| 61. |
- Hemminki, Kari, et al.
(författare)
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Cancer in immigrants as a pointer to the causes of cancer.
- 2014
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Ingår i: European Journal of Public Health. - : Oxford University Press (OUP). - 1101-1262 .- 1464-360X. ; 24 Suppl 1, s. 64-71
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Tidskriftsartikel (refereegranskat)abstract
- The early cancer studies on immigrants, which started to appear some 50 years ago, showed that the incidence in cancers changes to the level of the new host country in one or two generations. These findings were fundamental to the understanding of the environmental etiology of human cancer. Many immigrant groups originate from countries with no cancer registration, and, hence, the immigrant studies may provide estimates on the indigenous cancer rates. The Swedish Family-Cancer Database has been an important source of data for immigrant studies on various diseases. The Database covers the Swedish population of the past 100 years, and it records the country of birth for each subject. A total of 1.79 million individuals were foreign born, Finns and other Scandinavians being the largest immigrant groups. Over the course of years, some 30 publications have appeared relating to cancer in immigrants. In the present article, we will review more recent immigrant studies, mainly among Swedish immigrants, on all cancers and emphasize the differences between ethnic groups. In the second part, we discuss the problem of reliable registration of cancer and compare cancer incidence among non-European immigrants with cancer incidence in countries of origin, as these have now active cancer registries. We discuss the experiences in cancer registration in Morocco and Egypt. We show the usefulness and limitations in predicting cancer incidence in the countries of origin.
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| 62. |
- Hemminki, Kari, et al.
(författare)
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Cancer risk in amyloidosis patients in Sweden with novel findings on non-Hodgkin lymphoma and skin cancer
- 2014
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Ingår i: Annals of Oncology. - : Elsevier BV. - 1569-8041 .- 0923-7534. ; 25:2, s. 511-518
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Tidskriftsartikel (refereegranskat)abstract
- Background: Systemic amyloidosis (SSA) is a common form of amyloidosis but it remains often unnoticed because of the slow progression in old patients. The cause for SSA is the accumulation of wild-type transthyretin amyloids in critical tissues. We provide here data showing that SSA may be associated with old-age non-Hodgkin lymphoma.Systemic amyloidoses include immunoglobulin light chain (AL) amyloidosis, serum amyloid (AA)-related amyloidosis and senile systemic amyloidosis (SSA). AL amyloidosis is associated with myeloma, and we showed recently that transthyretin-related hereditary amyloidosis was related to non-Hodgkin lymphoma (NHL). In SSA, amyloids constitute wild-type transthyretin. We wanted to analyze cancer risks in amyloidosis, particularly in SSA. Nonhereditary amyloidosis patients were identified from the Swedish Hospital Discharge and Outpatients Registers from years 1997 through 2010. Their cancer risk was assessed based on the Swedish Cancer Registry using standardized incidence ratio (SIR) between amyloidosis patients and the remaining population. To gain information about amyloidosis subtypes, we used the Swedish Prescribed Drug Register from years 2005 through 2010 to find out the specific medication prescribed. Among 1400 identified amyloidosis patients, cancer risk was increased for myeloma, NHL and squamous cell skin cancer. Myeloma and skin cancers were diagnosed 7-8 years earlier than in the population, whereas NHL was diagnosed in elderly patients. The SIR was 204 for myeloma in patients who received AL amyloidosis medication, and it was 17.22 in patients receiving rheumatoid arthritis medication, suggesting AA amyloidosis. In remaining patients, including SSA, NHL risk was 14.78, including lymphoplasmacytic lymphoma and Waldenstrom macroglobulinemia (51.41) and diffuse large B-cell lymphoma (18.69). In these patients, endometrial cancer (7.04) and cancer of unknown primary site (6.56) were also increased. SSA is likely to be a main cause of NHL in the elderly population. The present findings suggest a novel mechanism for amyloidosis-related cancer, highlighting the role of chronic stimulation by amyloid.
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| 63. |
- Hemminki, Kari, et al.
(författare)
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Co-Morbidity between Early-Onset Leukemia and Type 1 Diabetes - Suggestive of a Shared Viral Etiology?
