Title

Characteriziation of Differential Protein Regulation of Meningioma Aggressiveness

Presenter

Anna Cichocki

Abstract

Meningioma tumors are the most common primary brain tumor, yet there is no effective chemotherapy treatment; surgery is the only option. These tumors are classified into three WHO grades according to histopathy. Ninety percent of meningioma cases are benign, but can evolve to become cancerous unexpectedly. This research was conducted to find a biomarker for meningioma malignancy by investigating five potential biomarker proteins (AKAP12, Rb-1, p53, SMAD2/3, and Merlin) based on protein expression in benign compared to malignant tumors. Using western blot methods, these proteins were tested in specimen tissue samples and cell lines to determine differences in regulation across the grades. We found that AKAP12 and Rb-1 were down-regulated. These findings and prior research of other cancers led to the theory that AKAP12 and Rb-1 may be in the same phosphorylation cascade that is involved with the cell aggressiveness in meningiomas via CDKs and cyclin kinases, particularly cyclin D.

Faculty Sponsor

Leena Knight

Sponsor Department/Programs

Biology

Tracks

Cells and Sickness

Terms of Use

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Location

Science 100

Presentation Type

Oral Presentation

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Apr 11th, 9:30 AM Apr 11th, 9:45 AM

Characteriziation of Differential Protein Regulation of Meningioma Aggressiveness

Science 100

Meningioma tumors are the most common primary brain tumor, yet there is no effective chemotherapy treatment; surgery is the only option. These tumors are classified into three WHO grades according to histopathy. Ninety percent of meningioma cases are benign, but can evolve to become cancerous unexpectedly. This research was conducted to find a biomarker for meningioma malignancy by investigating five potential biomarker proteins (AKAP12, Rb-1, p53, SMAD2/3, and Merlin) based on protein expression in benign compared to malignant tumors. Using western blot methods, these proteins were tested in specimen tissue samples and cell lines to determine differences in regulation across the grades. We found that AKAP12 and Rb-1 were down-regulated. These findings and prior research of other cancers led to the theory that AKAP12 and Rb-1 may be in the same phosphorylation cascade that is involved with the cell aggressiveness in meningiomas via CDKs and cyclin kinases, particularly cyclin D.

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