1 in women and 1.6% in men in 2011. Increased risk of NHL associated with personal histories of some autoimmune diseases (ADs) is known. It is unclear whether there are other NHL-related ADs and whether this association holds across different sex, age and year of diagnosis, or NHL histological subtypes. Patients and methods: Over an average of 9.4-year (maximum 47 years) follow-up of 878 161 patients diagnosed in 1964-2010 with 33 different ADs, 3096 subsequent NHL were diagnosed (data: Swedish Cancer Registry). Results: Of 33 studied ADs, 21 showed significantly increased risk of NHL; 6 of them tended to increase the risk and none significantly decreased it. The overall standardized incidence ratio (SIR) for NHL after ADs was 1.6 [novel findings: immune thrombocytopenic purpura (ITP) = 7.5, polymyositis/dermatomyositis = 4.1, primary biliary cirrhosis = 3.9, myasthenia gravis = 2.2, Behcet = 1.7, rheumatoid fever = 1.7, ulcerative colitis = 1.5, polymyalgia rheumatica = 1.4, and chronic rheumatic heart disease = 1.4; confirmatory findings: autoimmune hemolytic anemia = 27.2, Sjgren = 4.9, Celiac = 4.8, systemic lupus erythematosus = 4.4, polyarteritis nodosa = 2.9, discoid lupus erythematosus = 2.7, sarcoidosis = 2.6, Crohn = 2.1, systemic sclerosis = 2.1, rheumatoid arthritis = 2.0, and Hashimoto/hypothyroidism and psoriasis = 1.4]. SIR for NHL diagnosis before age 60 (2.2) was significantly higher than that in older ages (age = 60: 1.5). The SIRs in women or men and in period 1993-2010 or 1964-1992 were similar. Risk of all common NHL histology subtypes significantly increased after ADs (cutaneous/peripheral T cell and anaplastic large T and null cell = 2.2; small B-cell lymphocytic = 1.7; diffuse large B cell = 1.6; follicular and mantel cell = 1.3). Conclusion: Many of 33 studied ADs (except for ankylosing spondylitis, diabetes type I graves/hyperthyroidism, multiple sclerosis, chorea minor, and pernicious anemia), especially when diagnosed at younger ages, were associated with higher risk of NHL. However, the absolute risk of NHL in many ADs is still small.
    Type of Publication: Journal article published
    PubMed ID: 25081899
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