-transparent.png){kind=logo}
A Western lifestyle has been implicated in the pathogenesis of prostate cancer. However, no clear association between obesity and prostate cancer has been shown. Leptin may stimulate prostate growth and angiogenesis, and receptors for leptin are present in the prostate. Leptin may, thus, be associated with increased risk of prostate cancer. One hundred forty-nine men with prostate cancer were identified (together with 298 matched referents) who, before diagnosis, had participated in population-based health surveys in Northern Sweden. Blood pressure, body mass index, and use of tobacco were recorded. Leptin, insulin, insulin-like growth factor I (IGF-I), IGF-I-binding proteins 1-3, testosterone, and sex hormone-binding globulin were analyzed in stored samples. Their influences on prostate cancer were estimated by conditional logistic regression analysis. Prostate cancer specimens were investigated for immunoreactivity for the leptin receptor. Relative risk (95% confidence intervals) estimates of prostate cancer over the quintiles of leptin were 1.0, 2.1 (1.1-4.1), 2.6 (1.4-4.8), 1.4 (0.7-2.7), and 1.6 (0.8-3.2). Adjustments for metabolic variables, testosterone, and IGF-I and its binding proteins did not attenuate this increased risk. Immunoreactivity for the leptin receptor was detected in normal, high-grade prostatic intraepithelial neoplasia lesions and malignant prostatic epithelium. Moderately elevated plasma leptin concentrations are associated with later development of prostate cancer. This may be due to direct effects of leptin on prostatic intraepithelial neoplasia lesions, or to indirect actions through other mechanisms. A critical fat mass related to an interior milieu favorable for prostate cancer development seems to exist, because intermediate but not high leptin levels are related to prostate cancer risk.
P Stattin, and
S Söderberg, and
G Hallmans, and
A Bylund, and
R Kaaks, and
U H Stenman, and
A Bergh, and
T Olsson
January 2005,
Oncology,
P Stattin, and
S Söderberg, and
G Hallmans, and
A Bylund, and
R Kaaks, and
U H Stenman, and
A Bergh, and
T Olsson
November 2003,
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology,
P Stattin, and
S Söderberg, and
G Hallmans, and
A Bylund, and
R Kaaks, and
U H Stenman, and
A Bergh, and
T Olsson
January 2015,
Journal of occupational and environmental medicine,
P Stattin, and
S Söderberg, and
G Hallmans, and
A Bylund, and
R Kaaks, and
U H Stenman, and
A Bergh, and
T Olsson
May 2008,
International journal of cancer,
P Stattin, and
S Söderberg, and
G Hallmans, and
A Bylund, and
R Kaaks, and
U H Stenman, and
A Bergh, and
T Olsson
April 2006,
Journal of occupational and environmental medicine,
P Stattin, and
S Söderberg, and
G Hallmans, and
A Bylund, and
R Kaaks, and
U H Stenman, and
A Bergh, and
T Olsson
June 2003,
Occupational and environmental medicine,
P Stattin, and
S Söderberg, and
G Hallmans, and
A Bylund, and
R Kaaks, and
U H Stenman, and
A Bergh, and
T Olsson
January 2008,
Prostate cancer and prostatic diseases,
P Stattin, and
S Söderberg, and
G Hallmans, and
A Bylund, and
R Kaaks, and
U H Stenman, and
A Bergh, and
T Olsson
October 2010,
Cancer causes & control : CCC,
P Stattin, and
S Söderberg, and
G Hallmans, and
A Bylund, and
R Kaaks, and
U H Stenman, and
A Bergh, and
T Olsson
December 2012,
BMC pediatrics,
P Stattin, and
S Söderberg, and
G Hallmans, and
A Bylund, and
R Kaaks, and
U H Stenman, and
A Bergh, and
T Olsson
September 2016,
Cancer causes & control : CCC,
