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Plasma Leptin Is Not Associated with Prostate Cancer Risk¹

Department of Urology and Andrology [P. S.], Oncological Center [R. J.], and Department of Public Health and Clinical Medicine [S. S., T. O.] Umeå University Hospital, 901 85 Umeå, Sweden; International Agency for Research on Cancer, Lyon, France [R. K.]; Institute of Clinical Biochemistry, Rikshospitalet, Oslo, Norway [R. G., E. J.]; and Department of Clinical Chemistry, Helsinki University Central Hospital, Helsinki, Finland [H. A., U-H. S.]

	Introduction

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Leptin, the adipocyte-produced hormone, has been shown to induce angiogenesis and proliferation in several tissues, and leptin receptors have been demonstrated in the prostate (1 , 2) . Circulating levels of leptin are strongly related to the amount of adipose tissue and androgenicity (1 , 3) . We hypothesized that leptin may provide a link between a Western lifestyle often resulting in excess weight, and prostate cancer. In a previous prospective study in The Northern Sweden Health and Disease Cohort, we found a significantly increased risk of prostate cancer up to a relative risk of 2.4 for intermediately elevated levels of plasma leptin (2) . The aim of the present study was to investigate the consistency of our previous finding in a different study population while taking putative hormonal confounders into consideration.

	Materials and Methods

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In a longitudinal study, we used prediagnostic serum samples from 200 cases of prostate cancer and 397 controls in the Janus Project in Norway, for which the procedure for recruitment and blood collection have been described in detail previously (4) . Cases, diagnosed at the earliest 3 months after blood collection, were identified through linkage with the Cancer Registry. Two controls were randomly selected from sets matched to the index case on age (± 1 year) and date (± 6 months) at blood sampling and on county. The study was approved by the Research Ethics Committee of Umeå University Hospital.

Leptin was determined with a double antibody radioimmunoassay (Linco Res., St. Louis, MO). Intrabatch coefficients of variation were between 3–5%, and interassay coefficient of variation was 6–12%. Testosterone and estradiol were quantitated by a time-resolved fluoroimmunoassay (DELFIA; Wallac, Turku, Finland). SHBG³ was quantitated by fluoroimmunoassay (AutoDELFIA; Wallac, Turku, Finland). Samples of matched subjects were analyzed in the same batch, without knowledge of the case-control status.

The relation between the hormones was evaluated by the Pearson correlation analysis. Conditional logistic regression analysis was used to estimate the odds ratios and 95% CIs. Calculations were made with the software SPSS (Chicago, IL). With 200 cases and 400 controls, there is 0.80 power (at a significance level of 0.05) to detect a mean difference in exposure corresponding to an expected odds ratio of disease of 1.84 between the top and bottom quartiles (assuming normal exposure distributions, rare disease, and a loglinear relationship of exposure to disease risk).

	Results

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The mean age of the subjects at blood collection was 49 years (SD, 7.3), and the mean time between blood collection and diagnosis was 17 years (SD, 5.5). There were weak but significant correlations between leptin and testosterone (r = -0.11; P = 0.007), and SHBG (r = -0.09; P = 0.02) but not to estradiol (r = -0.05; P = 0.2). No significant association between plasma leptin levels and prostate cancer risk was found, either in the whole study group or in strata of age or follow-up time (Table 1) . Adjustments for testosterone, estradiol, and SHBG, separately or combined, did not affect the odds ratio estimates.

	Discussion

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	Acknowledgments

 
The Janus Serum bank owned by The Norwegian Cancer Society provided the serum samples. We thank Karin Hjertkvist for technical assistance.

	Footnotes

 
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This study was supported by grants from The Nordic Cancer Union, The Swedish Cancer Society, and The Lions Research Foundation, Umeå, Sweden.

² To whom requests for reprints should be addressed, at Department of Urology, Umeå University Hospital, 901 85 Umeå, Sweden. Fax: 46-90-12-53-96; E-mail: par.stattin{at}urologi.umu.se

³ The abbreviations used are: SHBG, sex hormone-binding globulin; CI, confidence interval.

Received 10/18/02; revised 1/16/03; accepted 2/11/03.

	References

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3. Söderberg S., Olsson T., Eliasson M., Johnson O., Brismar K., Carlström K., Ahren B. A strong association between biologically active testosterone and leptin in non-obese men and women is lost with increasing (central) adiposity. Int. J. Obes. Relat. Metab. Disord., 25: 98-105, 2001.[Medline]
4. Stattin P., Adlercreutz H., Tenkanen L., Jellum E., Lumme S., Hallmans G., Harvei S., Teppo L., Stumpf K., Luostarinen T., Lehtinen M., Dillner J., Hakama M. Circulating enterolactone and prostate cancer risk: a Nordic nested case-control study. Int. J. Cancer, 99: 124-129, 2002.[Medline]
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