Der Einfluss von Risikofaktoren auf die Entstehung und das Verhalten von Prostatakarzinomen

The factors that determine the risk of developing clinical prostate cancer are not well known; however, a few have been identified. The frequency of autopsy-detected cancers is roughly the same in different parts of the world. This finding is in sharp contrast with the incidence of clinical prostate cancer, which differs widely between different geographical areas, being high in the USA and Northern Europe and low in Southeast Asia. However, if Japanese men move from Japan to Hawaii, their risk of prostate cancer increases, and if they move to California their risk increases even more and approaches that of American men. These findings indicate that exogenous factors affect the risk of progression from so-called latent prostate cancer to clinical prostate cancer. Factors such as food consumption, pattern of sexual behaviour, alcohol consumption, exposure to ultraviolet radiation and occupational exposure have all been discussed as being of aetiological importance. However, there are some controversial discussions about the contribution of various identified risk factors such as obesity, diabetes mellitus, nicotine consumption, and intake of NSAID to prostate cancer development. The assumption substantiates that exogenic factors such as obesity and resulting changes of the metabolism like hyperinsulinaemia and diabetes mellitus as well as consumption of nicotine has an influence. These factors have already been proven for other hormone dependent tumors like endometrium cancer, colorectal or mammary cancer [10,13,44,105,112,119]. The aim of the present scientific work was to validate the contribution of various individual risk factors to the development of prostate cancer and the biological aggressiveness of prostate cancer by comparing patients with prostate cancer to an age-matched control group of men without cancer deriving from 2 single institutions only. The identification of risk factors might help to establish effective strategies for prostate cancer prevention. With regard to the BMI-groups there was no correlation between BMI and stage of prostate cancer (p=0.860) even regardless the BMI-groups (p=0.127) there was no correlation between both quantities. The fact that no patient in the group with prostate cancer has a BMI>40 should be taken into account. The same result was identified with regard to the presence of lymph node metastases and the Gleason-Score correlating the tumor aggressiveness. With regard to the BMI with and without a distribution in groups there was no association to a participation of lymph nodes (p=0.118) or an increased Gleason-Score (p=0.084). A promoting influence of the consumption of nicotine on the development of prostate cancer was described. The results of our study demonstrate an equal distribution of consumption of nicotine of the groups with prostate cancer and in the control group: 14.3% of patients with prostate cancer consumed on average 14.2 cigarettes per day, 17.5% of patients from the control group were smokers with a daily consumption of 16.1 cigarettes (p=0.169, Fishers Exact Test). We could not find a difference in the distribution of tumor stage, lymph node involvement and Gleason Score compared to non-smokers with prostate cancer. We also couldn’t confirm the result of an increased aggressiveness of prostate cancer under consumption of nicotine as described by CERHAN et al. and FURUYA et al. [14,24]. In contrast to the described risks of prostate cancer a protective effect of the daily or long-term consumption of ASS and other NSAID has been reported. The evidence of tumor protection due to NSAID was not found in our patient groups. There was no significant difference between the patient group with prostate cancer which used ASS or other NSAID (28.6%) and the control group (26.6%) (p=0.486, Fisher´s Exact Test). Regarding the high-grade disease of prostate cancer we couldn’t show an advantage by using NSAID or ASS compared to the patients with prostate cancer who didn’t take these drugs. We received the same result, i.e. no advantage caused by taking NSAID or ASS, with regard to the tumor-stage (p=0.528, Chi²-Test), the portion of participation of lymph nodes (p=0.443, Fisher´s Exact Test) or the distribution of the Gleason-Score (p=0.25, Chi²-Test). To summarize, we can neither confirm the influence of the known risk factors: overweight, hyperinsulinaemia and diabetes mellitus and the consumption of nicotine nor the protective effect of NSAID and ASS on the formation and development of prostate cancer.