Angiocidin, a novel tumor-inhibiting protein, has been shown to reduce acute myeloid leukemia (AML) cells in vivo by almost two-thirds in pre-clinical experiments.
George P. Tuszynski, a professor of neuroscience in Temple University's School of Medicine who discovered Angiocidin, will present the findings during the American Society of Hematology's national meeting in Atlanta on Dec. 9.
AML causes certain white blood cells to stop maturing, resulting in their uncontrolled proliferation, which can lead to suppression of the immune system and often fatal secondary problems such as infections, including pneumonia, and an increased risk for bleeding.
In earlier in vitro studies using four AML cell lines and patient AML cells, Angiocidin demonstrated the ability to stimulate maturation in the affected white cells, causing them to behave and function like normal cells.
With 50 percent success in the in vitro patient studies, the researchers next focused on how Angiocidin would perform against cells from AML patients in vivo. Samples from a patient were injected into a special mouse model developed by Martin Carroll, associate professor of medicine at the University of Pennsylvania. Over a 14 week period, the leukemia cells engrafted to the bone marrow of the mice.
The mice were then given doses of Ara-C, Angiocidin or a combination of both. The chemotherapy agent Ara-C, or cytosine arabinoside, is standard-of-care for AML and kills cancer cells by inhibiting DNA synthesis.
Mice treated only with Angiocidin saw a 63 percent reduction in AML cells, while those treated with both experienced a 79 percent reduction in AML cells. Mice treated with Ara-C alone saw a reduction of only around 40 percent.