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and alcohol. In some countries, such as India and the Southeast Asian region, up to 50% of all cancers arise in the oral cavity. In these countries, betel quid consumption plays an important role. However, many cases of oral cancer develop without prior exposure to the previous agents. In these cases, viruses, diet, or genetic predisposition have been hypothesized to play the role (Rodu 2002, p. 511) In the field of molecular biology there are lots of studies to find out the genetic basis of tumor genesis. It is generally accepted that neoplasm arises from a series of genetic alterations that lead to cellular proliferation and differentiation (Warnakulasuriya and Johnson 1992, p.404). This genetic alteration may be induced by inactivation of tumor suppressor gene. The most common genetic abnormalities, found in different type of human cancers are the mutation of the tumor suppressor gene p53 (Chen, Yang and Li, 1996, p. 204). The p53 gene is located in the short arm of the chromosome no. 17 at the position of 17 p 13.1 (Warnakulasuriya and Johnson 1992, p. 404). The p53 pathway provides a physiological system for integrating signals from diverse insults and eliciting adaptive cellular responses that include growth arrest in G1 phase of cell cycle and apoptosis (Chang et al. 2000, p.56). Defects in the pathway are prevalent in cancer, most notably being associated with mis-sense mutations in p53 itself (Shahnavaz et al. 2000, p.407). Inactivation of p53 gene leads to the inability of a cell with DNA damage to induce cell cycle arrest to allow time for DNA repair or the induction of apoptosis (Piattelli et al. 2002, p.532). This leads to the inability of p53 to act as a transcription factor for some DNA repair enzymes and thus to the non-occurrence of downstream events. So the cell reluctantly turns on to a one way street that leads to malignant transformation (Neoplasia 1999, pp.260). The p53 gene mutation often results in a more stable gene product that is expressed as a tumor marker or biomarker by the tumor cells (Rich., Kerdpon & Reade, 1999) . According to most studies p53 is not detected in normal oral mucosa but it can be demonstrated with immunohistochemical techniques in oral squamous cell carcinoma (Chen, Yang and Li, 1996, p.204). Immunohistochemistry is a much simpler and easier method to detect expression of p53 protein than DNA sequencing (Castle et al. 1999, p.326). It can facilitate the identification of p53 over expression to specific cell types that molecular biological techniques can’t provide (Murti et al 1998). Therefore p53 immunohistochemistry may have a practical, clinical and pathological value (Shahnavaz et al. 2000, p. 407). To find out the pattern of specific mutation in oral squamous cell carcinoma, different studies have been done to assess the expression pattern of p53 oncoprotein (Cruz et al. 1998, p.99). But in our country no study has so far been done regarding expression pattern of p53 protein in oral precancerous lesions and oral squamous cell carcinoma. The present study was undertaken with the hope of achieving the goal in assessing the expression pattern of p53 protein in our country.

Thesis on oral cancer and bangladesh  

The term oral cancer encompasses all malignancies that originate in the oral tissues. Squamous cell carcinoma of the oral cavity comprises 9...

Thesis on oral cancer and bangladesh  

The term oral cancer encompasses all malignancies that originate in the oral tissues. Squamous cell carcinoma of the oral cavity comprises 9...