Sam Milanovich, MD, Lab

 Milanovich Lab

Primary Research Focus

Dr. Milanovich Bio

Sam Milanovich, MD, and his lab’s team focus on studying the genetic and epigenetic regulation of normal blood cell development and how mutations on these processes lead to leukemic transformation. The goal is to define mechanisms that lead to the formation of leukemia stem cells.

Defining critical oncogenic molecular mechanisms and pathways in leukemia stem cells will improve understanding of leukemogenesis, and why some patients are cured by conventional therapies while others relapse. These understandings will help Dr. Milanovich’s team to identify distinct subsets of patients who may benefit from different therapeutic approaches.

This information can ultimately be used when designing novel therapies to specifically target leukemia stem cells while limiting toxicities to normal blood development, ultimately improving outcomes for pediatric leukemia patients.

Sam Milanovich
  • Associate scientist in the Children's Health and Cancer Biology Research Centers
  • Assistant professor at the University of South Dakota Sanford School of Medicine, Department of Pediatrics
  • Bachelor of Arts in biology, minor in psychology at Augustana College, Sioux Falls, SD
  • Medical degree at University of North Dakota School of Medicine & Health Science, Grand Forks, ND
  • Post-doctoral fellowship at the Medical College of Wisconsin, Blood Center of Wisconsin, Milwaukee, WI

Milanovich Lab Milanovich Lab

Behind the research

Acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) comprise the most common childhood cancers. Despite recent advances in therapy, acute leukemia remains a major cause of pediatric morbidity and mortality. Leukemia arises when normally developing hematopoietic precursors acquire leukemogenic mutations that transform them from normal hematopoietic stem cells or progenitors into leukemia stem cells.

Leukemia stem cells generate a heterogeneous, genetically diverse population of tumor cells that make up the bulk of the clinically detected, disease-causing tumor. These stem cells are characterized by unlimited self-renewal and have many biological differences from the bulk (non-stem cell) leukemia cells. These differences may cause leukemia stem cells to be more resistant to chemotherapy than the bulk tumor cells. Resistance of leukemia stem cells to conventional treatment explains why many cancers relapse months or years after therapy initially appears to have eradicated all detectable disease.

The Milanovich Lab utilizes a variety of methods to study molecular genetics in leukemia patient samples, leukemia cell lines and mouse models of normal blood and leukemia development.

Resources Positions Available
View Samuel Milanovich's publications here. Join a dedicated team of researchers and help shape the future of cancer treatments. See open positions here.
Meet members of the Milanovich lab here.  
 
Contact Us  
Phone: (605) 312-6409  
Email: samuel.milanovich@sanfordhealth.org  
 

 

Lab News

March 2017 Sam Milanovich, MD, co-authored a research article in Leukemia with Dr. Sridhar Rao of the BloodCenter of Wisconsin.These studies identify a novel epigenetic mechanism of disease in acute myelogenous leukemia (AML) patients with cohesion mutations. "The cohesion subunit of Rad21 is a negative regulator of hematopoietic self-renewal through epigenetic repression of Hoxa7 and Hoxa9.

November 2016, Dr. Milanovich was featured in a story by The Dickinson Press. The article highlights Dr. Milanovich's inspiration to research new diagnostic and therapeutic options for cancer patients. http://www.thedickinsonpress.com/news/local/4148053-fathers-battle-melanoma-helped-inspire-sons-cancer-research

August 2016, Dr. Milanovich co-authored a paper entitled "The cohesin subunit Rad21 is a negative regulator of hematopoeietic self-renewal through epigenetic repression of Hoxa7 and Hoxa9" in the journal Leukemia. http://www.ncbi.nlm.nih.gov/pubmed/27554164

August 2016, Dr. Sam Milanovich was the recent coauthor on a study in the journal Leukemia that focuses on the role of the cohesin subunit Rad21 as a negative regulator of hematopoietic stem cell self-renewal through repression of two other factors, HoxA7 and HoxA9. Genetic studies have discovered that mutations in the cohesin complex, a cellular structure often found in Acute Myeloid Leukemia (a type of blood cancer). In this study, the describe for the first time the process and mechanisms behind how these mutations cause leukemia; identifying pathways that may help guide future treatment options for patients with cohesin-mutated leukemia. http://www.ncbi.nlm.nih.gov/pubmed/27554164

August 2016, Dr. Sam Milanovich was recently invited to serve as an ad-hoc reviewer for the chapter “Hematopoiesis and Regenerative Medicine” in an e-book: Frontiers in Stem Cell and Regenerative Medicine Research.

News Archive