The NIH awarded $11.5 million grant to The University of Utah to Study Sarcomagenesis.
Using a mouse genetic model as a host and Sarcomas as the disease, The Jones lab, led by Kevin Bruce Jones, MD, investigates the genetic and epigenetic underpinnings of cancer initiation.
The two parts of a cancer cell are the normal cell from which it began (often called the cell of origin) and the genetic or epigenetic changes that changed it from a normal cell to a cancer cell (often termed the transforming events or just transformation.) Developmental biology is at the crux of both of these events.
Molecular pathways which, often with only small differences, decide the process of cell dividing and growing into a muscle, bone, or a limb and yet, they also decide the potential to be the origin of a tumor and happenings to bring the change about.
About a third of all sarcomas that were found in the 1990s associate with translocations. Chromosomes, which exist in pairs, can have an arm of one of them break off and translocate and swap a position of an arm of another. Each translocated chromosome will have a new gene formed at the junction site. This new gene contains the beginning of one gene and end of another. This new gene may contain characteristics that neither parent gene has.
Mice are used to study how these translocation-created fusion oncogenes drive sarcomagenesis. Other genes can be readily manipulated to test the importance of other pathways.
“The Jones lab uses mouse models that can activate the expression of the SS18-SSX fusion oncogenes at specific times in specific tissues to model the development of synovial sarcoma, a deadly soft-tissue cancer with predilection for young adults. This model recently revealed a unique Achilles heel of this tumor in the mitochondrial apoptosis pathway, or the means by which cancer cells fight off death signals. Work is ongoing to prepare for translation of this knowledge into a clinical trial for patients.”
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The University of Utah BioResearch Product Faire™ March 29th, 2019
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