Colorado cancer researcher earns $1.4M ARRA grant
A two-year, $1.4 million American Recovery and Reinvestment Act grant will kick start dynamic research in acute myeloid leukemia, or AML, at the University of Colorado Cancer Center.
Dr. Christopher Porter, assistant professor of Pediatrics at the University of Colorado Denver School of Medicine and pediatric oncologist at The Children’s Hospital, is the beneficiary of the faculty recruitment grant. He will use the funds to employ high-tech screening tools to look for genes in AML that, when they are turned off, make it easier for conventional therapies to kill the cells.
About 12,800 American adults and children will be diagnosed with AML in 2009. While great strides have been made in curing other kinds of leukemia five year survival for AML is about 60 percent in children and less than 25 percent in adults.
"This grant gives me the freedom to do some experiments that may be a little bit riskier (than what typically gets federal funding) but have potential for very high reward," Porter said. "It also allows me to really improve the pace of research by hiring other folks to get it done in a better way by improving on the bioinformatics and screening methods that are currently available."
Porter will hire a research associate, a bioinformatics expert and a molecular biology or genetics expert to work on the project. ARRA grant recipients are required to use the funds to create or retain jobs and for projects that have high probability of moving quickly from the laboratory to the bedside.
Scientists believe that most cancers are driven by genes that are inappropriately expressed—turned on or off—in cells. Porter’s strategy will use small hairpin RNAs, or shRNAs, which are some of the cellular machinery that help control gene expression. Using a genome-wide shRNA library and next-generation gene sequencing technology as a screening tool, Porter will try to find out which shRNAs are less common or missing in AML cells that survive standard chemotherapy.
"These less common or missing shRNAs represent potential therapeutic targets to make AML cells more sensitive to standard therapy," Porter said, adding that this strategy for looking for treatment targets can apply to any cancer type.
"Once we have the system streamlined, I will be branching it out to other pediatric cancers," he said. "We’ll find these genes, validate them in animal models and find gene inhibiting drugs that work against them. The ultimate goal is to test a new treatment in clinical trials."