Stem Cell Biology Training Grant Trainees

Predoctoral trainees: Current students

Ifeola Akkinola

Ifeola Akkinola

MD/PhD dual-degree program, PhD in Integrative Biology & Physiology
Advisor: Angela Panoskaltsis-Mortari, PhD

I'm currently interested in regenerative medical research involving decellularized tissue. My main project in the lab is revealing the potential of iPSC-derived hemangioblasts for re-endothelization of pulmonary vessels.

Mikayla Hall

Mikayla Hall

PhD student, Biomedical Engineering
Advisor: Brenda Ogle, PhD

My project focuses on using the proteins of the extracellular matrix (ECM) to induce endothelial differentiation of induced pluripotent stem cells. I am also working to understand how ECM interacts with cells to influence differentiation to endothelial cells.

Miles Smith

Miles Smith
PhD student, Molecular, Cellular, Developmental Biology and Genetics
Advisor: R. Scott McIvor, PhD
 
Hunter syndrome is an X-linked lysosomal storage disease caused by a deficiency in the iduronate-2-sulfatase enzyme. In Hunter syndrome, the deficiency of iduronate-2-sulfatase in a cell results in a buildup of macromolecules known as glycosaminoglycans, which damage and disrupt the cell. My research focuses on exploring novel gene therapies for this disease that can ameliorate Hunter syndrome in both the body as well as the neurodegeneration in the central nervous system. Additionally, a therapy that addresses the neurodegeneration in Hunter syndrome could be expanded for use in other lysosomal storage diseases.

Garrett Draper

Garrett Draper

PhD student, Comparative Molecular Biosciences, Dept. of Pediatrics
Advisor: David Largaespada, PhD

The genetic tumor predisposition syndrome Neurofibromatosis type 1 (NF1) results from the inheritance of a mutant copy of NF1, a Ras-GAP tumor suppressor gene. Loss of the remaining wild-type allele in Schwann lineage cells leads to hyperactive Ras signaling, cell proliferation, and the formation of benign plexiform neurofibromas. These benign tumors can progress to lethal malignant peripheral nerve sheath tumors (MPNSTs). Although NF1 and other mutations have been associated with MPNST formation, their temporal dependence during Schwann cell development using a human cell model has not been studied. I aim to develop a model of induced MPNSTs (iMPNSTs) for a better understanding of the timing at which these mutations occur during Schwann cell development to result in MPNST formation.

Previous Trainees

2017-2019

  • Timothy Monko
  • Daniel Sorensen

2016-2018

  • Thera Lee
  • Natalya Goloviznina

2015-2017

  • Catherine Lee
  • Keith Sabin

2014-2015

  • Mathew Angelos
  • Christine Robinson

2013-2015

  • Jami Erickson
  • Michael Vanden Oever
  • Teng Zhang

2012-2015

  • Keli Holzapfel

2012-2013

  • Patrick Ferrell
  • Jacqueline Wendel

2011-2013

  • John Chan

2011-2012

  • David Knorr
  • Nathan Weidenhamer

2010-2012

  • Beau Webber

2011-2011

  • Krista Bluske