Patients with two forms of leukemia, who currently have no viable treatment options, may benefit from existing drugs developed for different types of cancer, according to a study conducted by researchers at the Knight Cancer Institute at Oregon Health & Science University (OHSU).
Researchers at The Jackson Laboratory have identified a molecule that prevents repair of some cancer cells, providing a potential new “genetic chemotherapy” approach to cancer treatment that could significantly reduce side effects and the development of treatment resistance compared with traditional chemotherapy.
A new, pre-clinical study by researchers at Virginia Commonwealth University Massey Cancer Center suggests that a novel drug combination could lead to profound leukemia cell death by disrupting the function of two major pro-survival proteins. The effectiveness of the therapy lies in its ability to target a pro-survival cell signaling pathway known as PI3K/AKT/mTOR, upon which the leukemia cells have become dependent.
.A new study on how the progression of acute lymphocytic leukemia (ALL) is influenced by the bone marrow environment has demonstrated for the first time that targeting a specialized protein known as osteopontin (OPN) may be an effective strategy to increase the efficacy of chemotherapy in patients with this type of blood cancer. Study data were published online today in Blood, the Journal of the American Society of Hematology (ASH).
Two children with an aggressive form of childhood leukemia had a complete remission of their disease-showing no evidence of cancer cells in their bodies-after treatment with a novel cell therapy that reprogrammed their immune cells to rapidly multiply and destroy leukemia cells. A research team from The Children’s Hospital of Philadelphia and the University of Pennsylvania published the case report of two pediatric patients Online First today in The New England Journal of Medicine. It will appear in the April 18 print issue.
Scientists at Griffith University’s Institute for Glycomics and The Saban Research Institute of Children’s Hospital Los Angeles have discovered a critical weakness in leukaemic cells, which may pave the way to new treatments.
Scientists at the Walter and Eliza Hall Institute have for the first time visualised the molecular changes in a critical cell death protein that force cells to die.
The finding provides important insights into how cell death occurs, and could lead to new classes of medicines that control whether diseased cells live or die.
A new drug for patients with acute myeloid leukemia (AML) marked by a specific type of genetic mutation has shown surprising promise in a Phase II clinical trial. In more than a third of participants, the leukemia was completely cleared from the bone marrow, and as a result, many of these patients were able to undergo potentially curative bone marrow transplants, according to investigators at the Johns Hopkins Kimmel Cancer Center and nine other academic medical centers around the world. Many of the participants who did well with the new drug, quizartinib or AC220, had failed to respond to prior therapies.
Nine of twelve leukemia patients who received infusions of their own T cells after the cells had been genetically engineered to attack the patients’ tumors responded to the therapy, which was pioneered by scientists in the Perelman School of Medicine at the University of Pennsylvania. Penn Medicine researchers will present the latest results of the trial today at the American Society of Hematology’s Annual Meeting and Exposition.
- An estimated 10,200 Americans will die of acute myeloid leukemia (AML) in 2012, so new ways of treating the disease are needed.
- This study uses a novel class of experimental drugs to halt a process that helps AML cells develop and survive.
- The findings show that the agent is promising and should be considered for clinical trials testing.