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Pterygium is a chronic condition characterized by the encroachment of altered conjunctiva into the normal cornea. Several factors have been proposed as causative agents in the development of pterygium, however the exact mechanism of its pathogenesis is still unclear, even if several investigators consider pterygium an ultraviolet radiation (UV)-related disease. It is a relatively benign process, but since it displays tumor-like features, it has been proposed to be a neoplastic-like growth disorder (1). Vitamin D performs a number of functions outside of calcium homeostasis. Vitamin D status has been inversely associated with risk for various cancer, since Vitamin D inhibits cell proliferation, activates apoptotic pathways, inhibits angiogenesis, and exerts prodifferentiative effects in a wide variety of cancers (2). Since the antitumor actions of vitamin D are mediated primarily through Vitamin D receptor (VDR), and little is known about this subject in pterygium, the knowledge of VDR status may be important in understanding the pathogenesis of the disease. Keeping in mind all pathogenetic pterygium features, such as excessive cell proliferation, inflammation, fibrosis, extracellular matrix remodelling and intense neovascularization, we might suppose an alteration in the Vitamin D pathway. Therefore, the purpose of the study was to demonstrate, by immunohistochemistry on formalin-fixed and paraffin embedded sections of primary pterygium, the presence of VDR in pterygium, and to correlate it with the serum level of Vitamin D, in order to evaluate a possible role of Vitamin D pathway in the pathogenesis of the disease. The results will be discussed., Italian Journal of Anatomy and Embryology, Vol. 120, No. 1 (Supplement) 2015

It has been suggested that the invasive and metastatic potential of melanoma cells reflects their ability to undergo epithelial-mesenchymal transition (EMT)-like phenotypic changes (1). Important hallmarks of EMT include the loss of E-cadherin expression and increased expression of the cell adhesion molecule N-cadherin. This cadherin switch leads melanoma cells to lose contact with keratinocytes in the epi- dermis and interact instead with stromal fibroblasts and endothelial cells, thus promoting dermal and vascular melanoma invasion (2). In melanoma, up-regulation of N-cadherin can be induced by the overexpression of the transmembrane receptor Notch1, thus providing a mechanism that underlines increased melanoma cell adhesion, survival, growth, and tumor progression when Notch signaling is activated (3). In this study, the expression of N-cadherin and Notch1 was evaluated by immuno- histochemical analysis in primary cutaneous melanomas and lymph node metastases. First, we evaluated the prognostic impact of high N-cadherin expression on sur- vival in melanoma patients. Second, we correlated the expression of N-cadherin with the full clinicopathological data of patients. Third, we investigated the relationship between the expression of N-cadherin and Notch1. Moreover, N-cadherin expression was evaluated in dysplastic melanocytic nevi and in normal skin. The results will be discussed., Italian Journal of Anatomy and Embryology, Vol. 120, No. 1 (Supplement) 2015

GR is a nuclear receptor which, when activated by its specific ligand, can act as a transcription factor that binds to glucocorticoid response elements (GRE) or negative GRE. It affects inflammatory responses, differentiation and cell proliferation. The ligand activated glucocorticoid receptor induces a G1 cell cycle arrest or apoptosis in immature thymocytes and impairs proliferation of fibroblasts of undifferentiated mammary epithelial cells. It impairs proliferation and differentiation of neural progenitor cells in vivo and in vitro. Glucocorticoids are widely used in cancer therapy and have cell type-specific pro- or antiapoptotic effects. In melanoma, however, the antitumor activity of glucocorticoids remains an open question. A recent report demonstrated that in mouse embryo tissue and in human undifferentiated cells, cytoplasmic accumulation of GR is determined by nestin in conjunction with vimentin, copolymerised into an intermediate filament system, and that this anchoring of GR to the nestin/vimentin etheromeric complex is related to the maintenance of a high proliferation rate. The aim of this study was to analyse the expression of subcellular GR in cutaneous melanoma by immunofluorescence, immunohistochemistry and laser scanning confocal microscopy and to evaluate any effect in melanoma progression. The results will be discussed., Italian Journal of Anatomy and Embryology, Vol 117, No 2 (Supplement) 2012

Human breast carcinoma is a heterogeneous disease embracing different phenotypes with different biological characteristics. Transcriptional profiling has identified five breast cancer subtypes, of which the “basal epithelial” is the most aggressive, with a predilection for younger women, and correlates with poor prognosis. Nestin, an intermediate filament protein, was originally identified as a marker of neuroepithelial stem/progenitor cells in the brain. Recently, it was observed that nestin is expressed in basal/myoepithelial cells of the normal mammary gland and was also later found in cancer stem like cells of many tumors. Some studies showed that nestin is robustly immunohistochemically expressed in basal epithelial and triple negative breast tumors and that its expression correlates with survival patients. The increased expression of survivin, a member of the inhibitor-of-apoptosis (IAP) protein family, has been demonstrated to be associated with resistance to apoptosis. It has been reported that survivin and other IAP proteins cooperate to activate kinase cascades that control cell motility, thus stimulating tumour cell invasion and promoting metastasis. This mechanism seems to play a central role in breast cancer progression and resistance to treatment. The p53 protein represents the final effector of the p14CDKN2AMDM2 pathway; in majority of human cancers, the TP53 gene is functionally inactivated. Lack or reduced expression levels of the p53 protein seem to be associated with a defective apoptotic response to genotoxic damage and, thus, to anticancer agents. In this study, we evaluated the immunohistochemical expression of nestin in association with an anti-apoptotic protein, such as survivin, and a tumor suppressor factor, such as p53, and with Ki-67 proliferation index in bioptic samples of T4 breast tumors. The results will be discussed., Italian Journal of Anatomy and Embryology, Vol 116, No 1 (Supplement) 2011

Nestin, a class VI intermediate filament (IF) protein of rapidly proliferating progenitor cells and regenerating tissue, is considered as cancer stem cell marker of malignancies of neuroectodermal origin. It may play a role in connecting the components of the cytoskeleton and coordinate changes in cell dynamics. It is well known nestin copolymerizes with class III IF-proteins into heteromeric filaments, mostly vimentin, an intermediate filament overexpressed in various type of cancer. Moreover, nestin contributes to the disassembly of vimentin during mitosis. Vimentin is considered to be an ectodermal, neural and pancreatic progenitor cells marker, and its presence was detected in pancreatic cancer stem-like cells. The cancer stem cell hypothesis suggests that mutated melanocyte stem cells are present in skin as precursors of melanoma cells. Several investigations have provided evidence that the genetic and/or epigenic alterations occurring in the multipotent tissue-specific adult stem cells and/or their early progenies may lead to their malignant transformation into cancer progenitor cells. Melanomagenesis and tumor progression are commonly described as ‘de-differentiation’ processes of transformed, mature melanocytes; recently, it has also been demonstrated that metastatic melanoma cell lines exhibit morphological, phenotypic and functional features of stem cell population. Our recent study suggests that nestin expression in both tumoral and endothelial cells may be considered as an important early prognostic marker in melanoma; on the other hand vimentin overexpression in cancer well correlates with accelerated tumor growth, invasion, and poor prognosis. Based on these considerations, the aim of our study was to investigate the colocalization of nestin and vimentin in primary melanoma by immunofluorescence, and its association with clinico-pathological features and patients survival., Italian Journal of Anatomy and Embryology, Vol 116, No 1 (Supplement) 2011

Italian Journal of Anatomy and Embryology, Vol 115, No 1/2 (Supplement) 2010

Italian Journal of Anatomy and Embryology, Vol 115, No 1/2 (Supplement) 2010