Timothy C. Hallstrom, PhD

Associate Professor, Department of Pediatrics

Timothy C. Hallstrom

Contact Info

halls026@umn.edu

Office Phone 612-626-2961

Fax 612-626-4074

Lab Phone 612-624-1910

Office Address:
Pediatric BMT
Masonic Cancer Research Building, MCRB 660D
425 East River Parkway
Minneapolis, MN 55455

Mailing Address:
Pediatrics BMT
MMC 366 Mayo
8366A (Campus Delivery Code)
420 Delaware St SE
Minneapolis, MN 55455

Administrative Assistant Name
Emily Kukacka

Administrative Phone
612-624-6926

Administrative Email
kukac003@umn.edu

Administrative Fax Number
612-626-4074

Postdoctoral Fellowship, Duke University, Durham, NC

PhD in Molecular Biology, University of Iowa, Iowa City, IA

Summary

Dr. Hallstrom received his Ph.D. in Molecular Biology at the University of Iowa in 1999. He then did post-doctoral studies with Joseph Nevins at Duke University studying the control of Rb/E2F induction of proliferation and apoptosis. He joined the University of Minnesota in 2007 as an assistant professor in the Department of Pediatrics Hematology and Oncology division.

Awards & Recognition

  • Elected Member, Society for Pediatric Research (2010-present)
  • Robert M. and Barbara R. Bell Award recipient, Duke Comprehensive Cancer Center for exceptional abilities in basic or translational research in areas relating to the diagnosis, cause, prevention or treatment of cancer (2007)

Research

Research Summary/Interests

Immune Response in Pediatric Retinoblastoma Tumors

Our research interests focus on two major areas. The first is on the pediatric cancer retinoblastoma, which forms in the retina of children and infants. This cancer is caused by deregulation of the Rb/E2F pathway. We developed a novel mouse retinoblastoma model that develops rapid bilateral tumors in both eyes. Recently, we learned that these tumors express a gene expression “signature” that causes recruitment and accumulation of immune cells to these tumors. Since this is a highly sought after clinical goal, we are elucidating the mechanisms of immune cell recruitment so they can be targeted to kill cancer cells.

Epigenetics of Retinal Development

The second major research interest is in the epigenetic control mechanisms responsible for normal retinal development. These mechanisms can malfunction in pediatric retinoblastoma, and may be harnessed during retinal regeneration to produce new retinal cell types after they’ve been lost. In particular, we study the retinal function of an epigenetic regulator called UHRF2, which binds to a DNA epigenetic base called 5-hydroxymethylcytosine (5hmC). It is still poorly understood how 5hmC accumulates during retinal development and how this leads to proper retinal gene expression. Furthermore, 5hmC is widely lost in human tumors, including retinoblastoma, although the mechanism behind its loss is unclear, as is the anti-tumor effectiveness of restoring 5hmC. We utilize genome-wide approaches to understand the altered gene expression and 5hmC distribution in retinal cells lacking the Uhrf2 gene.

Publications

Sarver AL, Xie C, Riddle MJ, Forster CL, Wang X, Lu H, Wagner W, Tolar J, Hallstrom TC. (2021) “Retinoblastoma tumor cell proliferation is negatively associated with immune-modulatory signals and immune infiltration”. Under revision, Lab Investigation.

Wang X. Sarver AL, Lu H, Xie C, Forster CL, Hallstrom TC. (2021) Reduced TET expression and 5hmC levels delay neural progenitor cell cycle progression and differentiation in Uhrf2 mutant retina. Under revision, Development.

Xie C, Freeman MJ, Forster CL, Hallstrom TC. (2017) “Retinoblastoma cells activate the AKT pathway and are vulnerable to anti-PI3K/mTOR therapeutics” Oncotarget.doi: 10.18632/oncotarget.16970.

Lu H, Bhoopatiraju S, Wang H, Schmitz NP, Forster CL, Verneris MR, Linden MA and Hallstrom TC. (2016) Loss of UHRF2 expression is associated with human neoplasia, promoter hypermethylation, decreased 5-hydroxymethylcytosine, and high proliferative activity. Oncotarget. 7(46):76047-76061.

Filtz EA, Emery A, Lu H, Forster CL, Karasch C, Hallstrom TC. (2015) Rb1 and Pten co-deletion in osteoblast precursor cells causes rapid lipoma formation in mice. PLOS ONE.10(8):e0136729. doi: 10.1371/journal.pone.0136729. eCollection 2015.

Xie C, Lu H, Nomura A, Hanse EA, Forster CL, Parker JB, Linden MA, Karasch C, Hallstrom TC. (2015) Co-deleting Pten with Rb in retinal progenitor cells in mice results in fully penetrant bilateral retinoblastomas.Molecular Cancer. 14(1) 93.

Lu H, Hallstrom TC. (2013) The nuclear protein UHRF2 is a direct target of the transcription factor E2F1 in the induction of apoptosis. J Biol Chem. 288(33):23833-43.