- 2012
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Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7:6
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Tidskriftsartikel (refereegranskat)abstract
- Background: Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) are common early-onset malignancies. Their causes are largely unknown but infectious etiology has been implicated. Type 1 diabetes (T1D) is an autoimmune disease for which infectious triggers of disease onset have been sought and increasing pointing to enteroviruses. Based on our previous results on co-morbidity between leukemia and T1D, we updated the Swedish dataset and focused on early onset leukemias in patients who had been hospitalized for T1D, comparing to those not hospitalized for T1D. Methods and Findings: Standardized incidence ratios (SIRs) were calculated for leukemia in 24,052 patients hospitalized for T1D covering years 1964 through 2008. T1D patients were included if hospitalized before age 21 years. Practically all Swedish children and adolescents with T1D are hospitalized at the start of insulin treatment. SIR for ALL was 8.30 (N = 18, 95% confidence interval 4.91-13.14) when diagnosed at age 10 to 20 years after hospitalization for T1D and it was 3.51 (13, 1.86-6.02) before hospitalization for T1D. The SIR for ALL was 19.85 (N = 33, 13.74-27.76) and that for AML was 25.28 (8, 10.80-50.06) when the leukemias were diagnosed within the year of T1D hospitalization. The SIRs increased to 38.97 (26, 25.43-57.18) and 40.11 (8, 17.13-79.42) when T1D was diagnosed between ages 10 to 20 years. No consistent time-dependent changes were found in leukemia risk. Conclusion: A shared infectious etiology could be a plausible explanation to the observed co-morbidity. Other possible contributing factors could be insulin therapy or T1D related metabolic disturbances.
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| 64. |
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| 65. |
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| 66. |
- Hemminki, Kari, et al.
(författare)
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Do discordant cancers share familial susceptibility?
- 2012
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Ingår i: European Journal of Cancer. - : Elsevier BV. - 1879-0852 .- 0959-8049. ; 48, s. 1200-1207
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: Cancer syndromes manifest at many sites albeit with variable penetrance. Genome-wide association (GWA) studies have identified susceptibility loci shared by many types of cancer. Yet, a population level search for shared susceptibility between discordant cancers has been hampered because of lacking population sizes. METHODS: Over 1.1million patients in the nation-wide Swedish Family-Cancer Database were analysed for discordant familial cancers covering 33 sites. Standardised incidence ratios (SIRs) were calculated for patients whose family members had a defined cancer compared to those whose family members did not have that cancer. Three independent tests for each pair of cancer sites were done using different family relationships. RESULTS: Lung cancer showed 13 significant discordant associations but most of them were with sites for which smoking is a risk factor. An exception was the clustering of lung cancer and endocrine cancers. Four discordant associations reached a minimal significance level of 5×10(-6): colorectum-endometrium, breast-ovary, breast-prostate and melanoma-squamous cell carcinoma of the skin. The association of melanoma and nervous system cancer reached a minimal significance of 10(-4). Discarding lung cancer, all other associations were based on a single test whereby they were liable to be chance associations. CONCLUSIONS: This study showed the extraordinary requirements for statistical power in study of multiple cancer sites. In addition to the smoking related sites, associations between breast and prostate cancers, melanoma and nervous system tumours and lung and endocrine tumours found strong statistical support. Within the present sample size limits, we found no evidence of an overall susceptibility to cancer.
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| 67. |
- Hemminki, Kari, et al.
(författare)
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Does the Breast Cancer Age at Diagnosis Differ by Ethnicity? A Study on Immigrants to Sweden
- 2011
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Ingår i: The Oncologist. - : Oxford University Press (OUP). - 1083-7159 .- 1549-490X. ; 16:2, s. 146-154
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Tidskriftsartikel (refereegranskat)abstract
- Background. Age-specific incidence rates for breast cancer in low-risk and high-risk ethnic populations differ by age at which the incidence maximum is reached: around 50 years in low-risk populations and over 60 years in high-risk populations. The interpretation of these differences remains unsettled, one line primarily referring to biological differences, the second one to cohort effects of rapidly increasing rates in young populations, and the third one to incomplete registration of cancer in the elderly. Methods. The nationwide Family-Cancer Database was used to analyze standardized incidence ratios (SIRs) and age at diagnosis of breast cancer in female immigrants to Sweden by their region of origin compared with women native to Sweden matched on birth year and other relevant factors. Results. We showed first that the SIRs for breast cancer were lower in many immigrant groups compared with natives of Sweden; women from Turkey had the lowest SIR of 0.45, followed by those from Chile (0.54) and Southeast Asia (0.57). Women from nine regions showed an earlier mean age at diagnosis than their matched Swedish controls, the largest differences being 5.5 years for women from Turkey, 5.1 years for those from Asian Arab and "Other African" countries, 4.3 years for those from Iran, and 4.0 years for those from Iraq. Conclusions. The results show that in many immigrant groups, the diagnostic age is earlier (< 50 years) than in natives of Sweden (> 50 years), suggesting that true biological factors underlie the differences. These factors may explain much of the international variation in breast cancer incidence. Identifying these factors should advance understanding of breast cancer etiology and prevention. The Oncologist 2011; 16: 146-154
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| 68. |
- Hemminki, Kari, et al.
