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Late-Breaking Data Highlighting Research Advances in Several Blood Disorders to Be Presented At the American Society of Hematology Annual Meeting
Date:12/6/2008

ofile and did not reveal any new or unexpected safety concerns.

TET2 is a Novel Tumor SuppressorGene Inactivated in Myeloproliferative Neoplasms: Identification of a Pre-JAK2 V617FEvent [LBA-3]

Francois Delhommeau, M.D., Saint-Antoine Hospital,Paris, France

*Abstract LBA-3 is being presented on Saturday, December 6, at 2:00 p.m. at the ASH press conference on treatment advances in leukemia and lymphoma. The embargo for this abstract will break at that time.

This research unveiled a new tumor suppressor gene called TET2 (Ten-Eleven Translocation-2), which is altered in 14 percent of patients with myeloproliferative disorders, providing scientists with a greater understanding of the underlying biology of these conditions, as well as a potential target for the development of future treatments.

All blood cells start out as hematopoietic, or blood-forming, stem cells and have the potential to become mature red blood cells, white blood cells, or platelets. Myeloproliferative disorders develop when the DNA of a stem cell is altered in the bone marrow, causing the overproduction of some blood cells.

Previous research has detected mutations in other genes -- JAK2 and MPL -- in the blood stem cells of patients with myeloproliferative disorders. These JAK2 and MPL defects cause the overproduction of mature malignant blood cells, but multiple lines of evidence suggest that these are not the only molecular lesions responsible for abnormalities in the stem cell in these disorders. Greater analysis of blood cell development in myeloproliferative disorders with the JAK2 V617Fmutation led researchers to identify two subsets of patients. The first su
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SOURCE American Society of Hematology
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