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Sökning: L773:0008 543X OR L773:1097 0142 > Sundquist Kristina

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1.
  • Crump, Casey, et al. (författare)
  • Perinatal and Familial Risk Factors for Acute Lymphoblastic Leukemia in a Swedish National Cohort
  • 2015
  • Ingår i: Cancer. - : Wiley. - 1097-0142 .- 0008-543X. ; 121:7, s. 1040-1047
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUNDPerinatal factors including high birth weight have been found to be associated with acute lymphoblastic leukemia (ALL) in case-control studies. However, to the best of our knowledge, these findings have seldom been examined in large population-based cohort studies, and the specific contributions of gestational age and fetal growth remain unknown. METHODSThe authors conducted a national cohort study of 3,569,333 individuals without Down syndrome who were born in Sweden between 1973 and 2008 and followed for the incidence of ALL through 2010 (maximum age, 38 years) to examine perinatal and familial risk factors. RESULTSThere were 1960 ALL cases with 69.7 million person-years of follow-up. After adjusting for potential confounders, risk factors for ALL included high fetal growth (incidence rate ratio [IRR] per additional 1 standard deviation, 1.07; 95% confidence interval [95% CI], 1.02-1.11 [P =.002]; and IRR for large vs appropriate for gestational age, 1.22; 95% CI, 1.06-1.40 [P =.005]), first-degree family history of ALL (IRR, 7.41; 95% CI, 4.60-11.95 [P<.001]), male sex (IRR, 1.20; 95% CI, 1.10-1.31 [P<.001]), and parental country of birth (IRR for both parents born in Sweden vs other countries, 1.13; 95% CI, 1.00-1.27 [P =.045]). These risk factors did not appear to vary by patient age at the time of diagnosis of ALL. Gestational age at birth, season of birth, birth order, multiple birth, parental age, and parental education level were not found to be associated with ALL. CONCLUSIONSIn this large cohort study, high fetal growth was found to be associated with an increased risk of ALL in childhood through young adulthood, independent of gestational age at birth, suggesting that growth factor pathways may play an important long-term role in the etiology of ALL. Cancer 2015;121:1040-1047. (c) 2014 American Cancer Society. The authors conducted what, to their knowledge, is the largest population-based cohort study to date to examine perinatal and familial risk factors for acute lymphoblastic leukemia (ALL) among approximately 3.5 million individuals born in Sweden between 1973 and 2008. High fetal growth was found to be associated with an increased risk of ALL in childhood through young adulthood, independent of gestational age at birth, suggesting that growth factor pathways may play an important long-term role in the etiology of ALL.
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2.
  • Hemminki, Kari, et al. (författare)
  • Autoimmune diseases as comorbidities for liver, gallbladder, and biliary duct cancers in Sweden
  • 2023
  • Ingår i: Cancer. - : Wiley. - 0008-543X .- 1097-0142. ; 129:8, s. 1227-1236
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Autoimmune diseases are associated with many cancers but there is a lack of population-based studies with different autoimmune diseases that have a long follow-up. This is also true of hepatobiliary cancers, which include hepatocellular cancer (HCC) and rarer entities of gallbladder cancer (GBC), intra- and extrahepatic cholangiocarcinoma (iCCA and eCCA), and ampullary cancer. Methods: Diagnostic data on 43 autoimmune diseases were collected from the Swedish Inpatient Register from 1987 to 2018, and cancer data were derived from the national cancer registry from 1997 onward. Relative risks were expressed as standardized incidence ratios (SIRs). Results: In a population of 13.6 million, 1.1 million autoimmune diseases were diagnosed and subsequent hepatobiliary cancer was diagnosed in 3191 patients (17.2% of cancers). SIRs for HCC were 2.73 (men) and 2.86 (women), 3.74/1.96 for iCCA, 2.65/1.37 for GBC, 2.38/1.64 for eCCA, and 1.80/1.85 for ampullary cancer. Significant associations between autoimmune disease and HCC were observed for 13 autoimmune diseases, with the highest risks being for autoimmune hepatitis (48.92/73.53, men/women) and primary biliary cirrhosis (38.03/54.48). GBC was increased after six autoimmune diseases, with high SIRs for ulcerative colitis (12.22/3.24) and men with Crohn disease (9.16). These autoimmune diseases were also associated with a high risk of iCCA, which had seven other associations, and eCCA, which had five other associations. Ampullary cancer occurrence was increased after four autoimmune diseases. Conclusion: An autoimmune disease is a common precursor condition for hepatobiliary cancers. This calls for careful control of autoimmune disease symptoms in each patient and encouragement to practice a healthy lifestyle.
