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  • 1
    Keywords: CLASSIFICATION ; DIAGNOSIS ; INFORMATION ; COHORT ; cohort study ; DISEASE ; POPULATION ; RISK ; RISKS ; LYMPHOMA ; MALIGNANCIES ; AGE ; leukemia ; SWEDEN ; DATABASE ; familial risk ; CANCER DATABASE ; RELATIVES ; LONG-TERM SURVIVORS ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; MULTIPLE-MYELOMA ; DENMARK ; HETEROGENEITY ; multiple myeloma ; MALIGNANCY ; AGGREGATION ; SUBTYPE ; INTERVAL ; familial aggregation ; SIZE ; ANTICIPATION ; CLINICAL CHARACTERISTICS ; LYMPHOPROLIFERATIVE TUMORS ; PSEUDOAUTOSOMAL LINKAGE
    Abstract: The importance of genetic factors in the etiology of non-Hodgkin lymphoma (NHL) is suggested by case-control and cohort studies. Most previous studies have been too small to estimate accurately risks of specific categories of lymphoproliferative malignancies in relatives of NHL cases or to quantify the contribution of NHL case characteristics to familial risk. We have overcome sample size limitations and potential recall bias by using large databases from Sweden and Denmark. Diagnoses of lymphoproliferative malignancies were compared in 70,006 first-degree relatives of 26,089 NHL cases (including 7,432 with subtype information) versus 161,352 first-degree relatives of 58,960 matched controls. Relatives of NHL cases were at significantly increased risk for NHL [relative risk (RR), 1.73; 95% confidence interval (95% CI), 1.39-2.15], Hodgkin lymphoma (RR, 1.41; 95% Cl, 1.0-1.97), and nonsignificantly for chronic lymphocytic leukemia (CLL; RR, 1.31; 95% CI, 0.93-1.85). No increased risk was found for multiple myeloma among case relatives. Findings with respect to siblings compared with parents and offspring or with respect to age at diagnosis of proband were inconsistent. In both populations, relatives of cases with an aggressive NHL subtype were at substantially increased risk of NHL (combined RR, 3.56; 95% CI, 1.80-7.02). We conclude that NHL has an important familial component, which is shared with Hodgkin lymphoma and CLL. We estimate that the absolute lifetime risk for a first-degree relative of an NHL case to develop NHL is 3.6% (compared with a population risk of 2.1%) and higher if the index case had an aggressive subtype of NHL
    Type of Publication: Journal article published
    PubMed ID: 16214923
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  • 2
    Keywords: CANCER ; radiotherapy ; carcinoma ; human ; neoplasms ; DIAGNOSIS ; RISK ; PATIENT ; kidney ; RISK-FACTORS ; CARCINOGENESIS ; colon ; ASSOCIATION ; BREAST ; LYMPHOMA ; AGE ; OVARIAN-CANCER ; risk factors ; CERVICAL-CANCER ; RATES ; cancer risk ; REGISTRATION ; CANCER-PATIENTS ; adenocarcinoma ; TOBACCO ; pancreatic cancer ; LONG-TERM SURVIVORS ; YOUNG ; REGISTRY ; REPRODUCTIVE FACTORS ; ASSOCIATIONS ; ENDOMETRIAL ; PANCREATIC-CANCER ; cancer registries ; TESTICULAR CANCER ; LYMPHOMAS ; cancer registry ; pooled analysis ; RISK-FACTOR ; CANCERS ; REGISTRIES ; CANCER-DIAGNOSIS ; pancreatic neoplasms ; MALIGNANT NEOPLASMS ; neoplasms,second primary
    Abstract: Studies of pancreatic cancer in the setting of second primary malignant neoplasms can provide etiologic clues. An international multicenter study was carried out using data from 13 cancer registries with a registration period up to year 2000. Cancer patients were followed up from the initial cancer diagnosis, and the occurrence of second primary malignant neoplasms was compared with expected values derived from local rates, adjusting for age, sex, and period of diagnosis. Results from individual registries were pooled by use of a fixed-effects model. People were at higher risk of developing pancreatic cancer within 10 years of a diagnosis of cancers of the