Abstract

Background Malignant gliomas are the most common and lethal intracranial tumors. Glioma exhibit a relentless malignant progression characterized by widespread invasion throughout the brain, resistance to traditional and newer targeted therapeutic approaches. The classical genetic alterations in glioma target pathways governing cellular proliferation, cellular survival (apoptosis and necrosis), invasion, and angiogenesis. The p16 is the second most altered tumor suppressor gene and frequent mutations and deletions of p16 in human cancer cell lines first suggested an important role for p16 in carcinogenesis. The Bmi-1 is an important oncogene and its expression is found to be elevated in many types of cancers. Role of Bmi1 copy number variation in glioma is still under debate. In this study we analyzed the alterations in p16 and Bmi1 genes in glioma.

Highlights

  • Malignant gliomas are the most common and lethal intracranial tumors

  • We concluded that the p16 deletion is a common alteration found in glioma and Bmi1 gene amplification is not the common mechanism to increase the expression of this protein in glioma

  • Submit your manuscript to BioMed Central and take full advantage of: Results Our results showed that there is 20% of p16 deletion in our samples and the deletion pattern vary with exons

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Summary

Background

Malignant gliomas are the most common and lethal intracranial tumors. Glioma exhibit a relentless malignant progression characterized by widespread invasion throughout the brain, resistance to traditional and newer targeted therapeutic approaches. The classical genetic alterations in glioma target pathways governing cellular proliferation, cellular survival (apoptosis and necrosis), invasion, and angiogenesis. The p16 is the second most altered tumor suppressor gene and frequent mutations and deletions of p16 in human cancer cell lines first suggested an important role for p16 in carcinogenesis. The Bmi-1 is an important oncogene and its expression is found to be elevated in many types of cancers. Role of Bmi copy number variation in glioma is still under debate. In this study we analyzed the alterations in p16 and Bmi genes in glioma

Conclusions
Material and methods
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