ScienceDaily (Feb. 7, 2007) — Patients with so-called clonal myeloid disorders, such as myelofibrosis and some leukemias, often have bone marrow cells that are defective in making new blood cells, a process called hematopoiesis. Defective hematopoiesis may cause severe side effects and even death.

Laboratory studies have found that the bone marrow from patients with clonal myeloid disorders and defective hematopoiesis express abnormally high levels of various growth factors.

In a new study, Takayuki Nakayama, M.D, Ph.D., of the National Cancer Institute, and colleagues looked at the role of one of these growth factors, fibroblast growth factor 2 (FGF-2), in mouse and human cells. They found that FGF-2 inhibits a gene that is critical in regulating hematopoiesis. When they injected FGF-2 into mice, they found that the growth factor did indeed disrupt normal hematopoiesis.

"Thus, FGF-2 represents a promising therapeutic target for correction of hematologic abnormalities of clonal myeloid disorders and, potentially, other diseases," the authors conclude.

Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jncicancerspectrum.oxfordjournals.org/.

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The above story is reprinted from materials provided by Journal of the National Cancer Institute, via EurekAlert!, a service of AAAS.

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