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3.
  • Liu, Xiangdong, et al. (författare)
  • The impact of type 2 diabetes mellitus on cancer-specific survival: A follow-up study in sweden.
  • 2012
  • Ingår i: Cancer. - : Wiley. - 1097-0142 .- 0008-543X. ; 118:5, s. 1353-1361
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Earlier studies have suggested that type 2 diabetes mellitus (T2DM) alters the risk of developing a variety of cancers, but little has been known about the impact of T2DM on cancer prognosis. On the basis of nationwide population-based Swedish registries, the authors of this report compared the cause-specific survival among cancer patients with and without T2DM. METHODS: Patients with T2DM were identified from the nationwide Swedish Hospital Discharge Register, and cancers were recorded from the Swedish Cancer Registry. Hazard ratios (HRs) were calculated using Cox regression models to compare variations in cause-specific survival between cancer patients with and without T2DM. RESULTS: Of the 1016,105 cancer patients, 16,123 had been hospitalized with T2DM before their diagnosis of cancer. The mortality rate was significantly higher among cancer patients with T2DM than among those without T2DM (cause-specific HR, 1.38; 95% confidence interval, 1.35-1.41). There were no differences in TNM stage distribution among cancer patients with or without T2DM for the main cancers, with an exception of tumor and metastatic classifications for breast cancer and prostate cancer, respectively. CONCLUSIONS: The current results indicated that patients with T2DM who are diagnosed with a subsequent cancer are at an increased risk for cause-specific mortality compared with patients who have cancer without T2DM.
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4.
  • Mukama, Trasias, et al. (författare)
  • Familial risk of breast cancer by dynamic, accumulative, and static definitions of family history
  • 2020
  • Ingår i: Cancer. - : Wiley. - 0008-543X .- 1097-0142. ; 126:12, s. 2837-2848
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Familial breast cancer risk studies usually overlook the dynamic nature of family history. Methods: The authors assessed the effect of incorporating the timing of cancer diagnosis events into the assessment of familial risks of breast cancer in first-degree and second-degree relatives in a nationwide cohort study of 5,099,172 women (follow-up was between 1958-2015). Family history was assessed using 3 approaches: 1) as a static variable (ever having a relative with breast cancer); 2) as accumulative history; and 3) as a dynamic variable (time-dependent variable). Results: For women aged <50 years, familial risk was mostly higher when family history was assessed as a dynamic variable compared with using a static or accumulative family history. For example, the cumulative risk of receiving a breast cancer diagnosis until age 50 years for women with a history of breast cancer in 1 first-degree relative was 2.6% (95% CI, 2.5%-2.7%) using the static method, 2.4% (95% CI, 2.3%-2.4%) using the accumulative method, and 3.1% (95% CI, 3.0%-3.2%) using the dynamic method. Relative risk in women aged <50 years with a breast cancer diagnosis in a sister was 1.40-fold (95% CI, 1.31-fold to 1.48-fold) using the static method, 1.66-fold (95% CI, 1.57-fold to 1.76-fold) using the accumulative method, and 2.28-fold (95% CI, 2.07-fold to 2.51-fold) using the dynamic method. Conclusions: The results of the current study demonstrated that assessing family history as static, accumulative, or dynamic results in different familial risk estimates. The answer as to which method to use for family history assessment depends on the implications of the study, with the dynamic method appearing to be better suited for risk stratification studies, the accumulative method being the most convenient in practice and the least favored for risk prediction, and the static method being suitable for etiological impact and risk attribution studies.
