7039 POSTER Establishing a Dose Response Relationship for the Treatment of Prostate Cancer With External Beam Radiotherapy: a Meta-analysis

2011 ◽  
Vol 47 ◽  
pp. S496
Author(s):  
Y. Trada ◽  
A. Plank ◽  
J.M. Martin
2020 ◽  
Vol 8 (1) ◽  
pp. 12-28
Author(s):  
Jinhui Zhao ◽  
Di Gao ◽  
Yanhui Li ◽  
Tim Stockwell ◽  
Jun Ma

Aims: Meta-analyses have suggested a dose-response relationship between level of alcohol use and risk of prostate cancer, but the populations in the included studies are predominantly Caucasian. Many Chinese language studies have not been included in published reviews and/or meta-analyses. The present meta–analysis accessed research reports in both English and Chinese language sources in order to investigate this relationship specifically among Chinese people. Methods: Searches in five large Chinese biomedical bibliographic databases were made for case–control and cohort studies of alcohol consumption and prostate cancer incidence and death (ICD–10: C61) up to May 2017. Studies were coded for design, outcome, drinker and non-drinkers, extent of control for confounding and other study characteristics. Mixed models were used to estimate relative risk (RR) of incidence or death from prostate cancer due to alcohol consumption with study level controls for designs, drinker bias and types of drinkers. Findings: A total of 415 studies were identified of which 25 (20 in Chinese from five Chinese databases and 5 in English from published meta-analyses) satisfied inclusion criteria providing 36 risk estimates of prostate cancer for drinkers versus non-drinkers. There was a total of 36 OR estimates; 27 using patients as controls and 9 using healthy people. Nine studies (14 OR estimates) specified reference abstainers as “never drank” or “no drinking”. Adjusted RR estimates indicated a significantly increased risk of prostate cancer among drinkers (RR=1.46, 95% CI: 1.40 – 1.52, t-test P<0.001) compared to non-drinkers. Dose-response relationships (t-test P<0.001) were evident in three studies that assessed level of alcohol intake. Conclusions: There is a significantly higher risk of prostate cancer incidence among Chinese drinkers than non-drinkers, with some evidence of a dose-response relationship. However, almost all the identified studies suffered from former and/or occasional drinker biases. Few studies had adequate measures of level of alcohol intake and further well-designed studies are required.


2020 ◽  
Vol 38 (26) ◽  
pp. 3024-3031 ◽  
Author(s):  
William C. Jackson ◽  
Holly E. Hartman ◽  
Robert T. Dess ◽  
Sam R. Birer ◽  
Payal D. Soni ◽  
...  

PURPOSE In men with localized prostate cancer, the addition of androgen-deprivation therapy (ADT) or a brachytherapy boost (BT) to external beam radiotherapy (EBRT) have been shown to improve various oncologic end points. Practice patterns indicate that those who receive BT are significantly less likely to receive ADT, and thus we sought to perform a network meta-analysis to compare the predicted outcomes of a randomized trial of EBRT plus ADT versus EBRT plus BT. MATERIALS AND METHODS A systematic review identified published randomized trials comparing EBRT with or without ADT, or EBRT (with or without ADT) with or without BT, that reported on overall survival (OS). Standard fixed-effects meta-analyses were performed for each comparison, and a meta-regression was conducted to adjust for use and duration of ADT. Network meta-analyses were performed to compare EBRT plus ADT versus EBRT plus BT. Bayesian analyses were also performed, and a rank was assigned to each treatment after Markov Chain Monte Carlo analyses to create a surface under the cumulative ranking curve. RESULTS Six trials compared EBRT with or without ADT (n = 4,663), and 3 compared EBRT with or without BT (n = 718). The addition of ADT to EBRT improved OS (hazard ratio [HR], 0.71 [95% CI, 0.62 to 0.81]), whereas the addition of BT did not significantly improve OS (HR, 1.03 [95% CI, 0.78 to 1.36]). In a network meta-analysis, EBRT plus ADT had improved OS compared with EBRT plus BT (HR, 0.68 [95% CI, 0.52 to 0.89]). Bayesian modeling demonstrated an 88% probability that EBRT plus ADT resulted in superior OS compared with EBRT plus BT. CONCLUSION Our findings suggest that current practice patterns of omitting ADT with EBRT plus BT may result in inferior OS compared with EBRT plus ADT in men with intermediate- and high-risk prostate cancer. ADT for these men should remain a critical component of treatment regardless of radiotherapy delivery method until randomized evidence demonstrates otherwise.


Author(s):  
Makoto Hibino ◽  
Yoichiro Otaki ◽  
Elsa Kobeissi ◽  
Han Pan ◽  
Hiromi Hibino ◽  
...  