pharynx, stomach, gallbladder, larynx, lung, cervix, corpus uteri, bladder, and eye and 10 years or later following a diagnosis of cancers of the stomach, colon, gallbladder, breast, cervix, placenta, corpus uteri, ovary, testis, bladder, kidney, and eye, as well as Hodgkin's and non-Hodgkin's lymphomas. Pancreatic cancer was connected with smoking-related cancers, confirming the etiologic role of tobacco. The associations with uterine and ovarian cancers suggest that reproductive factors might be implicated in pancreatic carcinogenesis. The elevated pancreatic cancer risk in young patients observed among several types of cancer implies a role of genetic factors. Radiotherapy is also suggested as a risk factor
    Type of Publication: Journal article published
    PubMed ID: 16421239
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  • 3
    Keywords: CANCER ; carcinoma ; CELL ; LUNG ; PROSTATE ; COHORT ; EXPOSURE ; incidence ; liver ; RISK ; PATIENT ; kidney ; primary ; SKIN ; BREAST ; BREAST-CANCER ; LYMPHOMA ; DIFFERENCE ; DECREASE ; NUMBER ; AGE ; COUNTRIES ; PROSTATE-CANCER ; RATES ; skin cancer ; MELANOMA ; SWEDEN ; COLON-CANCER ; STOMACH ; SIR ; UNITED-STATES ; AUSTRALIA ; second cancer ; SKIN-CANCER ; basal cell carcinoma ; NON-HODGKINS-LYMPHOMA ; CELL CARCINOMA ; ONCOLOGY ; REGISTRY ; pancreas ; cancer registries ; non-Hodgkin lymphoma ; methods ; cancer registry ; CANCER INCIDENCE ; female ; CANCERS ; REGISTRIES ; E ; colorectal ; BASAL-CELL CARCINOMA ; second primary cancer ; SUN EXPOSURE ; vitamin D ; VITAMIN-D ; ULTRAVIOLET-RADIATION ; SUBSEQUENT RISK ; D METABOLITES
    Abstract: Background: Skin cancers are known to be associated with sun exposure, whereas sunlight through the production of vitamin D may protect against some cancers. The aim of this study was to assess whether patients with skin cancer have an altered risk of developing other cancers. Methods: The study cohort consisted of 416,134 cases of skin cancer and 3,776,501 cases of non-skin cancer as a first cancer extracted from 13 cancer registries. 10,886 melanoma and 35,620 non-melanoma skin cancer cases had second cancers. The observed numbers (0) of 46 types of second primary cancer after skin melanoma, basal cell carcinoma or non-basal cell carcinoma, and of skin cancers following non-skin cancers were compared to the expected numbers (E) derived from the age, sex and calendar period specific cancer incidence rates in each of the cancer registries (O/E = SIR, standardised incidence ratios). Rates from cancer registries classified to sunny countries (Australia, Singapore and Spain) and less sunny countries (Canada, Denmark, Finland, Iceland, Norway, Scotland, Slovenia and Sweden) were compared to each other. Results: SIR of all second solid primary cancers (except skin and lip) after skin melanoma were significantly lower for the sunny countries (SIR(S) = 1.03; 95% CI 0.99-1.08) than in the less sunny countries (SIR(L) = 1.14; 95%CI 1.11-1.17). The difference was more obvious after non-melanoma skin cancers: after basal cell carcinoma SIR(S)/SIR(L) = 0.65 (9S%CI = 0.58-0.72); after non-basal cell carcinoma SIR(S)/SIR(L) = 0.58 (95%CI = 0.50-0.67). In sunny countries, the risk of second primary cancer after non-melanoma skin cancers was lower for most of the cancers except for lip, mouth and non-Hodgkin lymphoma. Conclusions: Vitamin D production in the skin seems to decrease the risk of several solid cancers (especially stomach, colorectal, liver and gallbladder, pancreas, lung, female breast, prostate, bladder and kidney cancers). The apparently protective effect of sun exposure against second primary cancer is more pronounced after non-melanoma skin cancers than melanoma, which is consistent with earlier reports that non-melanoma skin cancers reflect cumulative sun exposure, whereas melanoma is more related to sunburn. (c) 2007 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 17540555
