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1.
  • Wolk, A., et al. (författare)
  • Nutrition and renal cell cancer
  • 1996
  • Ingår i: Cancer Causes and Control. - London, United Kingdom : Rapid Science Publisher. - 0957-5243. - 0957-5243 (Print) 0957-5243 (Linking) ; 7:1, s. 5-18
  • Tidskriftsartikel (refereegranskat)abstract
    • Epidemiologic evidence on the relation between nutrition and renal cell cancer is reviewed. Kidney cancer, comprising 1.7 percent of all malignant diseases diagnosed worldwide, shows about a 20-fold international variation in the incidence in men and 10-fold in women. This substantial variation indicates an important causal role of environmental factors. Renal cell (parenchymal) cancer (RCC) accounts for about 80 percent of all kidney cancers. While the etiology of RCC is incompletely understood, analytic epidemiologic studies provide consistent support for a positive association of obesity with risk of RCC; the dose-response observed supports a causal relationship. Only a few prospective studies, all of them limited in size, have been published, while ecologic and case-control studies suggest that diet may be important in the etiology of RCC. However, contradictory results and methodologic limitations in some case-control studies prevent definite conclusions concerning diet and RCC. A positive association of protein and fat intake, as well as their main food sources (meat, milk, fats), with risk of RCC-as suggested by ecologic studies-has no clear support in analytic epidemiologic studies. A protective effect of vegetables and fruits has been observed in most case-control studies, while the majority do not show an association between alcohol, coffee, and risk of RCC. Recent reports indicated an increased risk of RCC associated with consumption of fried/sauteed meat and low intakes of magnesium or vitamin E. An apparent positive association with total energy intake, perhaps due to bias, needs further investigation.
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  • Adami, Johanna, et al. (författare)
  • Smoking and the risk of leukemia, lymphoma, and multiple myeloma (Sweden)
  • 1998
  • Ingår i: Cancer Causes and Control. - 0957-5243 .- 1573-7225. ; 9:1, s. 49-56
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>While several epidemiologic studies have indicated a link between smoking and the risk of developing hematolymphoproliferative cancers (chiefly leukemias, lymphomas, and multiple myelomas), in particular myeloid leukemia, the role of tobacco in the etiology of these neoplasms remains unclear. To evaluate the potential impact of tobacco use on development of leukemia, lymphoma, and multiple myeloma, we conducted a cohort study of 334,957 Swedish construction workers using prospectively collected exposure-information with complete long-term follow-up. A total of 1,322 incident neoplasms occurred during the study period, 1971-91. We found no significant association between smoking status, number of cigarettes smoked, or duration of smoking and the risk of developing leukemias, lymphomas, or multiple myeloma. There was a suggestion of a positive association between smoking and the risk of developing Hodgkin's disease, although the rate ratios were not significantly elevated, except for young current smokers. No positive dose-risk trends emerged. Our study provides no evidence that smoking bears any major relationship to the occurrence of leukemias, non-Hodgkin's lymphomas, or multiple myeloma.</p>
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  • Alexeyev, Oleg, et al. (författare)
  • Association between the presence of bacterial 16S RNA in prostate specimens taken during transurethral resection of prostate and subsequent risk of prostate cancer (Sweden)
  • 2006
  • Ingår i: Cancer Causes and Control. - Dordrecht : Kluwer Academic Publishers. - 0957-5243 .- 1573-7225. ; 17:9, s. 1127-1133
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>Objective</strong>: To study bacterial 16S RNA in archival prostate samples from 352 patients with benign prostate hyperplasia (BPH) and evaluate whether the presence of bacterial DNA was different in those who later developed prostate cancer (<em>n</em> = 171) and in the matched controls that did not progress to cancer (<em>n</em> = 181).</p><p><strong>Methods</strong>: 16S DNA PCR followed by cloning and sequencing the positive samples.