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Placental Seratonin Critical For Brain Development
Plant Hormone Reveals Molecule Critical To Embryo
April 21, 2011--------News Archive
Insecticide Linked to Decrease In Cognitive Function
'Thirdhand Smoke' Poses Danger to Unborn Lungs
A Way To Predict Premature Birth?
Ovarian Cancer May Originate in Fallopian Tube
Parents Like Genetic Testing for Their Kids
Interventions Don't Always Net Healthy Newborn
New Approach to Treating MLL Leukemia In Babies?
The study involved a type of leukemia called mixed lineage leukemia, or MLL leukemia. Only 25 to 50 percent of babies diagnosed with MLL leukemia survive.
The study demonstrated how it may be possible to kill cancerous MLL cells by targeting a protein called DOT1. Researchers showed that, without the DOT1 protein, cancerous MLL cells died, said Charles Hemenway, MD, PhD, senior author of the study.
"We are focusing on the unique biology of MLL leukemia," Hemenway said.
The study was presented at the 2011 meeting of the American Association for Cancer Research in Orlando, Fla.
Between 5 and 10 percent of all leukemias are MLL positive. In children older than 1 who have MLL leukemia, the survival rate is about 75 percent. By comparison, the survival rate for most other childhood leukemias is about 90 percent. Adults who have MLL leukemia also have lower survival rates than any other type of leukemia.
MLL leukemia is caused by a mutation in the MLL gene. The mutated gene codes for an abnormal protein, turning a blood cell into a cancer cell. For reasons researchers don't understand, MLL is more resistant to chemotherapy than other forms of leukemia.
In previous studies, Loyola researchers developed a small molecule, called PFWT, to bind to the MLL protein. By binding to the MLL protein, the PFWT molecule effectively disables the protein, causing it to die. Later this year Hemenway plans to begin testing PFWT molecules on mice with MLL leukemia.
The new study also found a second possible way to attack MLL cells, by targeting the DOT1 protein. DOT1 works together with the MLL protein and is critical for keeping MLL cancer cells alive.
After culturing MLL cells from mice, researchers removed the gene coding for the DOT1 protein without which the cancerous cells died.
Loyola researchers are collaborating with researchers from Nemours/Alfred I. duPont Hospital for Children in Wilmington, Del., to identify additional molecules that could also disable DOT1.
Hemenway feel this double-barrel approach - targeting both the DOT1 and MLL proteins - potentially could be a more effective treatment than current chemotherapy against MLL, with fewer side effects. But it will take years of additional research and testing before such a treatment would be available for patients.
Hemenway is the Ronald McDonald House Charities Endowed Professor in Pediatric Oncology and division director of Pediatric Hematology/Oncology at Loyola University Chicago Stritch School of Medicine. Other co-authors are first author Ming-Jin Chang, a visiting doctoral student at Stritch and Jeffrey Lynn, PhD, a postdoctoral researcher at Cleveland Clinic who previously studied in Hemenway's lab.
The study was supported by the Leukemia & Lymphoma Society.