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Sökning: WFRF:(Fallah Mahdi) > (2010-2014)

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1.
  • Chen, Tianhui, et al. (författare)
  • Effect of a Detailed Family History of Melanoma on Risk for Other Tumors: A Cohort Study Based on the Nationwide Swedish Family-Cancer Database
  • 2014
  • Ingår i: Journal of Investigative Dermatology. - : Elsevier BV. - 1523-1747 .- 0022-202X. ; 134:4, s. 930-936
  • Tidskriftsartikel (refereegranskat)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.
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3.
  • Chen, Tianhui, et al. (författare)
  • Risk of subsequent cancers in renal cell carcinoma survivors with a family history.
  • 2014
  • Ingår i: European Journal of Cancer. - : Elsevier BV. - 1879-0852 .- 0959-8049. ; 50:12, s. 2108-2118
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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4.
  • Fallah, Mahdi, et al. (författare)
  • Autoimmune diseases associated with non-Hodgkin lymphoma: A nationwide cohort study.
  • 2014
  • Ingår i: Annals of Oncology. - : Elsevier BV. - 1569-8041 .- 0923-7534. ; 25:10, s. 2025-2030
  • Tidskriftsartikel (refereegranskat)abstract
    • The cumulative risk of NHL in Sweden by age 80 years has increased to 1.1 in women and 1.6% in men in 2011. Increased risk of non-Hodgkin lymphoma (NHL) associated with personal histories of some autoimmune diseases (ADs) are 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.
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  • Fallah, Mahdi, et al. (författare)
  • Familial melanoma by histology and age: Joint data from five Nordic countries.
  • 2014
  • Ingår i: European Journal of Cancer. - : Elsevier BV. - 1879-0852 .- 0959-8049. ; 50:6, s. 1176-1183
  • Tidskriftsartikel (refereegranskat)abstract
    • We aimed to estimate lifetime cumulative risk of melanoma (CRM) in relatives of patients with melanoma by histology and age at diagnosis in patients and relatives.
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8.
  • Fallah, Mahdi, et al. (författare)
  • Nonendocrine Cancers Associated with Benign and Malignant Parathyroid Tumors.
  • 2011
  • Ingår i: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 1945-7197 .- 0021-972X. ; 96, s. 1108-1114
  • Tidskriftsartikel (refereegranskat)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.
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9.
  • Fallah, Mahdi, et al. (författare)
  • Risk of thyroid cancer in first-degree relatives of patients with non-medullary thyroid cancer by histology type and age at diagnosis: a joint study from five Nordic countries
  • 2013
  • Ingår i: Journal of Medical Genetics. - : BMJ. - 0022-2593 .- 1468-6244. ; 50:6, s. 373-382
  • Tidskriftsartikel (refereegranskat)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.
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10.
  • Fallah, Mahdi, et al. (författare)
  • Risk of thyroid cancer in relatives of patients with medullary thyroid carcinoma by age at diagnosis
  • 2013
  • Ingår i: Endocrine-Related Cancer. - 1479-6821. ; 20:5, s. 717-724
  • Tidskriftsartikel (refereegranskat)abstract
    • The familial risk of medullary thyroid carcinoma (MTC alone or as part of multiple endocrine neoplasms, MEN2A/MEN2B) is high, so we aimed to answer open questions about the lifetime cumulative risk of thyroid cancer (LCRTC at 0-79 years) among relatives of MTC patients by age and sex. For this nationwide study, a cohort of 3217 first-/second-degree relatives (FDRs/SDRs) of 389 MTC patients diagnosed in 1958-2010 in the Swedish Family-Cancer Database was followed for the incidence of thyroid cancer. The LCRTC in female relatives of patients with early-onset MEN2B (diagnosis age <25 years) was 44-57%, representing 140-520 times increase over the risk in their peers without a family history of endocrine tumors (men: LCRTC=22-52%, 320-750 times) depending on the number of affected FDRs/SDRs. The LCRTC in female relatives of patients with late-onset MEN2B (diagnosis age >= 25 years) was about 15-43% (men=24%). The LCRTC among relatives of early-onset MTC-alone patients was 3-20%. The LCRTC among relatives of late-onset MTC-alone patients was 5-26%. The LCRTC in female relatives of MEN2A patients was 16-63% (men=52%). The relatives of patients with early-onset MTC exhibited a high tendency to develop early-onset thyroid cancer. Simply available data on the number of FDRs and even SDRs affected with MTC and their age at diagnosis were quite informative for the estimation of the risk of thyroid cancer in probands. In settings where genetic testing is not available or affordable for all, evidence-based cumulative risks reported in this nationwide study may help physicians to identify very high-risk individuals.
