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Kristen Maslar –Research Statement This past summer, I attend the CPRIT Undergraduate Summer Research Program at MD Anderson Cancer Center in Houston, Texas. Dr. Brown’s Lab focuses on breast cancer research, specifically triple negative breast cancer research. During my time at MD Anderson, I was assigned an independent research project, which was presented on my final day of the internship. Being assigned an independent project helped me to formulate my own hypothesis and ask relevant questions related to my hypothesis. Also, it provided me with a foundation of new techniques and skills that would correlate with my research at my undergraduate university. For this project, I specifically researched ASPM and its effects on triple negative breast cancer. ASPM, abnormal spindle-like microcephaly-associated protein, is a mitotic spindle regulatory protein assisting in microtubule polymerization and centriole stabilization. It is expressed at low levels in normal tissues; however, previous studies in Dr. Brown’s lab identified ASPM as being both mutated and amplified in early lesions and invasive breast cancer. Based on this information, I ran several pertinent experiments to test the effects on ASPM. For these tests, I learned which cell lines were appropriate to use based on their distinguishing characteristics, ranging from premalignant cells (MCF10A/DCIS.com) to various types of triple negative breast cancer cell lines (MDA231, MDA468). Overall, the main approach for each experiment was knocking down ASPM using siASPM for each cell type. I learned how to set up and run a qPCR and immunofluorescence, which were used to validate the results in cell lines. Later, using the same knockdown technique, I analyzed the effect of ASPM inhibition on growth of normal, premalignant and invasive breast cancer cells using growth assays

Research Statement

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Kristen Maslar –Research Statement

This past summer, I attend the CPRIT Undergraduate Summer Research Program at MD Anderson Cancer Center in Houston, Texas. Dr. Brown’s Lab focuses on breast cancer research, specifically triple negative breast cancer research. During my time at MD Anderson, I was assigned an independent research project, which was presented on my final day of the internship. Being assigned an independent project helped me to formulate my own hypothesis and ask relevant questions related to my hypothesis. Also, it provided me with a foundation of new techniques and skills that would correlate with my research at my undergraduate university.

For this project, I specifically researched ASPM and its effects on triple negative breast cancer. ASPM, abnormal spindle-like microcephaly-associated protein, is a mitotic spindle regulatory protein assisting in microtubule polymerization and centriole stabilization. It is expressed at low levels in normal tissues; however, previous studies in Dr. Brown’s lab identified ASPM as being both mutated and amplified in early lesions and invasive breast cancer.

Based on this information, I ran several pertinent experiments to test the effects on ASPM. For these tests, I learned which cell lines were appropriate to use based on their distinguishing characteristics, ranging from premalignant cells (MCF10A/DCIS.com) to various types of triple negative breast cancer cell lines (MDA231, MDA468). Overall, the main approach for each experiment was knocking down ASPM using siASPM for each cell type. I learned how to set up and run a qPCR and immunofluorescence, which were used to validate the results in cell lines. Later, using the same knockdown technique, I analyzed the effect of ASPM inhibition on growth of normal, premalignant and invasive breast cancer cells using growth assays and cell cycle analysis, which were also new techniques acquired during my time at MD Anderson.

From the multiple experiments performed, the data indicated that knockdown of ASPM halted the cell cycle, leading the apoptosis. Therefore, the results suggested that ASPM may be a biomarker for breast cancer forming potential, as well as a putative prophylactic target.