Is c-kit Gene Product involved in Epithelial-Mesenchymal Transition in Tongue Squamous Cell Carcinoma? A Pilot Study Oriented Towards Patient Outcome
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2017, Vol 1, Issue 3
Abstract
SSC: Squamous Cell Carcinomas; EMT: Epithelial-Mesnchymal Transition; PDGF: Platelet- Derived Growth Factor; SCF: Stem Cell Factor; HPF: High-Power –Fields; SMA: Smooth Muscle Antigen; PDGF: Platelet-Derived Growth Factor; GIST: Gastrointestinal Stromal Tumors.Over 90% of head and neck cancers are squamous cell carcinomas (SCC) which are the most common malignancies in the oral cavity. In spite of improved therapeutic procedures, SCCs generally exhibit poor prognosis and in addition, treatment results in significant functional and cosmetic defects. Several factors contribute to a poor prognosis for upper aerodigestive tract SCC patients including the delayed detection of cancerous lesions and the tendency to develop multifocal malignancy and premalignant lesions as a consequence of field cancerization. It has been generally accepted that prompt detection of early oral cancer or epithelial dysplasia is required to improve prognosis. Therefore it is important to identify markers for carcinoma progression. As with other cancers, most deaths of oral cancer, amongst them tongue cancers with greatest prevalence, result from local invasion and distant metastases. The landmark of carcinoma progression during the invasive and metastatic phases is epithelial cell plasticity and dedifferentiation, which is similar to epithelial-mesnchymal transition (EMT) that occurs during embryonic development. EMT is the process that cells undergo to switch from a polarized epithelial phenotype to a motile mesenchymal phenotype. This process can occur during embryonic development, wound healing, fibrosis and cancer progression and has extensively reviewed in the last ten years (kalluri and Nielsen 2003, thiery 2003, schiller 2004,thiery and sleeman2006) [1-3]. Loss of epithelial cell polarity and acquisition of motility results from the disappearance of cell junction adherence molecules, reorganization of cytoskeleton and redistribution of organelles (thiery and sleeman2006). Uncovering the mechanism for EMTs is one strategy to predict tumor progression and possibly develop therapeutic intervention. This is complicated by the diversity of molecular mechanisms contributing to the plasticity of epithelial cells in different tissues (gotzmann 2004) [4]. Several signal transduction pathways emerged as important for EMT, such as autocrine factors: EGF, HGF Insulinlike growth factor, platelet –derived growth factor, Want signaling, notch signaling, and Hedgehog signaling. These pathways are also controlled by crosstalk between each other and with RTK/Ras and TGF-b/bone morphogenic protein signaling.
Authors and Affiliations
DM Allon, Irit Allon, Ilana Kaplan, Dan Guttman
Keywords
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- EP ID EP570574
- DOI 10.26717/BJSTR.2017.01.000269
- Views 144
- Downloads 0
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