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5.
  • Mukama, Trasias, et al. (författare)
  • Risk-adapted starting age of breast cancer screening in women with a family history of ovarian or other cancers : A nationwide cohort study
  • 2021
  • Ingår i: Cancer. - : Wiley. - 0008-543X .- 1097-0142. ; 127:12, s. 2091-2098
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: There is a lack of evidence-based recommendations for the age at which women with a family history of cancers other than breast cancer should start breast cancer screening. METHODS: Using Swedish family cancer data sets, the authors conducted a nationwide cohort study including 5,099,172 Swedish women born after 1931 (follow-up, 1958-2015). Accounting for calendar time, they calculated the relative risk of breast cancer for women with a family history of a discordant cancer in 1 first-degree relative. Furthermore, the authors used 10-year cumulative risk to determine the ages at which women with a family history of discordant cancer reached risk thresholds at which women in the general population were recommended to start breast cancer screening. RESULTS: A family history of cancer at 15 sites was associated with an increased risk of breast cancer. Among women younger than 50 years, the highest risk of breast cancer was observed for those with a family history of ovarian cancer (standardized incidence ratio, 1.44; 95% confidence interval, 1.26-1.64). In these women, the risk of breast cancer associated with a family history at other cancer sites ranged from 1.08-fold for prostate cancer to 1.18-fold for liver cancer. When breast cancer screening was recommended to be started at the age of 50 years for the general population, women with 1 first-degree relative with ovarian cancer attained the threshold risk for screening at the age of 46 years. Women with a family history of other discordant cancers did not reach the risk thresholds for screening at younger ages. CONCLUSIONS: Many cancers showed familial associations with breast cancer, but women with a family history of these cancers (except for ovarian cancer) did not reach risk thresholds for screening at younger ages.
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6.
  • Xu, Xing, et al. (författare)
  • Risk of invasive prostate cancer and prostate cancer death in relatives of patients with prostatic borderline or in situ neoplasia : A nationwide cohort study
  • 2020
  • Ingår i: Cancer. - : Wiley. - 1097-0142 .- 0008-543X. ; 126:19, s. 4371-4378
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The question of whether having a family history of prostatic borderline or in situ neoplasia (PBISN) is associated with an increased risk of invasive prostate cancer (PCa) or death from PCa remains unanswered. The objective of the current study was to provide an evidence-based risk estimation for the relatives of patients with PBISN.METHODS: Nationwide Swedish family cancer data sets were used for the current study, including data regarding all residents of Sweden who were born after 1931 and their parents. Standardized incidence ratios (SIRs), standardized mortality ratios (SMRs), and lifetime cumulative risks of PCa were calculated for men with different constellations of family history. Family history was defined as a dynamic (time-dependent) variable considering changes during follow-up (1958-2015).RESULTS: Of the 6,343,727 men in the current study, a total of 238,961 developed invasive PCa and 5756 were diagnosed with PBISN during the follow-up. Men with 1 first-degree relative who was diagnosed with PBISN had a 70% increased risk of invasive PCa (SIR, 1.7; 95% confidence interval, 1.5-1.9) and PCa death (SMR, 1.7; 95% confidence interval, 1.3-2.2) compared with men with no family history of PBISN or invasive PCa. These were rather close to estimates in men with 1 first-degree relative diagnosed with invasive PCa (SIR, 2.1 and SMR, 1.8). A higher risk of PCa in family members was found among patients with a family history of PBISN and/or PCa diagnosed before age 60 years. The results in terms of cumulative risk resembled this trend.CONCLUSIONS: A family history of PBISN appears to be as important as a family history of invasive PCa with regard to an increased risk of invasive PCa or PCa mortality. Such a history should not be overlooked in PCa screening recommendations or in future research regarding familial PCa.
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