scholarly journals Protective effect of Chuquiraga spinosa extract on N -methyl-nitrosourea (NMU) induced prostate cancer in rats

2017 ◽  
Vol 5 (2) ◽  
pp. 47-52 ◽  
Author(s):  
Jorge Arroyo-Acevedo ◽  
Oscar Herrera-Calderón ◽  
Roberto Chávez-Asmat ◽  
Andrea Anampa-Guzmán ◽  
Víctor Chumpitaz-Cerrate ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protective Effect ◽  
Methyl Nitrosourea

scholarly journals Protective effect of carboxymethyl-glucan (CM-G) against DNA damage in patients with advanced prostate cancer

2010 ◽  
Vol 34 (1) ◽  
pp. 131-135 ◽  
Author(s):  
Marciane Magnani ◽  
Raul Jorge Hernan Castro-Gomez ◽  
Mateus Prates Mori ◽  
Hellen Kuasne ◽  
Emerson Pereira Gregório ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Damage ◽  
Protective Effect ◽  
Advanced Prostate Cancer

scholarly journals Protective effect of Chuquiraga spinosa Lessing associated with simvastatin on N-Nitroso-N-methylurea (NMU)-induced prostate cancer in rats

2019 ◽  
Vol Volume 12 ◽  
pp. 6555-6562
Author(s):  
Jorge Luis Arroyo-Acevedo ◽  
Juan Pedro Rojas-Armas ◽  
Oscar Herrera-Calderón ◽  
Roberto Chávez-Asmat ◽  
Hugo Jesús Justil-Guerrero ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protective Effect

Protective effect of green tea against prostate cancer: A case-control study in southeast China

2003 ◽  
Vol 108 (1) ◽  
pp. 130-135 ◽  
Author(s):  
Le Jian ◽  
Li Ping Xie ◽  
Andy H. Lee ◽  
Colin W. Binns
Keyword(s):  
Prostate Cancer ◽  
Protective Effect ◽  
Green Tea ◽  
Case Control Study ◽  
Case Control ◽  
Southeast China ◽  
Control Study

scholarly journals Do sex hormones confound or mediate the effect of chronotype on breast and prostate cancer? A Mendelian randomization study.

2021 ◽  
Author(s):  
Bryony L Hayes ◽  
Timothy Robinson ◽  
Siddhartha P. Kar ◽  
Katherine S Ruth ◽  
Konstantinos K Tsilidis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Prostate Cancer ◽  
Cancer Risk ◽  
Protective Effect ◽  
Sex Hormones ◽  
Prostate Cancer Risk ◽  
Total Testosterone ◽  
Testosterone Levels ◽  
Bioavailable Testosterone ◽  
Breast And Prostate Cancer

BACKGROUND Previous research has demonstrated that a morning-preference chronotype is protective against both breast and prostate cancer. Sex hormones have been implicated in relation to both chronotype and the development of both cancers. This study aims to assess whether sex hormones confound or mediate the effect of chronotype on breast and prostate cancer risk using a Mendelian Randomization (MR) framework. METHODS We obtained genetic variants strongly (p<5x10-8) associated with chronotype and sex hormones (total testosterone, bioavailable testosterone, sex hormone binding globulin (SHBG), and oestradiol from previously published genome-wide association studies (GWAS) that had been undertaken in UK Biobank and 23andMe (n=244,207 females and n=205,527 males). These variants were used to investigate causal relationships with risk of breast and prostate cancer using summary data from the largest available consortia in breast (nCases/nControls=133,384/ 113,789) and prostate cancer (nCases/nControls=79,148/61,106). This was achieved using a series of MR approaches: univariable, bidirectional and multivariable. Results Overall, we found evidence for a protective effect of genetically predicted tendency towards morning preference on both breast (OR=0.93, 95% CI:0.88, 1.00) and prostate (OR=0.90, 95% CI:0.83, 0.97) cancer risk. There was evidence that an increased tendency to morning preference reduces bioavailable testosterone levels in both females (mean SD difference=-0.08, 95% CI:-0.12, -0.05) and males (mean SD difference=-0.06, 95% CI:-0.09, -0.03), and reduces total testosterone levels in females (mean SD difference=-0.07, 95% CI:-0.10, -0.03). We also found evidence to support higher total and bioavailable testosterone increasing the risk of breast cancer (OR=1.15, 95% CI:1.07, 1.23, OR=1.10, 95% CI:1.01, 1.19 respectively) and higher bioavailable testosterone increasing prostate cancer risk (OR=1.22, 95% CI:1.08, 1.37). While findings from univariable and bidirectional MR analyses indicated that testosterone may lie on the causal pathway between chronotype and cancer risk, there was evidence for a bidirectional association between chronotype and testosterone in females, implicating testosterone as both a confounder and mediator of the chronotype effect on breast cancer risk. However, the effects of chronotype remained largely unchanged when accounting for testosterone in multivariable MR, suggesting that any confounding or mediating effect is likely to be minimal. Conclusions This study has extended previous findings regarding the protective effect of chronotype on breast cancer and found evidence to suggest that morning preference also reduces prostate cancer risk in men. While testosterone levels were found to be closely linked with both chronotype and cancer risk, there was inconsistent evidence for the role of testosterone in mediating the effect of morning preference chronotype on both breast and prostate cancer. Findings regarding the potential protective effect of chronotype on both breast and prostate cancer risk are clinically interesting. However, this may not serve as a direct target for intervention, since it is difficult to modify someone's morning/evening preference. Given this, further studies are needed to investigate the mechanisms underlying this effect and to identify other potential modifiable intermediates.

