کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3979845 | 1257379 | 2015 | 7 صفحه PDF | دانلود رایگان |
• Pre-clinical work has now clarified metformin (met) action in breast cancer (Bca).
• Host and disease characteristics might differentially impact met outcome in Bca.
• Ongoing trials of met in Bca are increasingly focused on host and disease features.
• Definition of target population is a pre-requisite for appropriate outcome interpretation.
• The “schism” between the pre-clinical and clinical setting is no longer sustainable.
Although preclinical work is vital in unraveling the molecular tenets which apply to metformin action in breast cancer, it is by nature unable to capture the host’s response to metformin in terms of insulin-mediated effects and related changes in the hormonal and metabolic asset at the systemic level. The latter might sound seemingly paradoxical when considering the inveterate use of metformin in dysmetabolisms and pathologic conditions with underlying hormonal disruption.Bridging the gap between the molecular target and characteristics of breast cancer patients may help lab-based experiments and clinical work converge into one or more well characterized sub-populations instead of a sub optimally selected one. An appropriate patient selection is the main key to the most suitable outcome interpretation and amelioration, in an attempt to meet our patients needs midway between overestimation of benefits and efficacy dilution for any given intervention and/or co-intervention.
Journal: Cancer Treatment Reviews - Volume 41, Issue 5, May 2015, Pages 441–447