Non-Hodgkin's lymphoma affecting the stomach, but not other sites, is associated with previous H. pylori infection. A causative role for the organism is plausible, but remains unproved.

HPV-16 infection may be a risk factor for squamous-cell carcinoma of the head and neck.

Key words: prostate cancer; 25(OH)-vitamin D 3 ; serum bankVitamin D deficiency has been implicated as risk factor for prostate cancer. 1 In cell culture studies, vitamin D metabolites have had protective action against cancer development (for review see Ylikomi et al. 2 ). Normal and malignant prostate cells contain vitamin D receptor (VDR), 3-5 which mediates the antiproliferative action of 1,25(OH) 2 -vitamin D 3 . 6 In addition to the antiproliferative action of 1,25(OH) 2 -vitamin D 3 , it can cause apoptosis, 7 induce differentiation, 8 inhibit telomerase expression, 9 inhibit tumor cell invasiveness 10 and suppress tumor-induced angiogenesis. 11 Several epidemiologic studies have reported that high serum vitamin D levels or sunlight may protect against prostate cancer. 3,4,[12][13][14][15] Factors that affect prostate cancer include age, dark skin and environment, e.g., latitude and diet. 16 These factors might be linked to vitamin D availability. 17,18 Furthermore, high fish (rich in vitamin D) consumption appears to correlate with lower prostate cancer risk. 19 In addition, VDR gene polymorphism may contribute to the risk of prostate cancer. 20 -24 There is also a study showing no correlation between serum vitamin D metabolites and prostate cancer in Maryland (USA), 25 but the authors concluded that the power of their study was limited. In another study on U.S. male physicians, only a weak protection against prostate cancer was found with the highest quartile of serum 1␣,25(OH) 2 -vitamin D 3 . 26 Similarly, no correlation was found in Hawaii. 27 There are 2 physiologically interesting metabolites of vitamin D, 1␣,25(OH) 2 -vitamin D 3 , regulating calcium homeostasis for bones and muscles in extremely narrow limits, and 25(OH)-vitamin D 3 , regulating target (prostate) cell proliferation and differentiation through activation to 1␣,25(OH) 2 -vitamin D 3 in the target (prostate) cell. Serum 25(OH)-vitamin D 3 is produced by liver 25-hydroxylase, the rate of the synthesis being directly proportional to vitamin D 3 serum concentration. 28 Therefore, serum 25(OH)-vitamin D 3 reflects vitamin D availability in the organism. Serum concentration of 25(OH)-vitamin D 3 is so high that it might possess a significant biologic activity in target cells, but it is also a precursor for the biologically more active 1␣,25(OH) 2 -vitamin D 3 . Prostate as well as many other target organs can activate 25(OH)-vitamin D 3 through 1␣-hydroxylation 29,30 and inactivate it through 24-hydroxylation. 31 In an epidemiologic study, we found that low concentrations (Ͻ40 nmol/l) of 25(OH)-vitamin D in serum were associated with a 1.7-fold increased risk of prostate cancer. 3,4 Since the power of our study was limited, preventing extensive analysis of the data, and we are partners in the Nordic Specimen Banks for Cancer Causes and Control, we had an opportunity to extend our study to other Scandinavian countries located geographically at the same latitude. Our aim was to determine whether our finding could be replicated in a la...

Obesity, a risk factor for colorectal cancer, is associated with elevated serum levels of leptin, the adipocyte-derived hormone, and insulin. Experimental and epidemiologic studies have indicated a role for insulin in the pathogenesis of colon cancer, and recent experimental studies have suggested a similar role for leptin. In a case-control study nested in the Janus Biobank, Norway, we measured serum levels of leptin and C-peptide (a marker of pancreatic insulin secretion) in cryopreserved prediagnostic sera from men (median age, 45 years) who were diagnosed with cancer of the colon (n ‫؍‬ 235) or rectum (n ‫؍‬ 143) after blood collection (median time, 17 years), and among 378 controls matched for age and date of blood collection. Obesity, a consequence of a positive energy balance caused by high intake of an energy-dense diet and a sedentary lifestyle, is a risk factor for colorectal cancer. 1,2 The association has been stronger and more consistent for men than for women as demonstrated in a recent metaanalysis, 1 although the association may be of similar magnitude in premenopausal women as for men. 3,4 Obesityinduced changes in hormonal metabolism may be a link to cancer risk. 1 Circulating levels of insulin are increased in obesity, and insulin has been postulated to be such a link. 5 The anabolic signals of insulin can promote tumor development by inhibiting apoptosis and by stimulating cell proliferation. 6 In contrast, data from epidemiologic studies are limited and only 2 prospective studies to date have shown an association between insulin exposure and colon cancer risk, 7,8 while another prospective study found no significant association. 9 The adipose tissue is an important endocrine organ, in which several hormones are produced, among them leptin. 10 Circulating leptin levels are closely related to the percentage and amount of adipose tissue (correlations of body mass index, BMI, with circulating levels ranging from 0.5 to 0.8) and leptin is also related to other factors in the metabolic syndrome, including insulin resistance and serum insulin levels. Leptin conveys information to the brain about the size of energy stores and leptin levels are increased by overfeeding. Energy restriction, a well-established protective factor against cancer, 11 decreases leptin levels. 11,12 Leptin is also involved in regulation of blood pressure, angiogenesis and wound healing. 12,13 In recent experimental studies, leptin stimulated growth of colon cancer cells. 14 -16 In view of these data, we hypothesized that leptin is a link between obesity and colon cancer. We describe the results from a nested case-control study on the association of prediagnostic serum levels of leptin and C-peptide with cancers of the colon and the rectum. MATERIAL AND METHODSThe Janus Project in Norway was started in 1973 and contains blood samples from about 600,000 subjects. The samples have been collected from men who participated in county health examinations, mostly for cardiovascular diseases, and from blood donors. The participants ...

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