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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: neoplasms ; FOLLOW-UP ; RISK ; UNITED-STATES ; CHILDREN ; SURVIVORS ; EWINGS-SARCOMA ; soft-tissue sarcoma ; WILMS-TUMOR ; childhood solid cancer ; INTERNATIONAL-CLASSIFICATION ; second malignant neoplasm
    Abstract: Children diagnosed with noncentral nervous system solid cancers (NCNSSC) experience several adverse late effects, including second malignant neoplasm. The aim of our study was to assess the risk of specific second malignancies after a childhood NCNSSC. Diagnosis and follow-up data on 10,988 cases of NCNSSC in children (0-14 years) were obtained from 13 registries. Standardized incidence ratios (SIRs) with 95% confidence intervals (CI) and cumulative incidence of second malignancies were computed. We observed 175 second malignant neoplasms, yielding a SIR of 4.6, 95% CI: 3.9-5.3. When considering second cancers with at least 10 occurrences, highest relative risks were found for second malignant bone tumors (SIR = 26.4, 16.6-40.0), soft tissue sarcomas (SIR = 14.1, 6.7-25.8) and myeloid leukemia (SIR = 12.7, 6.3-22.8). Significant increased risks for all malignancies combined were observed after sympathetic nervous system tumors (SIR = 11.4, 5.2-21.6), retinoblastomas (SIR = 7.3, 5.4-9.8), renal tumors (SIR = 5.7, 3.8-8.0), malignant bone tumors (SIR = 5.6, 3.7-8.2), soft tissue sarcomas (SIR = 4.7, 3.2-6.8), germ-cell, trophoblastic and other gonadal neoplasms (SIR = 2.5, 1.1-4.9), carcinomas and other malignant epithelial neoplasms (SIR = 2.2, 1.4-3.3). The highest risk of a second malignancy of any type occurred 5 to 9 years after NCNSSC (SIR = 9.9, 6.8-13.9). The cumulative incidence of second malignancies 10 years after the first neoplasm was eight times higher among NCNSSC survivors than in the general population, with the absolute difference between observed and expected cumulative incidence still increasing after 50 years of follow-up. Children who survived a NCNSSC experience a large increased risk of developing a new malignancy, even many years after their initial diagnosis
    Type of Publication: Journal article published
    PubMed ID: 21520035
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  • 6
    Keywords: carcinoma ; RISK ; GENOME ; DISCOVERY ; smoking ; COLORECTAL-CANCER ; molecular epidemiology ; HETEROGENEITY ; SCIENCE ; ENVIRONMENTAL-FACTORS
    Abstract: Cancer research is drawing on the human genome project to develop new molecular-targeted treatments. This is an exciting but insufficient response to the growing, global burden of cancer, particularly as the projected increase in new cases in the coming decades is increasingly falling on developing countries. The world is not able to treat its way out of the cancer problem. However, the mechanistic insights from basic science can be harnessed to better understand cancer causes and prevention, thus underpinning a complementary public health approach to cancer control. This manuscript focuses on how new knowledge about the molecular and cellular basis of cancer, and the associated high-throughput laboratory technologies for studying those pathways, can be applied to population-based epidemiological studies, particularly in the context of large prospective cohorts with associated biobanks to provide an evidence base for cancer prevention. This integrated approach should allow a more rapid and informed translation of the research into educational and policy interventions aimed at risk reduction across a population.
