Plastic Surgery Research Council
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Presenter: Yuan Liu, MD
Co-Authors: Jones R; Slotcavage R; Chang S; Carpenter J; Tulenko T
Cooper University Hospital

Introduction: The use of radiation therapy in cancer is limited by its side effects such as tissue necrosis, fibrosis, and non-healing wounds. These effects are suspected to be the result of radiation-dependent depletion or alteration of tissue-specific stem cells. We hypothesized that adipose-derived stem cells (ASCs) which have been exposed to radiation therapy in the course of cancer treatment will be fewer in number, proliferate less rapidly, and will exhibit a diminished differentiation capacity when compared to non-radiated cells.

Methods: During the course of revision surgery in subjects who had breast cancer and bilateral mastectomy with reconstruction, two samples of adipose tissue were harvested from the lateral thorax: one sample from the side ipsilateral to the tumor within the radiated field, and the other from the contralateral, non-radiated side. ASCs was isolated from specimens using standard collagenase digestion and centrifugation techniques, counted to determine SVF yield, and plated. Growth Curves were done. Cells were also plated in endothelial differentiation medium and allowed to fully differentiate to an endothelial-like phenotype over a two week period. At the end of the two week period, the differentiation capacity of these cells was assessed by examining differential gene expression using Real Time PCR.

Results: No difference was seen in SVF or ASC yield between R+ and R- cells. No difference was seen in proliferation rate based on growth curves. A difference was seen, however, in endothelial differentiation capacity based on expression levels of CD31, von Willibrand Factor vWF) and endothelial nitric oxide synthase. The R+ cells showed an 3-fold reduction in CD31 expression, a near 20-fold reduction in von Willibrand factor and a greater than 20-fold reduction in endothelial nitric oxide synthase (eNOS).

Conclusion: These preliminary results suggest that while radiated ASCs are no less in number, their ability to differentiate into an endothelial phenotype and form microvascular networks in vitro and in vivo may be impaired, perhaps clarifying a mechanism of chronic radiation damage.

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