scholarly journals Should diabetic women with breast cancer have their own intervention studies?

2011 ◽  
Vol 19 (1) ◽  
pp. C13-C17
Author(s):  
David A Potter ◽  
Douglas Yee ◽  
Zhijun Guo ◽  
Mariangellys Rodriguez

This commentary on ‘Calorie restriction and rapamycin inhibit MMTV-Wnt-1 mammary tumor growth in a mouse model of postmenopausal obesity’ by Nogueiraet al., published in this issue ofEndocrine-Related Cancer, addresses the challenges of translating diet, exercise, and pharmacologic trials in diabetic mouse mammary tumor models to human studies. We propose that trials specifically designed to test such interventions in diabetic women with breast cancer would be valuable and informative.

2011 ◽  
Vol 19 (1) ◽  
pp. 57-68 ◽  
Author(s):  
Leticia M Nogueira ◽  
Sarah M Dunlap ◽  
Nikki A Ford ◽  
Stephen D Hursting

Obesity is an established risk and progression factor for postmenopausal breast cancer. Interventions to decrease caloric intake and/or increase energy expenditure beneficially impact tumor progression in normoweight humans and animal models. However, despite the increasingly high global prevalence of obesity, the effects and underlying mechanisms of these energy balance modulating interventions are poorly characterized in obese individuals. The goal of this study was to better characterize the mechanism(s) responsible for the link between energy balance and breast cancer progression in the postmenopausal obesity context. We compared the effects of calorie restriction (CR), treadmill exercise (EX), and mammalian target of rapamycin (mTOR inhibitor) treatment on body composition, serum biomarkers, cellular signaling, and mammary tumor growth in obese mice. Ovariectomized C57BL/6 mice were administered a diet-induced obesity regimen for 8 weeks, then randomized into three treatment groups: control (semipurified diet fedad libitum, maintained the obese state); 30% CR (isonutrient relative to control except 30% reduction in carbohydrate calories); and EX (control diet fedad libitumplus treadmill exercise). Mice were implanted with syngeneic MMTV-Wnt-1 mammary tumor cells at week 12. Rapamycin treatment (5 mg/kg every 48 h) started at week 14. Tumors were excised at week 18. CR and rapamycin (but not EX) significantly reduced final tumor weight compared to control. In follow-up analysis, constitutive activation of mTOR ablated the inhibitory effects of CR on Wnt-1 mammary tumor growth. We conclude that mTOR inhibition may be a pharmacologic strategy to mimic the anticancer effects of CR and break the obesity–breast cancer progression link.


2015 ◽  
Vol 12 (5) ◽  
pp. 324-330 ◽  
Author(s):  
Sun-Hyun Kim ◽  
Seong-Mi Choi ◽  
Byung-Soo Youn ◽  
Han-Soo Kim

Oncogene ◽  
2012 ◽  
Vol 32 (8) ◽  
pp. 961-967 ◽  
Author(s):  
N Alikhani ◽  
R D Ferguson ◽  
R Novosyadlyy ◽  
E J Gallagher ◽  
E J Scheinman ◽  
...  

1987 ◽  
Vol 27 (1-3) ◽  
pp. 209-214 ◽  
Author(s):  
M. Sluyser ◽  
B. Moncharmont ◽  
G. Ramp ◽  
C.C.J. de Goeij ◽  
S.G. Evers

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