The protective effect of diabetes mellitus against prostate cancer: Role of sex hormones

The Prostate ◽  
2009 ◽  
Vol 69 (16) ◽  
pp. 1744-1750 ◽  
Author(s):  
N. Baradaran ◽  
H. Ahmadi ◽  
S. Salem ◽  
M. Lotfi ◽  
Y. Jahani ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Diabetes Mellitus ◽  
Protective Effect ◽  
Sex Hormones

Impact of flaxseed supplementation and dietary fat restriction on prostate cancer proliferation and other biomarkers: Results of a Phase II randomized controlled trial (RCT) using a presurgical model

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 1510-1510 ◽  
Author(s):  
S. L. George ◽  
T. J. Polascik ◽  
D. M. Albala ◽  
P. J. Walther ◽  
J. Moul ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protective Effect ◽  
Dietary Fat ◽  
Controlled Trial ◽  
Specific Antigen ◽  
Sex Hormone Binding Globulin ◽  
Total Testosterone ◽  
Sample Mean ◽  
Cell Counts ◽  
Mib 1

1510 Background: Diet may play a key role in the etiology of prostate cancer (PC). Dietary fat restriction (DFR) and flaxseed supplementation (FS) may reduce risk, though results are mixed. We undertook an RCT to test the comparative effects of these dietary regimens on the biology of the prostate and other biomarkers. Methods: PC patients (N=161) scheduled ≥ 21 days prior to prostatectomy were block randomized on race (black vs non-black) and biopsy Gleason sum (<7 vs 7+) to these diets: 1) control; 2) FS (30 g/day); 2) DFR (<20% total energy); or 4) FS+DFR. Blood was drawn upon accrual and prior to surgery and analyzed for prostate specific antigen (PSA), sex hormone binding globulin (SHBG), total testosterone (T), insulin-like growth factor 1 (IGF1), IGF binding protein 3 (IGFBP3), c- reactive protein (CRP), and total and low density lipoprotein cholesterol (TC & LDL-C). Proliferation (MIB-1) and apoptosis (TUNEL) was assessed in the malignant and benign prostate. Results: Complete data were collected on 93% of the sample; mean length on protocol was 30 days. Median MIB-1 positive (+) cells/total nuclei ratios were: 1=2.38;2=1.71;3=2.93;4=1.58. Primary analyses suggest a significant protective effect (p=0.016) of FS. Secondary analyses of MIB-1 + nuclei (controlling for total cell counts) show increased proliferation with DFR (p=.017), and a significant interaction with FS and DFR (p<.0001). No differences were observed between groups with regard to PC apoptosis, and histology of benign tissue. No differences were observed between arms for PSA, SHBG, T, IGF1, IGFBP3 or CRP. Significant differences were observed between arms for changes in serum lipids and body weight [ΔTC = +9/-26/-46/-37 mg/dL; ΔLDLC = -14/-17/-29/-21 mg/dL and Δ weight = +0.3/-1.3/-1.7/-1.1 kg (p’s<.05)]; effects were attributed to DFR and not FS. Side effects did not differ between arms Conclusions: Preliminary findings suggest that FS is safe and exerts a protective effect (main effect or via interaction with DFR) on PC. Data also provide further support of DFR for cardiovascular disease, though its role in PC is less clear. Further controlled analyses and additional studies are needed to confirm findings. No significant financial relationships to disclose.

scholarly journals Nonsteroidal anti-inflammatory drugs and prostate cancer: a systematic review of the literature and meta-analysis

