Cancer has been thought to progress as a linear series of genetic events. Researchers have suspected all tumor cells in leukemia share the same genetic abnormalities and growth properties, but new findings suggest that is not the case.
The new discovery unveils how genetic abnormalities transform normal cells into leukemic cells and the steps that have to happen to make those cells abnormal and aggressive. The new research also shed light on "how leukemic cells at different steps of genetic evolution respond to therapy, or contribute to relapse," said Dr. John Dick, Senior Scientist at OCI's Campbell Family Institute for Cancer Research, the research arm of Princess Margaret Hospital, and the McEwen Centre for Regenerative Medicine at University Health Network.
This means defective genes and their individual leukemia cell carriers are arranged in a more complex way than previously suspected.
The researchers also found that leukemia cells taken from patients with acute lymphoblastic leukemia (ALL) are comprised of multiple families of genetically distinct leukemia cells. The traced this cellular "family tree" back to its roots and found the cells that promote the disease persist through generations, and even separate to evolve other cancer families that are genetically distinct.
The finding could yield more effective target therapies.
Dr. Dick said deciphering the "complexity of cellular relationships and the existence of distinct genetic families of leukemia cells" will help researchers determine why some cancer cells are not destroyed by therapy and eventually regrow and cause disease relapse.
Acute lymphoblastic leukemia is a cancer of white blood cells in which malignant, immature white blood cells over-multiply in bone marrow. The disease is most common in childhood, and prognosis is generally good with a cure rate of about 80 percent. Adults with the disease face a 45 percent to 60 percent chance of long-term, disease-free survival.