PubMed · 14077764
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C LORDY, E B RIBEIRO. 1963. [STRUMA POSTBRANCHIALIS].. https://pubmed.ncbi.nlm.nih.gov/14077764/
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Primary adenocarcinoma of the nasolacrimal drainage system is a highly uncommon diagnosis, which is presumably derived from malignantly transformed glandular cells that are interspersed amongst the epithelium of the nasolacrimal duct. The patients usually present with unspecific orbital or sinus-nasal symptoms. An appropriate therapeutic regime consists of a preferably early, radical resection and local postoperative radiation therapy. This brief contribution deals with an especially uncommon case of a carcinoma of the nasolacrimal drainage system. On his first presentation, the 62-year old patient complained about right sided epiphora which had been present over the last few weeks. Eight years prior to presentation, he had been treated for a nasolacrimal duct stenosis by endoscopic dacryocystorhinostomy on this side. Diagnostic imaging revealed a soft tissue mass in the right nasolacrimal duct which was removed by a combined extra-endonasal approach. The final histopathological evaluation was adenocarcinoma. Following postoperative radiotherapy, the patient has been free of disease for 42 months. The occurrence of adenocarcinoma of the nasolacrimal drainage system in the setting of previous surgery may provide a new insight into the clinical spectrum of the natural history of this disease.
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Transforming growth factor (TGF) beta is a potent regulator of cell-matrix and cell-cell adhesions (collectively termed cellular adhesions). Cellular adhesions play crucial roles in controlling the differentiation of epithelial cells and in maintaining the integrity of the epithelium. Loss of TGF beta-responsiveness is thought to be an important early initiating event in the malignant progression of epithelial cancer. In the TGFbeta-responsive human colon adenocarcinoma Moser cells, TGFbeta promotes cellular adhesions and suppresses their malignant phenotype. TGFbeta promotes cell-matrix adhesion by inducing the synthesis of extracellular matrix (ECM) adhesion molecules and the expression of integrin receptors for these molecules (termed ECM remodeling). TGFbeta promotes cell-cell adhesion through the induction of E-cadherin expression, an epithelial associated homotypic cell-cell adhesion molecule, which also functions as a tumor suppressor in colon cancer. How TGFbeta regulates E-cadherin expression is not known. In this study, we showed that the induction of E-cadherin by TGFbeta was mediated through the activation of focal adhesion kinase (FAK), a major signaling molecule in focal adhesion contacts and that the activation of FAK was due to ECM remodeling and increased cell-matrix interactions. Thus, TGFbeta regulates cell-cell adhesion through its ability to remodel the ECM and to activate FAK through ECM remodeling.