2013 ◽  
Vol 3 (4) ◽  
pp. 323 ◽  
Author(s):  
Siavash Jafari ◽  
Mahyar Etminan ◽  
Kourosh Afshar
Keyword(s):  
Prostate Cancer ◽  
Protective Effect ◽  
Journal Club ◽  
Meta Analysis ◽  
Cancer De La Prostate ◽  
Inclusion Criteria ◽  
Inflammatory Drugs ◽  
Observational Design ◽  
Anti Inflammatory ◽  
Significant Protective Effect

Prostate cancer is the most common visceral cancer in men. Manystudies have shown that nonsteroidal anti-inflammatory drugs(NSAIDs) may reduce the risk of prostate cancer. We systematicallysearched all relevant databases (MEDLINE, EMBASE, The CochraneCollaboration, CINAHL, Database of Abstracts of Review of Effectsand ACP Journal Club) to March 2008. We also explored bibliographiesof the articles, pertinent journals and conferences. Weselected relevant articles according to predefined inclusion criteriaby 2 independent reviewers. We used both fixed and randomeffectmodels for meta-analysis. We performed subgroup and sensitivityanalysis based on predefined variables. From 962 extractedarticles, 20 met the inclusion criteria with a total of 25 768 participants.All the studies had an observational design. There wasa statistically significant protective effect for NSAIDs on risk ofprostate cancer (odds ratio [OR] 0.92, 95% confidence interval[CI] 0.86–0.97). Subgroup analysis did not show any effect of studydesign or quality score on the results. There was a small but statisticallysignificant protective effect for acetylsalicylic acid (ASA)(OR 0.95, 95% CI 0.91–1.00). Exposure to non-ASA NSAIDs wasassociated with a slightly reduced likelihood of prostate cancer(OR 0.92, 95% CI 0.85–1.00). With the available data, we werenot able to determine an optimum dosage for NSAIDs. We concludethat taking NSAIDs may reduce the risk of prostate cancer.Nevertheless, the effect is small.Le cancer de la prostate est le cancer viscéral le plus fréquentchez l’homme. Bon nombre d’études ont montré que les antiinflammatoiresnon stéroïdiens (AINS) pouvaient réduire le risquede cancer de la prostate. Notre objectif était de réaliser une revuesystématique et une méta-analyse des articles publiés sur les effetsdes AINS dans la réduction du risque de cancer de la prostate.Toutes les bases de données pertinentes (MEDLINE, EMBASE,Collaboration Cochrane, CINAHL, Database of Abstracts of Reviewof Effects et ACP Journal Club) ont été systématiquement consultéesen mars 2008. On a également examiné la bibliographie des articlesdégagés et des revues et conférences pertinentes. Les articlespertinents ont été sélectionnés en fonction de critères d’inclusionprédéfinis par 2 analystes indépendants. Pour la méta-analyse,on a eu recours à des modèles à effets fixes et à effets aléatoires.Une analyse par sous-groupes et une analyse de sensibilité ont étéeffectuées à l’aide de variables prédéfinies. Sur les 962 articlesdégagés, 20 satisfaisaient aux critères d’inclusion, pour un totalde 25 768 sujets. Toutes les études étaient de type observationnel.On a noté un effet protecteur statistiquement significatif sur lerisque de cancer de la prostate avec les AINS (rapport de cotes de0,92; IC à 95 % de 0,86 à 0,97). L’analyse par sous-groupes n’arévélé aucun effet du plan de l’étude ou du score de qualité surles résultats. On a noté un effet protecteur léger mais tout de mêmesignificatif sur le plan statistique avec l’aspirine (RC 0,95; IC à95 % de 0,91 à 1,00). L’exposition à des AINS autres que l’aspirinea été associée à une probabilité légèrement moindre de cancer dela prostate (RC 0,92, IC à 95 % de 0,85 à 1,00). Les donnéesdisponibles ne nous ont pas permis de déterminer la posologieoptimale des AINS. Nous avons observé un effet favorable possibleassocié à la prise d’AINS dans la réduction du risque de cancerde la prostate, mais cet effet est minime.

Polymorphisms in estrogen related genes may modify the protective effect of isoflavones against prostate cancer risk in Japanese men

2010 ◽  
Vol 19 (2) ◽  
pp. 131-137 ◽  
Author(s):  
Tomoko Sonoda ◽  
Hiromu Suzuki ◽  
Mitsuru Mori ◽  
Taiji Tsukamoto ◽  
Akira Yokomizo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Protective Effect ◽  
Prostate Cancer Risk ◽  
Japanese Men
Sign in / Sign up

Export Citation Format

Share Document