Epigenetic Modifying Drugs and Cohesin Mutations in Leukemia

Ellen Drake, Oberlin College

Location

Science Center, A155

Document Type

Presentation

Start Date

4-24-2015 1:30 PM

End Date

4-24-2015 2:30 PM

Abstract

Acute myeloid leukemia (AML) affects more than 50,000 people annually, and approximately 50 percent of patients will succumb to this disease. New mutations in the cohesin complex pathway have recently been identified in 10-20 percent of patients with AML. Although cohesin’s role in alignment of sister chromatids is well described, recent studies have shown there to be no differences in karyotypic abnormality. This suggests an alternate mechanism for cohesin leading to disease. This genetic defect is always monoallelic in patients and results in predicted nonsense mediated decay. Given the dose effect nature of these abnormalities, they may be potential targets for therapeutic intervention. My goal is to determine the pharmacologic sensitivity of isogenic hematopoietic cells with cohesin subunit knockdown achieved by RNA interference.

Notes

Session 1, Panel 2 - Cellular Expression: Studies in Mutation, Digestion, and Mutualism
Moderator: Taylor Allen, Associate Professor of Biology

Major

Biology

Advisor(s)

Taylor Allen, Biology

Project Mentor(s)

Michael Moore, Biology

April 2015

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Apr 24th, 1:30 PM Apr 24th, 2:30 PM

Epigenetic Modifying Drugs and Cohesin Mutations in Leukemia

Science Center, A155

Acute myeloid leukemia (AML) affects more than 50,000 people annually, and approximately 50 percent of patients will succumb to this disease. New mutations in the cohesin complex pathway have recently been identified in 10-20 percent of patients with AML. Although cohesin’s role in alignment of sister chromatids is well described, recent studies have shown there to be no differences in karyotypic abnormality. This suggests an alternate mechanism for cohesin leading to disease. This genetic defect is always monoallelic in patients and results in predicted nonsense mediated decay. Given the dose effect nature of these abnormalities, they may be potential targets for therapeutic intervention. My goal is to determine the pharmacologic sensitivity of isogenic hematopoietic cells with cohesin subunit knockdown achieved by RNA interference.