</p><p><strong>Results</strong>: In 96/352 (27%) of the prostate tissue specimens 16S RNA were detected. Sequence analysis revealed <em>Propionibacterium acnes</em> as the predominant microorganism (23% of 16S RNA positive patients). The second most frequent isolate—<em>Escherichia coli</em> was found in 12 (12%) patients. The other isolates included <em>Pseudomonas</em> sp. (3 patients), <em>Actinomyces</em> sp. (2), <em>Streptococcus mutans</em> (1), <em>Corynebacterium</em> sp. (2),<em>Nocardioides</em> sp. (1), <em>Rhodococcus</em> sp. (1) <em>Veillonella</em> sp. (2). In <em>P. acnes</em> positive samples 62% exhibited severe histological inflammation versus 50% in the bacteria-negative group (<em>p</em> = 0.602). The presence of <em>P. acnes</em> in the prostate was associated with prostate cancer development (OR 2.17, 95% CI 0.77–6.95).</p><p><strong>Conclusions</strong>: This study has revealed <em>P. acnes</em> as the most common bacteria in the prostate in BPH. Further studies are needed to clarify its role in contributing to the development of prostatic inflammation and prostate cancer.</p>
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  • Almquist, Martin, et al. (författare)
  • Metabolic factors and risk of thyroid cancer in the Metabolic syndrome and Cancer project (Me-Can)
  • 2011
  • Ingår i: Cancer Causes and Control. - Springer. - 0957-5243 .- 1573-7225. ; 22:5, s. 743-751
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Objective  To investigate metabolic factors and their possible impact on risk of thyroid cancer. Methods  A prospective cohort study was conducted based on seven population-based cohorts in Norway, Austria, and Sweden, in the Metabolic syndrome and Cancer project (Me-Can). Altogether 578,700 men and women with a mean age of 44.0 years at baseline were followed for on average 12.0 years. Relative risk of incident thyroid cancer was assessed by levels of BMI, blood pressure, and blood levels of glucose, cholesterol, triglycerides, and by a combined metabolic syndrome (MetS) score. Risk estimates were investigated for quintiles, and a <em>z</em> score distribution of exposures was analyzed using Cox proportional hazards regression. Results  During follow-up, 255 women and 133 men were diagnosed with thyroid cancer. In women, there was an inverse association between glucose and thyroid cancer risk, with adjusted RR: 95% CI was 0.61 (0.41–0.90), <em>p</em> trend = 0.02 in the fifth versus the first quintile, and a positive association between BMI and thyroid cancer risk with a significant trend over quintiles. There was no association between the other metabolic factors, single or combined (Met-S), and thyroid cancer. Conclusion  In women, BMI was positively, while blood glucose levels were inversely, associated with thyroid cancer.</p>
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10.
  • Andersson, Ulrika, et al. (författare)
  • The association between longer relative leukocyte telomere length and risk of glioma is independent of the potentially confounding factors allergy, BMI, and smoking
  • 2019
  • Ingår i: Cancer Causes and Control. - Springer. - 0957-5243 .- 1573-7225. ; 30:2, s. 177-185
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Purpose: Previous studies have suggested an association between relative leukocyte telomere length (rLTL) and glioma risk. This association may be influenced by several factors, including allergies, BMI, and smoking. Previous studies have shown that individuals with asthma and allergy have shortened relative telomere length, and decreased risk of glioma. Though, the details and the interplay between rLTL, asthma and allergies, and glioma molecular phenotype is largely unknown. Methods: rLTL was measured by qPCR in a Swedish population-based glioma case–control cohort (421 cases and 671 controls). rLTL was related to glioma risk and health parameters associated with asthma and allergy, as well as molecular events in glioma including IDH1 mutation, 1p/19q co-deletion, and EGFR amplification. Results: Longer rLTL was associated with increased risk of glioma (OR = 1.16; 95% CI 1.02–1.31). Similar to previous reports, there was an inverse association between allergy and glioma risk. Specific, allergy symptoms including watery eyes was most strongly associated with glioma risk. High body mass index (BMI) a year prior diagnosis was significantly protective against glioma in our population. Adjusting for allergy, asthma, BMI, and smoking did not markedly change the association between longer rLTL and glioma risk. rLTL among cases was not associated with IDH1 mutation, 1p/19q co-deletion, or EGFR amplification, after adjusting for age at diagnosis and sex. Conclusions: In this Swedish glioma case–control cohort, we identified that long rLTL increases the risk of glioma, an association not confounded by allergy, BMI, or smoking. This highlights the complex interplay of the immune system, rLTL and cancer risk.</p>
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