Host cellular paracrine regulation of tumor progression is an important determinant of tumor biology but one cell that has been ignored in this regulation is the myoepithelial cell. Myoepithelial cells surround normal ducts and precancerous lesions, especially of the breast and form a natural border separating proliferating epithelial cells from proliferating endothelial cells (angiogenesis). Myoepithelial cells may thus negatively regulate tumor invasion and metastasis. Whereas epithelial cells are susceptible targets for transforming events, myoepithelial cells are resistant. Therefore, it can be said that myoepithelial cells function as both autocrine as well as paracrine tumor suppressors. Our laboratory has found that myoepithelial cells secrete a number of suppressor molecules including high amounts of diverse proteinase inhibitors and angiogenic inhibitors but low amounts of proteinases and angiogenic factors compared to common malignant cell lines. This observation has been made in vitro, in mice, and in humans and suggests that myoepithelial cells exert pleiotropic suppressive effects on tumor progression. The gene expression profile of myoepithelial cells may explain the pronounced anti-invasive and anti-angiogenic effects of myoepithelial cells on carcinoma cells and may also account for the reduced malignancy of myoepithelial tumors, which are devoid of appreciable angiogenesis and invasive behavior.
Aims: The aim of this study was to determine the impact of diabetes mellitus (DM) on short-term overall survival and time to recurrence (TTR) in breast cancer patients, and examine the impact of breast cancer on glycemic control in DM. Methods: From a data set of newly diagnosed breast cancer patients (2007)(2008)(2009)(2010)(2011), we identified 109 patients with DM and 109 matched controls. Results: Hemoglobin A1c among cases did not significantly change over 1 year (p = 0.10). Cases and controls showed no differences in OS (hazard ratio: 1.25; 95% CI: 0.49-3.17) during the median follow-up of 2.2 years (range: 0.1-4.9 years) and no differences in TTR (hazard ratio: 1.00; 95% CI: 0.14-7.10). Conclusion: DM did not adversely affect metabolic control, short-term OS or TTR.
KEYWORDSCoexisting diabetes mellitus (DM) and cancer has been a topic of increasing interest [1]. DM is associated with an increased risk of development of many types of cancers [2][3][4]. Moreover, several studies have indicated that coexisting DM is associated with greater mortality in several types of cancers, including colorectal, endometrial, pancreas, liver and bladder [5,6]. A relationship between hyperglycemia and cancer mortality has also been noted [7,8].The link between DM and breast cancer is of particular interest, given the common risk factors of obesity, diet and hyperinsulinemia [2][3][4]. Current hypotheses regarding mechanisms of the link between DM and breast cancer can be found in two recent reviews [2,5]. Postulated
Practice points• The link between diabetes mellitus (DM) and breast cancer is of particular interest, given the common risk factors of obesity, diet and hyperinsulinemia.• Previous studies typically have not examined how DM might affect breast cancer mortality or how breast cancer might alter outcomes of patients with DM in a single analysis.• The purpose of this study was to examine whether breast cancer and its treatment affected glycemic control and therapy for DM and to assess its impact on short-term overall survival and time to recurrence.• The presence of breast cancer and its treatment did not negatively affect metabolic control among patients with DM in this cohort.• DM did not appear to affect either breast cancer overall survival or time to recurrence in the short term.For reprint orders, please contact: reprints@futuremedicine.com
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