Tumor-Inhibitor Protein Angiocidin Promotes Maturation of Leukemia Cells

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According to a presentation at the most recent meeting of the American Society of Hematology, a novel tumor-inhibiting protein called angiocidin appears to reduce leukemia cells by as much as two-thirds in pre-clinical experiments.

The presentation was given by the discoverer of angiocidin, Temple University School of Medicine's George P. Tuszynski.

In acute myeloid leukemia (AML), white blood cells do not mature. Consequently they proliferate, causing immunosuppression and some fatal problems, including pneumonia and other infections, along with bleeding problems.

Angiocidin's Unique Ability

Unlike many other anti-cancer drugs and prospective drugs, angiocidin doesn't kill cancer cells; rather it has shown the unique ability to encourage maturation in the white cells that are not maturing in this disease, allowing them to behave—and work—like healthy white blood cells.

In vitro studies demonstrate that angiocidin has a 50% success rate against AML, so the next step was seeing whether the same success rate would be found in vivo. Researchers did this by using a cell line from a patient and injecting it into a mouse model. By week 14, the AML cells had engrafted into the mouse bone marrow.

The injected mice were then treated with one of three treatments:

  1. Ara-C (cytosine arabinoside, the current standard of care in AML)
  2. Angiocidin
  3. Ara-C plus angiocidin

The results:

  • Mice treated with Ara-C: 40% reduction in leukemia cells
  • Mice treated with angiocidin: 63% reduction in leukemia cells
  • Mice treated with both: 79% reduction in leukemia cells

While these results are promising, Tuszynski cautioned that pre-clinical results speak little to the potential results of the treatment in humans. However, they do answer the question of whether angiocidin can get into the bone marrow and prevent the growth of AML cells.

A further positive attribute to angiocidin is that it has shown little or no evidence of being toxic.

Source: MNT

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