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11.
  • Finne, Patrik, et al. (författare)
  • Lead-time in the European Randomised Study of Screening for Prostate Cancer.
  • 2010
  • Ingår i: European journal of cancer. - : Elsevier BV. - 1879-0852 .- 0959-8049. ; 46:17, s. 3102-3108
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Lead-time is defined as the time by which screening advances the diagnosis compared with absence of screening. A sufficiently long lead-time needs to be achieved so that cancer can be detected while still curable. A very short lead-time may indicate poor sensitivity of the screening test, while a very long lead-time suggests overdiagnosis. Material and methods In the first screening round, a total of 56,294 men aged 55–74 years were screened with serum prostate specific antigen (PSA) in five countries of the European Randomised Study of Screening for Prostate Cancer (ERSPC) with an overall detection rate (prevalence) of 2.8% (1972 prostate cancers). Prostate cancer incidence among 92,142 men randomly allocated to the control arm of the trial was also assessed. Lead-time was estimated as the time required to accumulate a similar cumulative risk of prostate cancer in the control arm to the detection rate in the intervention arm, i.e. from the ratio of detection rate (prevalence of screen-detected cases) and expected incidence (cumulative risk). Results Using a serum PSA cut-off of 4 ng/ml, the mean lead-time in the whole study population was estimated as 6.8 years (95% confidence interval (95% CI) 7.9–8.4). It was 8 years in The Netherlands, 6 in Sweden and Finland, 5 in Italy and 4 in Belgium. The mean lead-time was similar, 6–7 years, at ages 50–64 years, but close to 8 years among men aged 65–74 years. A lower PSA cut-off level of 3 ng/ml used in Sweden and The Netherlands prolonged the mean lead-time by approximately 1 year. Lead-time based on advanced prostate cancer only was slightly shorter, mean 5.3 years (95% CI 4.6–6.0). The lead-time for the second screening round was slightly shorter than that for the first (5.9, 95% CI 5.4–6.4), reflecting a similar relation between detection rate and control group incidence. Conclusion The lead-time for prostate cancer found in ERSPC substantially exceeded that found for breast, cervical and colorectal cancer screening. One round of prostate cancer screening can advance clinical diagnosis by 4–8 years. Overdiagnosis or detection of non-progressive tumours may contribute substantially to the lead-time.
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12.
  • Frank, Christoph, et al. (författare)
  • The population impact of familial cancer, a major cause of cancer
  • 2014
  • Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136. ; 134:8, s. 906-1899
  • Tidskriftsartikel (refereegranskat)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.
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  • Hemminki, Kari, et al. (författare)
  • Risk of cancer in patients with medically diagnosed hay fever or allergic rhinitis.
  • 2014
  • Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136. ; 135:10, s. 2397-2403
  • Tidskriftsartikel (refereegranskat)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.
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15.
  • Kharazmi, Elham, et al. (författare)
  • Familial risk of early and late onset cancer : nationwide prospective cohort study.
  • 2012
  • Ingår i: BMJ: British Medical Journal. - : BMJ. - 1756-1833. ; 345
  • Tidskriftsartikel (refereegranskat)abstract
    • To determine whether familial risk of cancer is limited to early onset cases. Nationwide prospective cohort study. SETTING : Nationwide Swedish Family-Cancer Database. All Swedes born after 1931 and their biological parents, totalling >12.2 million individuals, including >1.1 million cases of first primary cancer. Familial risks of the concordant cancers by age at diagnosis. The highest familial risk was seen for offspring whose parents were diagnosed at an early age. Familial risks were significantly increased for colorectal, lung, breast, prostate, and urinary bladder cancer and melanoma, skin squamous cell carcinoma, and non-Hodgkin's lymphoma, even when parents were diagnosed at age 70-79 or 80-89. When parents were diagnosed at more advanced ages (≥ 90), the risk of concordant cancer in offspring was still significantly increased for skin squamous cell carcinoma (hazard ratio 1.9, 95% confidence interval 1.4 to 2.7), colorectal (1.6, 1.2 to 2.0), breast (1.3, 1.0 to 1.6), and prostate cancer (1.3, 1.1 to 1.6). For offspring with a cancer diagnosed at ages 60-76 whose parents were affected at age <50, familial risks were not significantly increased for nearly all cancers. Though the highest familial risks of cancer are seen in offspring whose parents received a diagnosis of a concordant cancer at earlier ages, increased risks exist even in cancers of advanced ages. Familial cancers might not be early onset in people whose family members were affected at older ages and so familial cancers might have distinct early and late onset components.
