Epigenetic mechanisms of IKAROS tumor suppressor in acute lymphoblastic leukemia
Conference Year
2022
Abstract
Hematopoietic malignancies are defined by genetic and epigenetic aberrations. The hematopoietic transcription factor IKAROS, encoded by IKZF1, coordinates chromatin structure to promote normal hematopoietic gene networks and is commonly mutated in precursor B cell acute lymphoblastic leukemia (preB-ALL). In patient derived cell models of preB-ALL, rescue of IKAROS function leads to cell cycle arrest; however, the mechanism behind IKAROS tumor suppression is incompletely understood. Here we investigate epigenetic deregulation in preB-ALL patient cell models to elucidate the mechanism of IKAROS tumor suppression. We identify alterations in global DNA methylation and chromatin accessibility patterns which may promote leukemogenic gene networks.
Primary Faculty Mentor Name
Seth Frietze
Graduate Student Mentors
Princess Rodriguez, PhD, Hana Paculova, PhD
Faculty/Staff Collaborators
Joseph Boyd, MS, Hilde Schjerven, PhD
Status
Graduate
Student College
College of Nursing and Health Sciences
Program/Major
Cellular, Molecular and Biomedical Sciences
Primary Research Category
Biological Sciences
Epigenetic mechanisms of IKAROS tumor suppressor in acute lymphoblastic leukemia
Hematopoietic malignancies are defined by genetic and epigenetic aberrations. The hematopoietic transcription factor IKAROS, encoded by IKZF1, coordinates chromatin structure to promote normal hematopoietic gene networks and is commonly mutated in precursor B cell acute lymphoblastic leukemia (preB-ALL). In patient derived cell models of preB-ALL, rescue of IKAROS function leads to cell cycle arrest; however, the mechanism behind IKAROS tumor suppression is incompletely understood. Here we investigate epigenetic deregulation in preB-ALL patient cell models to elucidate the mechanism of IKAROS tumor suppression. We identify alterations in global DNA methylation and chromatin accessibility patterns which may promote leukemogenic gene networks.