Common habitual behaviors and synchronous colorectal cancer risk: a retrospective case-control study.

PURPOSE: The association of habitual behaviors with the prevalence of synchronous colorectal cancer (sCRC) is unknown. Here, we investigated whether these behaviors, which are known risk factors for colorectal polyps, may be related to sCRC risk. METHODS: We enrolled 17,093 patients who underwent cancer treatment between January 1995 and December 2016 and examined the association of age, sex, familial history of hereditary colorectal cancer (CRC), and status of three common habitual behaviors (smoking and alcohol and coffee consumption) with the prevalence of sCRC. RESULTS: Of the enrolled patients, 960 (5.6%) patients had sCRC. The independent risk factors for sCRC prevalence included advanced age, male sex, hereditary CRC, smoking, and daily alcohol consumption of more than one bottle (> 600 mL). Contrary to these factors, daily coffee consumption of more than one cup seemed to provide a protection from sCRC. In the Kaplan-Meier test, the significantly worse 5-year overall survival (OS) was noted in smokers with stage 0-III CRC. The effect of alcohol consumption on 5-year OS was significant in stages II and III. Compared with those without daily coffee consumption, patients with daily coffee consumption had significantly higher 5-year OS in stages I (93.0% vs. 86.4%), II (87.1% vs. 77.2%), III (71.5% vs. 61.9%), and IV (18.0% vs. 13.0%). CONCLUSIONS: sCRC prevalence was significantly associated with habitual behaviors. Patients with smoking or with daily alcohol consumption of one bottle had higher sCRC prevalence than did those without these habits. Coffee consumption could be a protective factor for lowering sCRC risk.

Evodiamine Induces Cell Growth Arrest, Apoptosis and Suppresses Tumorigenesis in Human Urothelial Cell Carcinoma Cells.

BACKGROUND/AIM: Evodiamine, an indole alkaloid derived from Evodia rutaecarpa, exhibits pharmacological activities including vasodilatation, analgesia, anti-cardiovascular disease, anti-Alzheimer's disease, anti-inflammation, and anti-tumor activity. MATERIALS AND METHODS: This study analyzes the anti-tumor effects of evodiamine on cellular growth, tumorigenesis, cell cycle and apoptosis induction of human urothelial cell carcinoma (UCC) cells. RESULTS: The present study showed that evodiamine significantly inhibited the proliferation of UCC cells in a dose- and time-dependent manner. Also, evodiamine suppressed the tumorigenesis of UCC cells in vitro. Moreover, evodiamine caused G2/M cell-cycle arrest and induced caspase-dependent apoptosis in UCC cells. Finally, we demonstrated that evodiamine exhibits better cytotoxic than 5-fluorouracil, a clinical chemotherapeutic drug, for UCC cells. CONCLUSION: Evodiamine induces growth inhibition, tumorigenesis suppression, cell-cycle arrest, and apoptosis induction in human UCC cells. Therefore, this agent displays a therapeutic potential for treating human UCC cells and is worthy for further investigation.

Chronic Cigarette Smoking Impairs Erectile Function through Increased Oxidative Stress and Apoptosis, Decreased nNOS, Endothelial and Smooth Muscle Contents in a Rat Model.

Cigarette use is an independent risk factor for the development of erectile dysfunction (ED). While the association between chronic smoking and ED is well established, the fundamental mechanism(s) of cigarette-related ED are incompletely understood, partly due to no reliable animal model of smoking-induced ED. The present study was designed to validate an in vivo rat model of chronic cigarette-induced ED. Forty 12-week old male Sprague-Dawley rats were divided into 4 groups. Ten rats served as control group and were exposed only to room air. The remaining 30 rats were passively exposed to cigarette smoke (CS) for 4 weeks (n = 10), 12 weeks (n = 10), and 24 weeks (n = 10). At the 24-week time point all rats were assessed with intracavernous pressure (ICP) during cavernous nerve electrostimulation. Blood and urine were collected to measure serum testosterone and oxidative stress, respectively. Corporal tissue was assessed by Western blot for neuronal nitric oxide synthase (nNOS). Penile tissues were subjected to immunohistochemistry for endothelial, smooth muscle, and apoptotic content. Mean arterial pressure (MAP) was significantly higher in 24-week cigarette exposed animals compared to the control animals. Mean ICP/MAP ratio and cavernosal smooth muscle/endothelial contents were significantly lower in the 12- and 24-week rats compared to control animals. Oxidative stress was significantly higher in the 24-week cigarette exposed group compared to control animals. Mean nNOS expression was significantly lower, and apoptotic index significantly higher, in CS-exposed animals compared to control animals. These findings indicate that the rat model exposure to CS increases apoptosis and oxidative stress and decreases nNOS, endothelial and smooth muscle contents, and ICP in a dose dependent fashion. The rat model is a useful tool for further study of the molecular and cellular mechanisms of CS-related ED.