Leukemia research by Cincinnati Children’s Hospital Medical Center gives us hope on a higher percentage of getting leukemia cured.
AML or Acute Myeloid Leukemia is caused by a disruption on the genetic programming of blood cells with the defect of chromosome 11q23. The survival rate is ranging from 20-40 percent. This urged the scientists of Cincinnati Children’s Hospital to look for a more effective treatment by doing a research with mice and donated human cells.
According to H. Leighton Grimes, PhD, principal investigator and Sarah Meyer, PhD, a former member of the Grimes Laboratory, the cancerous blood cells died and were replaced by healthy white blood cells when scientists blocked the target molecule on human AML cells in combination with other known treatments.
With the online publication of Journal of Experimental Medicine, the research suggests possible development on more effective treatment for AML, but according to Grimes, the findings of the research are not ready for clinical application.
Grimes, the director of the Cancer Pathology Program at Cincinnati Children’s Hospital said: “Our work provides a complete mechanistic look into the function of genetic and molecular programs driving this leukemia, and it exploits these processes to identify actionable therapeutic targets. We still have extensive additional testing to conduct in laboratory animal models of AML before knowing if this approach will translate to patient care.”
To identify sets of genes that show up in high numbers in MLL-AF9 leukemia, scientists conducted additional testing on the cells included computer-assisted analysis of the Molecular Signature Database. Additional biochemical testing on the cells was also conducted. With these tests, researchers found out that miR-196 directly targets and inhibits a gene called Cdkn1b/p27Kip1 (cyclin-Dependent Kinase Inhibitormolecular programming in leukemia stem cell that allows the cell to maintain aggressive MLL-AF9 leukemia.
According to Grimes normal blood stem cells or hematopoietic stem cells are not able to survive extensive cell division. The researchers discovered that when miR-196 targets Cdkn1b/p27Kip1, it quickens MLL-AF9 progression by abnormally linking stem cell activity with the growth of leukemia cells.
AML is killed depending on the dosage used with the experiment with human AML cell lines. Scientists are also applying this research with other tested treatments to see if they can get a more combined effect with AML treatment. Researchers approach the study to “represent a new opportunity for AML therapeutics.”