    Type of Publication: Journal article published
    PubMed ID: 25515230
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  • 7
    Keywords: CANCER ; LUNG ; lung cancer ; LUNG-CANCER ; WORKERS ; FRANCE
    Type of Publication: Journal article published
    PubMed ID: 12848246
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  • 8
    Keywords: human ; MODEL ; MODELS ; DISEASE ; DISEASES ; EPIDEMIOLOGY ; HISTORY ; RISK ; RISKS ; ARTHRITIS ; FAMILY ; CONTRAST ; ASSOCIATION ; SUSCEPTIBILITY ; LYMPHOMA ; family history ; SWEDEN ; case-control studies ; FAMILY-CANCER DATABASE ; RELATIVES ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; ULCERATIVE-COLITIS ; RELATIVE RISK ; DENMARK ; INFLAMMATORY-BOWEL-DISEASE ; AUTOIMMUNITY ; SYSTEMIC-LUPUS-ERYTHEMATOSUS ; MALIGNANCY ; case-control study ; population-based case-control study ; REGISTRY ; REGRESSION ; FAMILIES ; INCREASE ; RHEUMATOID-ARTHRITIS ; AUTOIMMUNE-DISEASES ; case control studies ; INTERVAL ; FAMILY-HISTORY ; HODGKIN-LYMPHOMA ; INCREASED RISK ; odds ratio ; HODGKIN LYMPHOMA ; REGISTRIES ; population-based ; autoimmune disease ; 1ST-DEGREE RELATIVES ; LUPUS-ERYTHEMATOSUS ; SARCOIDOSIS
    Abstract: Background: Personal history of autoimmune diseases is consistently associated with increased risk of non-Hodgkin lymphoma. In contrast, there are limited data on risk of Hodgkin lymphoma following autoimmune diseases and almost no data addressing whether there is a familial association between the conditions. Methods: Using population-based linked registry data from Sweden and Denmark, 32 separate autoimmune and related conditions were identified from hospital diagnoses in 7476 case subjects with Hodgkin lymphoma, 18 573 matched control subjects, and more than 86 000 first-degree relatives of case and control subjects. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) as measures of relative risks for each condition using logistic regression and also applied multivariable hierarchical regression models. All P values are two-sided. Results: We found statistically significantly increased risks of Hodgkin lymphoma associated with personal histories of several autoimmune conditions, including rheumatoid arthritis (OR = 2.7, 95% CI = 1.9 to 4.0), systemic lupus erythematosus (OR = 5.8, 95% Cl = 2.2 to 15.1), sarcoidosis (OR = 14.1, 95% CI = 5.4 to 36.8), and immune thrombocytopenic purpura (OR = infinity, P = .002). A statistically significant increase in risk of Hodgkin lymphoma was associated with family histories of sarcoidosis (OR = 1.8, 95% CI = 1.01 to 3.1) and ulcerative colitis (OR = 1.6, 95% CI = 1.02 to 2.6). Conclusions: Personal or family history of certain autoimmune conditions was strongly associated with increased risk of Hodgkin lymphoma. The association between both personal and family histories of sarcoidosis and a statistically significantly increased risk of Hodgkin lymphoma suggests shared susceptibility for these conditions
    Type of Publication: Journal article published
    PubMed ID: 16985251
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  • 9
    Keywords: CANCER ; carcinoma ; PATHWAY ; PATHWAYS ; RISK ; GENE ; TUMORS ; TIME ; DNA ; kidney ; MECHANISM ; RISK-FACTORS ; colon ; mechanisms ; SKIN ; ASSOCIATION ; LYMPHOMA ; NUMBER ; AGE ; DNA-REPAIR ; REPAIR ; DIETARY ; ADENOCARCINOMAS ; INDIVIDUALS ; SMALL-INTESTINE ; NONPOLYPOSIS COLORECTAL-CANCER ; 2ND PRIMARY NEOPLASMS ; DNA repair ; CLUSTER ; REGISTRY ; pancreas ; ASSOCIATIONS ; cancer registries ; INCREASE ; GLAND ; SMALL-BOWEL ; INTERVAL ; GENDER ; second primary cancers ; rectum ; cancer registry ; pooled analysis ; CANCER INCIDENCE ; registry-based study ; small intestine cancer