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16.
  • Mousavi, Seyed Mohsen, et al. (författare)
  • Age- and time-dependent changes in cancer incidence among immigrants to Sweden: colorectal, lung, breast and prostate cancers
  • 2012
  • Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136. ; 131:2, s. 122-128
  • Tidskriftsartikel (refereegranskat)abstract
    • To examine the role of gender, age at immigration and length of stay on incidence trends of common cancers, we studied risk of colorectal, lung, breast and prostate cancers in immigrants to Sweden from 1958 to 2008. The nationwide Swedish Family-Cancer Database was used to calculate standardized incidence ratios for common cancers among immigrants compared to Swedes. Immigrants were classified into high-risk countries when their risk was increased, into low-risk when their risk was decreased and into other when their risk was nonsignificant. Among those who immigrated at younger age (<30 years), we found an increasing trend for colorectal cancer risk in low-risk men and high-risk women. Among those who immigrated at older age (=30 years), a decreasing lung cancer risk in high-risk men and an increasing breast cancer risk in low-risk women were observed. The increasing trend of prostate cancer risk was independent of age at immigration. The risk trends for other immigrants were between the risks of low- and high-risk countries. The gender-specific shifts in cancer risks in immigrants toward the risk in natives indicate a major role of sex, age at immigration and environmental exposures in colorectal and lung cancers risks. In contrast, the unchanged trend of breast cancer among those who immigrated at younger ages and an increasing trend for those who migrated at older ages may suggest a limited effect for environmental exposures, especially at younger age. Our study points out a role of age at immigration on the risk trend of cancer.
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17.
  • Mousavi, Seyed Mohsen, et al. (författare)
  • Nervous system tumors in adult immigrants to Sweden by subsite and histology.
  • 2011
  • Ingår i: European Journal of Neurology. - : Wiley. - 1351-5101. ; 18, s. 766-771
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The coding of histology of nervous system (NS) tumors with various degrees of malignancies differs between cancer registries, whereby the comparison of incidence rates from one registry to another seems difficult. No study has systematically defined whether the change in the risk of NS tumors upon immigration in adulthood varies by subsite or histology. Therefore, we aimed to address this issue amongst the first-generation immigrants to Sweden based on a large uniform cancer registry data (1958-2006). Methods: The nationwide Swedish Family-Cancer Database (2008 version; >11.8 million individuals; 1.8 million immigrants; histology code in force since 1958) was used to calculate standardized incidence ratios (SIRs). We analyzed 28 981 adult cases of NS tumors amongst Swedes and 2519 amongst immigrants (age ≥30). Results: Significantly decreased risks for brain glioma were amongst German (SIR = 0.64), Eastern European (0.62), some Asian (0.71), Chilean (0.34), and African immigrants (0.52). We found an increased risk for brain meningioma amongst Finns (1.15) and former Yugoslavians (1.33), whilst only Norwegians (0.71) and Latin Americans (0.21) had a decreased risk. The risk for spinal ependymoma and astrocytoma was increased in Germans (3.66) and former Yugoslavians (8.89). We found no significant difference for peripheral nerve tumors between immigrants and the native Swedes. Conclusion: Significant differences between risk of NS tumors amongst immigrants and the native Swedes may suggest different risk factor profiles for glioma compared to meningioma indicating a higher etiological role of genetic background or childhood environmental risk factors rather than exposures after immigration.
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18.
