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Lactase persistence, dietary intake of milk, and the risk for prostate cancer in Sweden and Finland
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2007 (engelsk)Inngår i: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 16, nr 5, s. 956-961Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Prostate carcinoma is the most common cancer in men. Its primary pathogenesis is mostly unknown. Dairy products containing lactose have been suggested to be risk factors for prostate cancer. Digestion of lactose is dependent on lactase activity in the intestinal wall. A single nucleotide polymorphism C to T residing 13,910 bp upstream of the lactase gene has been shown to associate with the developmental down-regulation of lactase activity underlying persistence/nonpersistence trait. To find out whether lactase persistence is related to the risk for prostate cancer, we genotyped 1,229 Finnish and 2,924 Swedish patients and their 473 Finnish and 1,842 Swedish controls using solid-phase minisequencing. To explore if dairy products have an association with prostate cancer, we analyzed the milk consumption in the Swedish study consisting of 1,499 prostate cancer patients and 1,130 controls (Cancer Prostate in Sweden I study) using a questionnaire. Only the consumption of low-fat milk was found to be associated with increased risk of prostate cancer [odds ratio (OR), 1.73; 95% confidence interval (95% CI), 1.162.391. A statistically significantly higher (P < 0.01) lactose intake was observed among subjects with high lactase activity (C/T and T/T genotypes) compared with those with low lactase activity (C/C genotype). Lactase persistence did not associate with increased risk for prostate carcinoma in the Finnish (OR, 1.11; 95% CI, 0.83-1.47, P = 0.488) or in the Swedish populations (OR, 1.16; 95% CI, 0.91-1.46; P = 0.23). In conclusion, lactase persistence/nonpersistence contains no risk for prostate cancer. Analysis of different milk products showed some evidence for low-fat milk as a potential risk factor for prostate cancer.

sted, utgiver, år, opplag, sider
Univ Helsinki, Dept Med Genet, Helsinki 00251, Finland. Univ Helsinki, Cent Hosp, Mol Genet Lab, FIN-00014 Helsinki, Finland. Karolinska Inst, Dept Med Epidemiol & Biostat, S-10401 Stockholm, Sweden. Tampere Univ Hosp, Res Unit, FIN-33521 Tampere, Finland. Tampere Univ Hosp, Dept Clin Chem, FIN-33521 Tampere, Finland. Tampere Univ Hosp, Inst Med Technol, Canc Genet Lab, FIN-33521 Tampere, Finland. Tampere Univ Hosp, Dept Urol, FIN-33521 Tampere, Finland. Univ Tampere, Sch Med, FIN-33101 Tampere, Finland. Univ Milan, Dept Stat, I-20122 Milan, Italy. Univ Umea Hosp, Dept Surg & Perioperat Sci Urol & Androl, S-90185 Umea, Sweden.: AMER ASSOC CANCER RESEARCH , 2007. Vol. 16, nr 5, s. 956-961
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URN: urn:nbn:se:mdh:diva-40711DOI: 10.1158/1055-9965.EPI-06-0985ISI: 000246649200019PubMedID: 17507622OAI: oai:DiVA.org:mdh-40711DiVA, id: diva2:1246074
Tilgjengelig fra: 2018-09-06 Laget: 2018-09-06 Sist oppdatert: 2018-09-06bibliografisk kontrollert

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