    Abstract: Cancer of the small intestine is a rare neoplasm, and its etiology remains poorly understood. Analysis of other primary cancers in individuals with small intestine cancer may help elucidate the causes of this neoplasm and the underlying mechanisms. We included 10,946 cases of first primary small intestine cancer from 13 cancer registries in a pooled analysis. The observed numbers of 44 types of second primary cancer were compared to the expected numbers derived from the age-, gender- and calendar period-specific cancer incidence rates in each registry. We also calculated the standardized incidence ratios (SIR) for small intestine cancer as a second primary after other cancers. There was a 68% overall increase in the risk of a new primary cancer after small intestine carcinoma (SIR = 1.68, 95% confidence interval [CI] = 1.47-1.71), that remained constant over time. The overall SIR was 1.18 (95% CI = 1.05-1.32) after carcinoid, 1.29 (1.01-1.63) after sarcoma, and 1.27 (0.78-1.94) after lymphoma. Significant (p 〈 0.05) increases were observed for cancers of the oropharynx, colon, rectum, ampulla of Vater, pancreas, corpus uteri, ovary, prostate, kidney, thyroid gland, skin and soft (issue sarcomas. Small intestine cancer as a second primary was increased significantly after all these cancers, except after oropharyngeal and kidney cancers. Although some of the excess may be attributable to overdiagnosis, it is plausible that most additional cases of second primary cancers were clinically relevant and were due to common genetic (e.g., defects in mismatch or other DNA repair pathways) and environmental (e.g., dietary) factors. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16003748
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  • 10
    Keywords: CANCER ; radiotherapy ; SURVIVAL ; FOLLOW-UP ; RISK ; TUMORS ; kidney ; treatment ; BREAST-CANCER ; chemotherapy ; LONG-TERM SURVIVORS ; ETOPOSIDE ; TESTICULAR CANCER ; COMBINATION CHEMOTHERAPY ; leukaemia ; nonseminoma ; BLEOMYCIN ; NORWEGIAN MALE-PATIENTS ; SECONDARY LEUKEMIA ; seminomas
    Abstract: We investigated the risk of second malignancies among 29,511 survivors of germ-cell testicular cancer recorded in 13 cancer registries. Standardized incidence ratios (SIRs) were estimated comparing the observed numbers of second malignancies with the expected numbers obtained from sex-, age-, period- and population-specific incidence rates. Seminomas and nonseminomas, the 2 main histological groups of testicular cancer, were analyzed separately. During a median follow-up period of 8.3 years (0-35 years), we observed 1,811 second tumors, with a corresponding SIR of 1.65 (95% confidence interval (CI): 1.57-1.73). Statistically significant increased risks were found for fifteen cancer types, including SIRs of 2.0 or higher for cancers of the stomach, gallbladder and bile ducts, pancreas, bladder, kidney, thyroid, and for soft-tissue sarcoma. nonmelanoma skin cancer and myeloid leukemia. The SIR for myeloid leukemia was 2.39 (95% CI: 1.41-3.77) after seminomas. and 6.77 (95% CI: 4.14-10.5) after nonseminomas. It increased to 37.9 (95% CI: 18.9-67.8; based on 11 observed cases of leukemia) among nonseminoma patients diagnosed since 1990. SIRs for most solid cancers increased with follow-up duration, whereas they, did not change with year of testicular cancer diagnosis. Among subjects diagnosed before 1980, 20 year survivors of seminoma had a cumulative risk of solid cancer of 9.6% (95% CI: 8.7-10.5%) vs. 6.5% expected, whereas 20 years survivors of nonseminoma had a risk of 5.0% (95% CI: 4.2-6.0%) vs. 3.1% expected. In conclusion, survivors of testicular cancers have an increased risk of several second primaries, where the effect of the treatment seems to play a major role. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17096341
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