Jessica Blackburn, Ph.D.

Abeloff V Scholar*

Funded by Louisville Friends of V

Acute lymphoblastic leukemia is one of the most common and deadly childhood
cancers. Drugs that children are given often do not fully kill all of the leukemia cells.
A specialized cell, called a leukemia stem cell, preserves the leukemia through selfrenewal.
If one leukemia stem cell persists, the cancer can regrow and make a child
sick. Our goal is to find better ways to kill these cells so that we can cure patients.
One way that we do this is by studying leukemia stem cells in a zebrafish cancer
model, which is very similar to human disease. Here, we will use a new method to
find genes that are only expressed by leukemia stem cells. We will then look for
drugs that target these genes and can kill leukemia stem cells. The breakthroughs
that we make can be quickly applied to human disease because our studies are being
done in an animal model. Our research will give vital data about leukemia stem cells
and biology, and we hope we will discover new drugs to treat leukemia.

Bradley Bernstein, M.D., Ph.D. and John Mullen, M.D.

Support for the Liposarcoma Genome Project was funded by

Alex Gould and Friends in memory of Kathryn Gould.

Liposarcoma Genome Project –
Liposarcoma is the most common type of cancer that arises in soft tissue.  These tumors often present as low grade tumors initially, but a subset of patients will experience recurrence of a higher grade tumor.  Those patients who recur with higher grade tumors do poorly.  Therefore, our research focuses on understanding these high grade tumors.  We will explore the genetic changes between the low grade and high grade tumors in order to understand the molecular features that underlie high grade transformation.  We will begin by sequencing gene mutations in these tumors and surveying gene activity in each tumor type (Aim 1).   Mechanisms that govern which genes are on and off frequently involve how the DNA is packaged and structurally arranged in the cell.  Therefore, we will characterize the packaging (chromatin) and structure (topology) of the genomic DNA in these tumors (Aim 2).  By elucidating mechanisms by which tumor cells alter gene expression, we will better understand the genes and pathways that sustain them.  Finally, we will develop models of these tumors (Aim 3).  We can use these models to test driver genes and candidate therapeutic targets identified in our study.  We believe that our interdisciplinary team of clinicians and scientists is poised to complete the proposed aims, which should yield important insights into liposarcoma biology and guide future clinical strategies.

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