Abstract

The survival of patients with oral squamous cell carcinoma (OSCC) has not changed significantly in several decades especially woman, leading clinicians and investigators to search for promising molecular targets. To this case, we performed comprehensive genomic analysis of gene expression, copy number, methylation and point mutations in OSCC. Integrated analysis revealed more somatic events than previously reported, identifying four major driver pathways (mitogenic signaling, Notch, cell cycle, p53) and two additional key genes (p16, CDK4). The Notch pathway was defective in 66% of patients, and in follow-up studies of mechanism, functional NOTCH1 signaling inhibited proliferation of OSCC cell lines. Frequent mutation of CDK4/CDK6 defines a new molecular subtype of OSCC with few copy number changes. Although genomic alterations are dominated by loss of tumor suppressor genes, 80% of patients harbored at least one genomic alteration in a targetable gene, suggesting that novel approaches to treatment may be possible for this debilitating disease.

Keywords : malignant tumour,cauliflower alike,horn pearl formation

CHAPTER V CLOSING

5.1

Conclusion Oral Squamous Cell Carsinoma (OSCC) is caused by several multifactorial

like tobacco, alcohol, viruses, carcinogens, malnutrition, chronic candidiasis and radiation.Uncontrolled cell division also can change behavior of normal cell.If the behavior of the cell changed,it can expressed abnormal protein.Cell that have been mutate become dysplasia cell. Starting from mild dysplasia, moderate dysplasia, severe dysplasia, carcinoma in situ and then develop into invasive carcinoma.Tumor Suppressor Gene like p53 and p16 also can be accelerate growth of mutate cell. This suggests that p53 gene mutation may be an early step in the malignant conversion of Oral Squamous Cell Carsinoma.For that reason,it can be lead into malignant tumor.