scholarly journals The Impact of Diabetes on the Risk of Prostate Cancer Development according to Body Mass Index: A 10-year Nationwide Cohort Study

2016 ◽  
Vol 7 (14) ◽  
pp. 2061-2066 ◽  
Author(s):  
Jin Bong Choi ◽  
Hyong Woo Moon ◽  
Young Hyun Park ◽  
Woong Jin Bae ◽  
Hyuk Jin Cho ◽  
...  
2005 ◽  
Vol 173 (4S) ◽  
pp. 403-403
Author(s):  
Stephen J. Freedland ◽  
Martha K. Terris ◽  
Elizabeth A. Platz ◽  
Joseph C. Presti

Urology ◽  
2005 ◽  
Vol 66 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Stephen J. Freedland ◽  
Martha K. Terris ◽  
Elizabeth A. Platz ◽  
Joseph C. Presti

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Barbara Iyen ◽  
Stephen Weng ◽  
Yana Vinogradova ◽  
Ralph K. Akyea ◽  
Nadeem Qureshi ◽  
...  

Abstract Background Although obesity is a well-recognised risk factor for cardiovascular disease (CVD), the impact of long-term body mass index (BMI) changes in overweight or obese adults, on the risk of heart failure, CVD and mortality has not been quantified. Methods This population-based cohort study used routine UK primary care electronic health data linked to secondary care and death-registry records. We identified adults who were overweight or obese, free from CVD and who had repeated BMI measures. Using group-based trajectory modelling, we examined the BMI trajectories of these individuals and then determined incidence rates of CVD, heart failure and mortality associated with the different trajectories. Cox-proportional hazards regression determined hazards ratios for incident outcomes. Results 264,230 individuals (mean age 49.5 years (SD 12.7) and mean BMI 33.8 kg/m2 (SD 6.1)) were followed-up for a median duration of 10.9 years. Four BMI trajectories were identified, corresponding at baseline, with World Health Organisation BMI classifications for overweight, class-1, class-2 and class-3 obesity respectively. In all four groups, there was a small, stable upwards trajectory in BMI (mean BMI increase of 1.06 kg/m2 (± 3.8)). Compared with overweight individuals, class-3 obese individuals had hazards ratios (HR) of 3.26 (95% CI 2.98–3.57) for heart failure, HR of 2.72 (2.58–2.87) for all-cause mortality and HR of 3.31 (2.84–3.86) for CVD-related mortality, after adjusting for baseline demographic and cardiovascular risk factors. Conclusion The majority of adults who are overweight or obese retain their degree of overweight or obesity over the long term. Individuals with stable severe obesity experience the worst heart failure, CVD and mortality outcomes. These findings highlight the high cardiovascular toll exacted by continuing failure to tackle obesity.


2012 ◽  
Vol 442 (1) ◽  
pp. 151-159 ◽  
Author(s):  
Inma M. Berenjeno ◽  
Julie Guillermet-Guibert ◽  
Wayne Pearce ◽  
Alexander Gray ◽  
Stewart Fleming ◽  
...  

The PI3K (phosphoinositide 3-kinase) pathway is commonly activated in cancer as a consequence of inactivation of the tumour suppressor PTEN (phosphatase and tensin homologue deleted on chromosome 10), a major negative regulator of PI3K signalling. In line with this important role of PTEN, mice that are heterozygous for a PTEN-null allele (PTEN+/− mice) spontaneously develop a variety of tumours in multiple organs. PTEN is a phosphatase with selectivity for PtdIns(3,4,5)P3, which is produced by the class I isoforms of PI3K (p110α, p110β, p110γ and p110δ). Previous studies indicated that PTEN-deficient cancer cell lines mainly depend on p110β, and that p110β, but not p110α, controls mouse prostate cancer development driven by PTEN loss. In the present study, we investigated whether the ubiquitously expressed p110α can also functionally interact with PTEN in cancer. Using genetic mouse models that mimic systemic administration of p110α- or p110β-selective inhibitors, we confirm that inactivation of p110β, but not p110α, inhibits prostate cancer development in PTEN+/− mice, but also find that p110α inactivation protects from glomerulonephritis, pheochromocytoma and thyroid cancer induced by PTEN loss. This indicates that p110α can modulate the impact of PTEN loss in disease and tumourigenesis. In primary and immortalized mouse fibroblast cell lines, both p110α and p110β controlled steady-state PtdIns(3,4,5)P3 levels and Akt signalling induced by heterozygous PTEN loss. In contrast, no correlation was found in primary mouse tissues between PtdIns(3,4,5)P3 levels, PI3K/PTEN genotype and cancer development. Taken together, our results from the present study show that inactivation of either p110α or p110β can counteract the impact of PTEN inactivation. The potential implications of these findings for PI3K-targeted therapy of cancer are discussed.


Pain Medicine ◽  
2016 ◽  
Vol 18 (1) ◽  
pp. 25-35 ◽  
Author(s):  
Zachary L. McCormick ◽  
Sarah C. Choxi ◽  
David T. Lee ◽  
Austin Marcolina ◽  
Joel Press ◽  
...  

2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Jin Bong Choi ◽  
Jun-Pyo Myong ◽  
Yunhee Lee ◽  
Jun Sung Koh ◽  
Sung-Hoo Hong ◽  
...  

BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Kosj Yamoah ◽  
Charnita M. Zeigler-Johnson ◽  
Abra Jeffers ◽  
Bruce Malkowicz ◽  
Elaine Spangler ◽  
...  

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