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Articles by K. Hemminki
Total Records ( 3 ) for K. Hemminki
  J Ji , X Shu , X Li , K Sundquist , J Sundquist and K. Hemminki

Background: Sarcoidosis patients show dysregulated immune function, which may be related to subsequent cancer. We examined here the overall and specific cancer risks among Swedish subjects who had been hospitalized for sarcoidosis.

Methods: A sarcoidosis research database was created by identifying hospitalized sarcoidosis patients from the Swedish Hospital Discharge Register and by linking them with the Cancer Registry. Standardized incidence ratios (SIRs) were calculated for cancers in sarcoidosis patients compared with subjects without sarcoidosis.

Results: A total of 10 037 patients were hospitalized for sarcoidosis during years 1964–2004. Among them 1045 patients developed subsequent cancer, giving an overall SIR of 1.40 and 1.18 for cancer diagnosed later than 1 year of follow-up. A significant excess was noted for skin (squamous cell), kidney and nonthyroid endocrine tumors and additionally for non-Hodgkin's lymphoma and leukemia. Patients with multiple hospitalizations showed high risks.

Conclusions: A 40% overall excess incidence of cancer was noted among sarcoidosis patients, but the increase was confined mainly to the first year after hospitalization. However, the increased risks of skin cancer and non-Hodgkin's lymphoma and leukemia, especially for those with multiple hospitalizations or hospitalized at old age, call for clinical attention.

  P Vodicka , Z Polivkova , S Sytarova , H Demova , M Kucerova , L Vodickova , V Polakova , A Naccarati , Z Smerhovsky , M Ambrus , M Cerna and K. Hemminki

Background: The majority of human cancers arise from cells unable to maintain genomic stability. Recent prospective studies indicated that enhanced chromosomal aberrations (CAs) frequencies are predictive of gastrointestinal and lung cancers. However, studies on incident cancer patients are lacking; thus, we investigated chromosomal damage in newly diagnosed cancer patients and healthy individuals. Methods: We analyzed chromosomal damage in peripheral blood lymphocytes in a group of 300 incident cancer patients (with different malignancies) in comparison with 300 healthy controls. Results and Conclusions: The frequencies of aberrant cells (ACs) and CAs were significantly higher in patients (2.38 ± 1.56 and 2.53 ± 1.69, respectively) as compared with controls (1.81 ± 1.31 and 1.94 ± 1.47, respectively, P < 0.01). The percentual difference in chromatid-type aberrations (CTAs) between patients and controls was moderately significant (1.37 ± 1.20 and 1.11 ± 0.99, respectively, P ≤ 0.05), whereas the difference in chromosome-type aberrations (CSAs) was stronger (1.16 ± 1.24 versus 0.83 ± 1.12, P < 0.01). Using binomial logistic regression, the estimated odds ratios and 95% confidence interval for ACs were 1.33 (1.18–1.49), P < 0.01; for CAs, 1.27 (1.14–1.41), P < 0.01; for CTA 1.24 (1.07–1.44), P < 0.01 and for CSA, 1.27 (1.10–1.47), P < 0.01. By stratifying patients for distinct neoplasia, markers of chromosomal damage were significantly enhanced in patients with breast, prostate and head/neck cancers, whereas no effect was recorded in patients affected by gastrointestinal cancers. The present study shows for the first time evidence of increased chromosomal damage in lymphocytes of incident cancer patients compared with healthy controls. The effects were observed in different cancer types but as the number of patients was relatively small, further studies are warranted.

  X. Shu , J. Ji , X. Li , J. Sundquist , K. Sundquist and K. Hemminki
  Aims Type 1 diabetes mellitus (T1DM) is an autoimmune disease with potential mechanistic links to immune-related cancers. We aimed at examining the overall and specific cancer risks among hospitalized T1DM patients from the national registers in Sweden.
Methods A T1DM research cohort was created by identifying T1DM patients from the Hospital Discharge Register and linking them with the Cancer Registry. Standardized incidence ratios (SIRs) for subsequent cancers were calculated among patients with T1DM compared with those without T1DM.
Results Two hundred and fifty-eight cases were ascertained with subsequent cancers during the follow-up duration from 1964 to 2006, with an increased overall SIR of 1.17 (95% CI 1.04–1.33) among 24 052 T1DM patients identified at baseline. Significant excess was noted for gastric and skin (squamous cell carcinoma) cancers and for leukaemia. Increased risk of acute lymphatic leukaemia accounted for most of the variation of leukaemia risk (SIR = 5.31, 95% CI 3.32–8.05). Cancer risk varied with sex, age at first hospitalization and numbers of hospitalizations. The risk was higher in women compared with men and in those hospitalized for T1DM at age over 10 years compared with the younger patients. Higher risks were also found among those with more hospital visits.
Conclusion By quantifying the variations of overall and site-specific cancer risks after T1DM, the current study provides novel associations between T1DM and subsequent cancers, the mechanisms of which remain to be established.
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