Background: Hypertension or elevated blood pressure (BP) is an important risk factor for aortic dissection (AD); however, few prospective studies concerning this topic have been published. We investigated the association between hypertension/elevated BP and AD in two cohorts and conducted a meta-analysis of published prospective studies, including these two studies. Methods: We analyzed data from the Japan Specific Health Checkups (J-SHC) Study and UK Biobank, which prospectively followed 534,378 and 502,424 participants, respectively. Multivariable Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) for the association of hypertension/elevated BP with AD incidence in the UK Biobank and AD mortality in the J-SHC Study. In the meta-analysis, summary relative risks (RRs) were calculated using random effects models. A potential nonlinear dose-response relationship between BP and AD was tested using fractional polynomial models, and the best-fitting second-order fractional polynomial regression model was determined. Results: In the J-SHC Study and UK Biobank, there were 84 and 182 ADs during 4- and 9-year follow-up, and the adjusted HRs of AD were 3.57 (95% CI, 2.17-6.11) and 2.68 (95% CI: 1.78-4.04) in hypertensive individuals, 1.33 (95% CI: 1.05-1.68) and 1.27 (95% CI: 1.11-1.48) per 20-mmHg increase in systolic BP (SBP), and 1.67 (95% CI: 1.40-2.00) and 1.66 (95% CI: 1.46-1.89) per 10-mmHg increase in diastolic BP (DBP), respectively. In the meta-analysis, the summary RRs were 3.07 (95% CI 2.15-4.38, I2=76.7%, n=7 studies, 2,818 ADs, 4,563,501 participants) for hypertension and 1.39 (95% CI: 1.16-1.66, I2=47.7%, n=3) and 1.79 (95% CI: 1.51-2.12, I2=57.0%, n=3) per 20-mmHg increase in SBP and per 10-mmHg in DBP, respectively. The AD risk showed a strong, positive dose-response relationship with SBP and even more so with DBP. The risk of AD in the nonlinear dose-response analysis was significant at SBP >132 mmHg and DBP >75 mmHg. Conclusions: Hypertension and elevated SBP and DBP are associated with a high risk of AD. The risk of AD was positively dose-dependent, even within the normal BP range. These findings provide further evidence for the optimization of BP to prevent AD.


Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Jingkai Wei ◽  
Yuzhi Xi ◽  
Ruixue Hou ◽  
Alysse Kowalski ◽  
Hao Sun ◽  
...  

Introduction: Previous studies show that alpha-linolenic acid (ALA) is associated with reduced risk of coronary heart disease (CHD). However, it remains unclear whether and how dietary ALA doses are related to CHD. Hypothesis: We hypothesized that higher dietary ALA intake is associated with a greater reduction in risk of CHD. Methods: We searched PubMed, EMBASE, and Web of Science for prospective studies examining the association between dietary ALA intake and CHD risk. Dietary ALA intake was assigned or measured by self-report. Outcomes were reported as total and fatal CHD and/or myocardial infarction, which were obtained from blinded endpoint assessments or medical records. Two-stage fixed-effects dose-response meta-analyses were conducted to estimate the association between increasing ALA intake (relative to study-specific referents) and CHD. Results: Fifteen published articles were identified and included in the meta-analysis (13 cohort studies and 2 randomized controlled trials). The pooled analysis was based on 310,768 individuals with 12,049 events with a mean length of follow-up of 9.6 years. The analysis showed a J-shaped curve between ALA intake and relative risk of total CHD (Chi-square=21.08, p<0.001). ALA intake from 0.3-1.4g/day showed reduced risk of total CHD, while intake ≥2.5g/day was associated with increased risk of CHD, compared to people without ALA intake (Figure 1A). Approximately 1g/day of ALA intake was associated with the lowest risk of total CHD. ALA intake was linearly associated with fatal CHD - every 1g/day increase in ALA intake was associated with an 11% decrease in fatal CHD risk (95% CI: -0.16, -0.05) (Figure 1B). Conclusion: The J-shaped dose-response relationship based on our pooled analysis suggests that 1g/day of dietary ALA may be optimal for total CHD prevention. Though a higher dietary ALA intake was associated with reduced risk of fatal CHD, the excess total CHD risk at higher ALA intakes warrants further investigation, especially through randomized controlled trials.


2015 ◽  
Vol 181 (6) ◽  
pp. 374-384 ◽  
Author(s):  
Michael Goodman ◽  
K. M. Venkat Narayan ◽  
Dana Flanders ◽  
Ellen T. Chang ◽  
Hans-Olov Adami ◽  
...  

2018 ◽  
Vol 119 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Jingkai Wei ◽  
Ruixue Hou ◽  
Yuzhi Xi ◽  
Alysse Kowalski ◽  
Tiansheng Wang ◽  
...  

AbstractPrevious studies show inconsistent associations between α-linolenic acid (ALA) and risk of CHD. We aimed to examine an aggregate association between ALA intake and risk of CHD, and assess for any dose–response relationship. We searched the PubMed, EMBASE and Web of Science databases for prospective cohort studies examining associations between ALA intake and CHD, including composite CHD and fatal CHD. Data were pooled using random-effects meta-analysis models, comparing the highest category of ALA intake with the lowest across studies. Subgroup analysis was conducted based on study design, geographic region, age and sex. For dose–response analyses, we used two-stage random-effects dose–response models. In all, fourteen studies of thirteen cohorts were identified and included in the meta-analysis. The pooled results showed that higher ALA intake was associated with modest reduced risk of composite CHD (risk ratios (RR)=0·91; 95 % CI 0·85, 0·97) and fatal CHD (RR=0·85; 95 % CI 0·75, 0·96). The analysis showed a J-shaped relationship between ALA intake and relative risk of composite CHD (χ2=21·95, P<0·001). Compared with people without ALA intake, only people with ALA intake <1·4 g/d showed reduced risk of composite CHD. ALA intake was linearly associated with fatal CHD – every 1 g/d increase in ALA intake was associated with a 12 % decrease in fatal CHD risk (95 % CI −0·21, −0·04). Though a higher dietary ALA intake was associated with reduced risk of composite and fatal CHD, the excess composite CHD risk at higher ALA intakes warrants further investigation, especially through randomised controlled trials.


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