Augmentation mammoplasty: effect on diagnosis of breast cancer

Breast augmentation for cosmetic purposes is an increasingly common procedure in the USA and UK. In the USA in 2003, a total of 254 140 breast augmentation procedures were carried out [American Society of Plastic Surgeons, http://www.plasticsurgery.org/newsroom/ Procedural-Statistics-Press-Kit-Index.cfm9-1-2005; 2006.(1)]. It has been previously estimated that between 1 and 1.5 million women in the USA have prosthetic breast implants [Cook RR, Delongchamp RR, Woodbury M, et at. The prevalence of women with breast implants in the United States, 1989. J Clin Epidemiol 1995;48:519-25.(2)]. The UK National Breast Implant Registry has recorded a rise in the numbers of women receiving breast implants, with over 13 000 procedures registered in 2001; an estimated 77% of these were for cosmetic purposes. No association has been found between the presence of breast implants in a breast and an increased risk of breast cancer, and this subject has been comprehensively reviewed elsewhere [Hoshaw SJ, Klein PJ, Clark BD, et al. Breast implants and cancer: causation, delayed detection, and survival. Plast Reconstr Surg 2001; 107:1393-407.(3)]. However, as the population of women with breast implants ages, an increasing number of them will develop breast cancer; a reflection of the fact that the incidence of the disease increases with increasing age. Debate continues on the effect of breast implants on the efficacy of mammography in diagnosing breast cancer, and the role of other imaging techniques for this purpose, as well as the limitations that the presence of implants place on percutaneous biopsy techniques. We review the Literature on the radiological and tissue diagnosis of breast cancer in women with a history of previous augmentation mammaplasty. (c) 2007 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.

Breast cancer following augmentation mammoplasty - a review of its impact on prognosis and management

The incidence of breast cancer in women with implants is increasing and will continue to do so for the foreseeable future due to the marked increase in breast implant insertion in recent years. Undoubtedly many of these women will wish to know whether the presence of implants worsens the prognosis of their breast cancer. Furthermore, the clinical management of such patients may be difficult, as aesthetic results are likely to be a major concern for women who have already undergone cosmetic surgery to the breast. There is no consensus on surgical approach to this scenario. This article reviews the literature on the prognosis of breast cancer patients with a history of augmentation mammoplasty and examines the available data regarding their surgical treatment. (c) 2007 Published by Elsevier Ltd on behalf of British Association of Plastic, Reconstructive and Aesthetic Surgeons.

Induction of epithelial to mesenchymal transition in PMC42-LA human breast carcinoma cells by carcinoma-associated fibroblast secreted factors

Background Breast carcinoma is accompanied by changes in the acellular and cellular components of the microenvironment, the latter typified by a switch from fibroblasts to myofibroblasts. Methods: We utilised conditioned media cultures, Western blot analysis and immunocytochemistry to investigate the differential effects of normal mammary fibroblasts (NMFs) and mammary cancer-associated fibroblasts (CAFs) on the phenotype and behaviour of PMC42-LA breast cancer cells. NMFs were obtained from a mammary gland at reduction mammoplasty, and CAFs from a mammary carcinoma after resection. Results We found greater expression of myofibroblastic markers in CAFs than in NMFs. Medium from both CAFs and NMFs induced novel expression of α-smooth muscle actin and cytokeratin-14 in PMC42-LA organoids. However, although conditioned media from NMFs resulted in distribution of vimentin-positive cells to the periphery of PMC42-LA organoids, this was not seen with CAF-conditioned medium. Upregulation of vimentin was accompanied by a mis-localization of E-cadherin, suggesting a loss of adhesive function. This was confirmed by visualizing the change in active β-catenin, localized to the cell junctions in control cells/ cells in NMF-conditioned medium, to inactive β-catenin, localized to nuclei and cytoplasm in cells in CAF-conditioned medium. Conclusion We found no significant difference between the influences of NMFs and CAFs on PMC42-LA cell proliferation, viability, or apoptosis; significantly, we demonstrated a role for CAFs, but not for NMFs, in increasing the migratory ability of PMC42-LA cells. By concentrating NMF-conditioned media, we demonstrated the presence of factor(s) that induce epithelial-mesenchymal transition in NMF-conditioned media that are present at higher levels in CAF-conditioned media. Our in vitro results are consistent with observations in vivo showing that alterations in stroma influence the phenotype and behaviour of surrounding cells and provide evidence for a role for CAFs in stimulating cancer progression via an epithelial-mesenchymal transition. These findings have implications for our understanding of the roles of signalling between epithelial and stromal cells in the development and progression of mammary carcinoma.

The evolution of mastectomies in the oncoplastic breast surgery era

Over time, surgical techniques have advanced to the point where oncological safety and aesthetic outcomes are the pillars of contemporary breast surgery. Variations of mastectomy came up and started allowing the oncological safety and the possibility of an immediate breast reconstruction. Nowadays the association between plastic surgical techniques and mastectomy with immediate breast reconstruction is one of the best alternatives to treat breast cancer and also improved overall aesthetic outcomes and favors the achievement of contralateral breast symmetry. Oncoplastic mastectomy is a feasible term and can be routinely used.

4-Hydroxylation of estrogens as marker of human mammary tumors.

Estrogen is a known risk factor in human breast cancer. In rodent models, estradiol has been shown to induce tumors in those tissues in which this hormone is predominantly converted to the catechol metabolite 4-hydroxyestradiol by a specific 4-hydroxylase enzyme, whereas tumors fail to develop in organs in which 2-hydroxylation predominates. We have now found that microsomes prepared from human mammary adenocarcinoma and fibroadenoma predominantly catalyze the metabolic 4-hydroxylation of estradiol (ratios of 4-hydroxyestradiol/2-hydroxyestradiol formation in adenocarcinoma and fibroadenoma, 3.8 and 3.7, respectively). In contrast, microsomes from normal tissue obtained either from breast cancer patients or from reduction mammoplasty operations expressed comparable estradiol 2- and 4-hydroxylase activities (corresponding ratios, 1.3 and 0.7, respectively). An elevated ratio of 4-/2-hydroxyestradiol formation in neoplastic mammary tissue may therefore provide a useful marker of benign or malignant breast tumors and may indicate a mechanistic role of 4-hydroxyestradiol in tumor development.