  • Rachakonda, P. Sivaramakrishna, et al. (författare)
  • TERT promoter mutations in bladder cancer affect patient survival and disease recurrence through modification by a common polymorphism
  • 2013
  • Ingår i: Proceedings of the National Academy of Sciences. - : Proceedings of the National Academy of Sciences. - 1091-6490 .- 0027-8424. ; 110:43, s. 17426-17431
  • Tidskriftsartikel (refereegranskat)abstract
    • The telomerase reverse transcriptase (TERT) promoter, an important element of telomerase expression, has emerged as a target of cancer-specific mutations. Originally described in melanoma, the mutations in TERT promoter have been shown to be common in certain other tumor types that include glioblastoma, hepatocellular carcinoma, and bladder cancer. To fully define the occurrence and effect of the TERT promoter mutations, we investigated tumors from a well-characterized series of 327 patients with urothelial cell carcinoma of bladder. The somatic mutations, mainly at positions - 124 and - 146 bp from ATG start site that create binding motifs for E-twenty six/ternary complex factors (Ets/TCF), affected 65.4% of the tumors, with even distribution across different stages and grades. Our data showed that a common polymorphism rs2853669, within a preexisting Ets2 binding site in the TERT promoter, acts as a modifier of the effect of the mutations on survival and tumor recurrence. The patients with the mutations showed poor survival in the absence [hazard ratio (HR) 2.19, 95% confidence interval (CI) 1.02-4.70] but not in the presence (HR 0.42, 95% CI 0.18-1.01) of the variant allele of the polymorphism. The mutations in the absence of the variant allele were highly associated with the disease recurrence in patients with Tis, Ta, and T1 tumors (HR 1.85, 95% CI 1.11-3.08). The TERT promoter mutations are the most common somatic lesions in bladder cancer with clinical implications. The association of the mutations with patient survival and disease recurrence, subject to modification by a common polymorphism, can be a unique putative marker with individualized prognostic potential.
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19.
  • Riihimäki, Matias, et al. (författare)
  • Metastatic sites and survival in lung cancer.
  • 2014
  • Ingår i: Lung Cancer. - : Elsevier BV. - 1872-8332 .- 0169-5002. ; 86:1, s. 78-84
  • Tidskriftsartikel (refereegranskat)abstract
    • Population-based data on metastatic sites and survival in site-specific metastases are lacking for lung cancer and for any cancer because most cancer registries do not record metastases. This study uses a novel population-based approach to identify metastases from both death certificates and national inpatient data to describe metastatic pathways in lung cancer patients.
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20.
  • Roudgari, Hassan, et al. (författare)
  • Prostate cancer risk assessment model: a scoring model based on the Swedish Family-Cancer Database
  • 2012
  • Ingår i: Journal of Medical Genetics. - : BMJ. - 0022-2593 .- 1468-6244. ; 49:5, s. 345-352
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Many prostate cancer (PC) risk assessment models have been developed, however almost none include familial history. Aim To produce a risk assessment model for PC based on familial background of related cancers. Method 976 859 independent index men aged >= 30 in year 1998 and their family members in the Swedish Family-Cancer Database (FCD2010) were randomly divided into development (60%) and validation (40%) datasets (follow-up 10 years). The HR from Cox model was used to extrapolate risk scores. Results Specified scores were: for PC in situ at age <60 years in index man, 5; for PC at age <60 years in each first-degree relative (FDR), 15; for PC at age >= 60 years in each FDR, 10; for PC at age <60 years in each second-degree relative, 5; for breast cancer in each FDR, 2; for oesophageal carcinoma in situ in index man, 2; and for oesophagus cancer in each FDR, 2. Based on the findings, if the milestone age for a PC screening programme was 60 years or more, the recommended starting age for the men with the score-group 6-10 would be 54 years; score-group 11-15, 52 years; score-group 16-20, 50 years; score-group 21-25, 44 years; and for the score-group 26+ it should start before age 40. The concordance index in development and validation sets was 0.885 (95% CI 0.883 to 0.888). No significant difference was found between curves from development and validation datasets (internally validated using twofold validation and bootstrapping). Conclusion Familial history of relevant malignancies can be used as risk factors to estimate a man's prior risk of developing PC. The prostate cancer risk assessment model could satisfactorily assess risk of developing prostate cancer.
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