Jackson Laboratory researcher develops better way to attack leukemia at its source
There is good news on the cancer and, more specifically, leukemia research front. Researchers led by Leonard Shultz at The Jackson Laboratory recently developed a new way to investigate a dangerous cancer, acute myelogenous leukemia, that promises to bring the medical field closer to a cure that has so far proven elusive. Clinical therapies for leukemia and other cancers are improving all the time, but cancer is a complicated and adaptable foe, so better techniques are needed to find more effective treatments and, better yet, preventions and cures.
Acute myelogenous leukemia (AML) is the most common adult leukemia. Chemotherapy treatments are generally effective at forcing the disease into remission, but in 70% of the cases there is a relapse, and 15% don’t respond to the initial treatment. Recent research has implicated a rare group of cancerous cells, called cancer stem cells, in the high incidence of cancer recurrence. Leukemic stem cells are rare and were only recently discovered, so researchers are still investigating their basic characteristics and function.
As reported online in Nature Biotechnology in October, Shultz and collaborators at Harvard Medical School and a number of Japanese institutions, including RIKEN, created a way to research human leukemia in mice. Using their system, the researchers characterized exactly where the stem cells locate within the bone marrow. Further, they demonstrated that leukemic stem cells can exclusively initiate and renew the disease, and that they are highly resistant to conventional chemotherapies that target fast-dividing cells.
The reason for the resistance is not yet entirely understood, but it’s thought that most stem cells are quiescent, or paused, in their cell division cycles and thereby evade chemotherapies. Working with the new research techniques, scientists now have the ability to focus on the development of patient-specific AML therapies that are targeted to leukemic stem cells.