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Surgical Stress Promotes Tumor Growth in Ovarian Carcinoma
Journal article   Open access   Peer reviewed

Surgical Stress Promotes Tumor Growth in Ovarian Carcinoma

Jeong-Won Lee, Mian M.K Shahzad, Yvonne G Lin, Guillermo Armaiz-Pena, Hee-Dong Han, Hye-Sun Kim, Eun Ji Nam, Nicholas B Jennings, Jyotsnabaran Halder, Lingegowda S Mangala, …
Clinical cancer research, Vol.15(8), pp.2695-2702
04/15/2009
DOI: 10.1158/1078-0432.CCR-08-2966
PMCID: PMC2746852
PMID: 19351748
url
https://doi.org/10.1158/1078-0432.CCR-08-2966View
Published (Version of record) Open Access

Abstract

Surgical stress has been suggested to facilitate the growth of pre-existing micrometastases as well as small residual tumor postoperatively. The purpose of this study was to examine the effects of surgical stress following either mastectomy or laparotomy on ovarian cancer growth and to determine underlying mechanisms responsible for increased growth. In both HeyA8 and SKOV3ip1 models, the mice in the laparotomy and mastectomy groups had significantly greater tumor weight ( P < 0.05) and nodules ( P < 0.05) compared to anesthesia only controls. There was no increase in tumor weight following surgery in the β-adrenergic receptor (ADRB)-negative RMG-II model. To block the influence of sympathetic nervous system activation by surgical stress, we used propranolol infusion via Alzet pumps. Propranolol completely blocked the effects of surgical stress on tumor growth, indicating a critical role for ADRB signaling in mediating the effects of surgical stress on tumor growth. In the HeyA8 and SKOV3ip1 models, surgery significantly increased microvessel density (CD31) and VEGF expression, which were blocked by propranolol treatment. These results indicate that surgical stress could enhance tumor growth and angiogenesis, and β-blockade might be effective in preventing such effects.
Ovarian Cancer Angiogenesis Surgery Adrenergic Receptor Stress

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