ABSTRACT
Although rare, subcutaneous air emphysema can occur during dental procedures such as endodontic treatment, surgical extractions, and preparing a tooth for an indirect or direct dental restoration. We report the development of a subcutaneous air emphysema that was introduced through the periodontal ligament of an untreated premolar after the use of an air syringe to dry the tooth.
Subject(s)
Bicuspid/surgery , Dental High-Speed Equipment/adverse effects , Subcutaneous Emphysema/etiology , Humans , Inlays/adverse effects , Inlays/methods , Male , Maxilla , Middle Aged , MouthABSTRACT
An understanding of the process by which tumor cells destroy the basement membrane of the surface epithelium, invade, and metastasize is essential to the development of novel treatment of head and neck squamous cell carcinoma (HNSCC). In recent years, there has been increased interest in the role of epithelial-mesenchymal transition (EMT) in invasion. EMT is a process that describes the development of motile, mesenchymal-like cells from non-motile parent epithelial cells. There are 3 known types of EMT that mediate development, wound healing, and carcinogenesis. This review summarizes studies of known EMT biomarkers in the context of HNSCC progression. The biomarkers discussed come from a wide range of proteins, including cell-surface proteins (E-cadherin, N-cadherin, and Integrins), cytoskeletal proteins (α-Smooth Muscle Actin, Vimentin, and ß-catenin), extracellular matrix proteins (Collagens, Fibronectin, and Laminin), and transcription factors (SNAIL1, SNAIL2, TWIST, and LEF-1). Overall, the findings of these studies suggest that EMT mediates HNSCC progression. The mechanistic role of the EMT markers that have been associated with HNSCC should be more clearly defined if new anti-HNSCC therapies to block EMT progression are to be developed.
Subject(s)
Biomarkers, Tumor/analysis , Carcinoma, Squamous Cell/pathology , Epithelial-Mesenchymal Transition/physiology , Neoplasm Invasiveness/pathology , Basement Membrane/pathology , Cell Adhesion/physiology , Cell Movement/physiology , Epithelial Cells/pathology , Head and Neck Neoplasms/pathology , Humans , Mesoderm/pathologyABSTRACT
Despite the dismal prognosis for patients with squamous cell carcinoma of the head and neck (SCCHN), there have been no novel treatments in over 40 years. Identification of novel tumor antigens in SCCHN will facilitate the identification of potential novel treatment targets. Tumor antigens are proteins selectively expressed by tumor cells and recognized by the host immune system. Phage-displayed tumor antigens were enriched by biopanning with normal and then SCCHN-specific serum. Ninety-six phage clones were sequenced for identification, and 21 clones were validated using Luminex. One of these proteins, L23, a novel tumor antigen in SCCHN, was validated as an oncogene. L23 is upregulated in SCCHN compared with normal keratinocytes. Knockdown of L23 inhibited proliferation, invasion and cell survival. Overexpression of L23 had the reverse effect. Overexpression of L23 in non malignant cells led to transformation. Injection of SCCHN cells with knockdown of L23 in mice, induced tumors that were significantly smaller than control tumors. In conclusion, the immunomic screen yielded a panel of antigens specific to SCCHN; one of these proteins, L23, is a novel oncogene in SCCHN.
Subject(s)
Antigens, Neoplasm/genetics , Autoantibodies/immunology , Biomarkers, Tumor/genetics , Carcinoma, Squamous Cell/immunology , Head and Neck Neoplasms/immunology , Ribosomal Proteins/genetics , Animals , Apoptosis/genetics , Biomarkers, Tumor/analysis , Biomarkers, Tumor/immunology , Carcinoma, Squamous Cell/genetics , Carcinoma, Squamous Cell/pathology , Case-Control Studies , Cell Line, Tumor , Cell Proliferation , Cell Surface Display Techniques , Gene Expression Regulation, Neoplastic , Head and Neck Neoplasms/genetics , Head and Neck Neoplasms/pathology , Humans , Keratinocytes/immunology , Mice , Mice, Nude , NIH 3T3 Cells , Oncogenes , Reference Values , Reproducibility of Results , Ribosomal Proteins/immunology , Squamous Cell Carcinoma of Head and NeckABSTRACT
Cytokines are critical mediators of inflammation and host defenses. Regulation of cytokines can occur at various stages of gene expression, including transcription, mRNA export, and post- transcriptional and translational levels. Among these modes of regulation, post-transcriptional regulation has been shown to play a vital role in controlling the expression of cytokines by modulating mRNA stability. The stability of cytokine mRNAs, including TNFα, IL-6, and IL-8, has been reported to be altered by the presence of AU-rich elements (AREs) located in the 3'-untranslated regions (3'UTRs) of the mRNAs. Numerous RNA-binding proteins and microRNAs bind to these 3'UTRs to regulate the stability and/or translation of the mRNAs. Thus, this paper describes the cooperative function between RNA-binding proteins and miRNAs and how they regulate AU-rich elements containing cytokine mRNA stability/degradation and translation. These mRNA control mechanisms can potentially influence inflammation as it relates to oral biology, including periodontal diseases and oral pharyngeal cancer progression.