(författare)
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Effect of autoimmune diseases on incidence and survival in subsequent multiple myeloma
- 2012
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Ingår i: Journal of Hematology & Oncology. - : Springer Science and Business Media LLC. - 1756-8722. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- Background: Patients with many types of autoimmune diseases (AIDs) are at an increased risk of cancer, which may depend on underlying dysregulation of the immune system or treatment. We systematically analyzed myeloma risk and survival in patients diagnosed with 33 different AIDs. Methods: Data on patients with AIDs were retrieved from the Swedish Hospital Discharge Register and were linked to myeloma diagnoses from the Cancer Registry. Standardized incidence ratios (SIR) and hazard ratios (HRs) were calculated for subsequent myeloma between 1964 and 2008. Results: Among patients with the 33 AIDs analyzed, 457 cases of myeloma were diagnosed. The overall SIR for myeloma was 1.12 and the overall HR was 0.92 and non-significant. SIRs for myeloma were significantly increased after ankylosing spondylitis (2.02) and systemic sclerosis (2.63). Only the HR for myeloma after rheumatic fever (5.27) was significantly increased. The SIR for myeloma before age 60 years was 1.45; the SIR for myeloma was only increased in the period 1964-1990 (1.31) and not later (1.04). Only the SIR for myeloma after ankylosing spondylitis was increased in the period 1991-2008 (2.09); the HRs for myeloma were increased after polymyositis/ dermatomyositis (6.44) and rheumatic fever (4.43) but there were only three deaths of myeloma after these AIDs. Conclusions: The present data showed an increase in myeloma SIR after two AIDs, ankylosing spondylitis and systemic sclerosis, and in HR after rheumatic fever. The overall myeloma risk after any AID was no longer increased in the latter follow-up period of 1991 through 2008.
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| 69. |
- Hemminki, Kari, et al.
(författare)
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Effect of autoimmune diseases on mortality and survival in subsequent digestive tract cancers
- 2012
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Ingår i: Annals of Oncology. - : Elsevier BV. - 1569-8041 .- 0923-7534. ; 23:8, s. 2179-2184
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Tidskriftsartikel (refereegranskat)abstract
- Patients with some autoimmune diseases (AIDs) are at increased risk of cancer, possibly a result of an underlying dysregulation of the immune system, medication, treatment or, probably, surveillance bias. Data on cancer mortality and survival in patients previously diagnosed with AIDs would provide novel information on these comorbidities and their clinical implications. Standardized mortality ratios (SMRs) and hazard ratios (HRs) were calculated for subsequent deaths from seven digestive tract cancers between 1964 and 2008 in patients hospitalized for any of 33 AIDs. There were 33 increased SMRs for specific cancers after a defined AID; similarly, 21 HRs were increased. Both the SMR and HR were increased after 10 autoimmune disorders, including pernicious anemia, systemic lupus erythematosus and psoriasis. Increased SMRs and unchanged HRs were noted for 23 cancers. Myasthenia gravis was associated with SMRs for five cancers but no increases in HRs. For nine cancers, including esophageal cancer after ulcerative colitis and rheumatoid arthritis, the SMR was unchanged but the HR increased. The increases in SMRs provide evidence that cancer risks were truly increased and largely unaffected by surveillance bias. The prognostic survival data should contribute to clinical evaluation and therapeutic planning.
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| 70. |
- Hemminki, Kari, et al.
(författare)
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Effect of autoimmune diseases on risk and survival in female cancers.
- 2012
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Ingår i: Gynecologic Oncology. - : Elsevier BV. - 1095-6859 .- 0090-8258. ; 127:1, s. 180-185
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: Patients with autoimmune (AI) diseases are diagnosed with increased frequencies of some cancers, which may depend on the underlying dysregulation of the immune system or treatment. Data on female cancers are limited. METHODS: We analyzed systematically risk and survival of female cancers of the breast, uterus, ovary and other genital organs in close to 200,000 patients diagnosed with any of 33 different AI diseases. Standardized incidence ratios (SIRs) for risk and hazard ratios (HRs) for survival were calculated for subsequent incident cancers or cancer deaths up to year 2008. RESULTS: For all breast cancer after any AI diseases, the SIR was 0.94; SIRs were modestly increased after two AI diseases and decreased after nine AI diseases, including Sjogren syndrome (0.46). For cervical cancer, the risk was increased after discoid lupus erythematosus (3.34) and systemic sclerosis (2.43). The HR was 2.12 in chronic rheumatic heart disease patients. The overall SIR for endometrial cancer was 0.85, with low SIR in ankylosing spondylitis (0.37); the HR was 4.05 for Sjogren syndrome. The SIR for ovarian cancer was increased for polymyositis/dermatomyositis (3.26) while the HR was increased for multiple sclerosis (2.43). The overall SIR for other genital cancers was increased to 1.54 and a very high risk of 35.88 was observed in localized scleroderma. CONCLUSIONS: Breast, endometrial and ovarian cancers were decreased after all AI diseases and most significant changes after individual AI diseases were towards lower risks. Probably treatment related factors explain the findings. For cervical and other genital cancers all significant changes were increased risks.
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