Molecular Changes in Oral Cancer Progression and Their Underlying Mechanisms - Essay Example

Alcohol has been found to be a primary risk factor in oral SCC.5 Other factors include tobacco consumption, genetic predisposition, viral infection, and denture related factors.2, 6, 7 The process of oral carcinogenesis is a multifactorial and multistep process occurring when epithelial cells are exposed to genetic alterations.8 Complex molecular changes associated with oncogenes, tumor suppressor genes (TSG), and other factors underlie the development and progression of oral cancer. A study of these molecular mechanisms is vital in order to better diagnose and detect oral cancer related alterations that are often invisible under a microscope.

8 The present paper outlines some of the molecular changes that are believed to contribute to oral cancer progression. The mechanisms underlying some of these molecular changes are also discussed. II. Progression of Oral Cancer The pathological progression of cancer takes place when normal cells are transformed to pre-malignant cells and then to malignant cells through the accumulation of mutations.9 The progression of oral cancer from dysplasia to the stage of metastasis is associated with multistage pathologic changes caused by molecular alterations.

10 The pathologic phenotypes involved in cancer progression include increase in cell proliferation, horizontal spread and survival, which are associated with molecular changes such as altered expression of molecules such as p53 that regulate cell cycle, altered growth factor response, altered protein metabolism and synthesis, and cell immortality associated with telomerase.10 The progression of oral cancer may also be attributed to other molecular changes that lead to the overproduction of growth factors, increase in the number of cell surface receptors, alterations in transcriptional factors and signal messengers, etc.8 III. Molecular Changes Contributing to the Progression of Oral Cancer As already stated, the progression of oral cancer occurs as a result of multistep genetic alterations resulting from molecular changes.

The normal functioning of the oncogenes and TSGs is altered due to which there is an increase in the production of growth factors, transcription factors, intracellular signal messengers and/or number of cell surface receptors.11 These alterations lead to phenotypic changes in the cell, which facilitate cell proliferation and suppress cell cohesion, subsequently enabling the infiltration of malignant cells.11 McGregor et al. have shown that the initial stages of oral cancer progression from the dysplasia stage are associated with loss of the expression of (RAR)-?

retinoic acid receptor, loss of expression of p16 cell cycle inhibitor, mutations in p53, and an increase in the levels of telomerase reverse transcriptase mRNA.12 There is an increase in the expression of the epidermal growth factor receptor after the dysplasia sta