Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 101, Issue 2, Pages 597-602Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0307203101
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Funding
- NCI NIH HHS [U01 CA084221, CA84221, CA84306, R01 CA072614, R37 CA072614, U01 CA084306, CA72614] Funding Source: Medline
- NIDDK NIH HHS [T32 DK007636, T32 DK07636] Funding Source: Medline
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RAS mutations are common in myeloid malignancies; however, it is not known whether oncogenic RAS can initiate leukemia. We show that expressing mutant K-RaSG12D protein from the endogenous murine locus rapidly induces a fatal myeloproliferative disorder with 100% penetrance characterized by tissue infiltration, hypersensitivity to growth factors, and hyperproliferation. Hematopoietic cells from diseased mice demonstrated increased levels of Ras-GTIP, but effector kinases were not constitutively phosphorylated and responded normally to growth factors. Oncogenic RAS is sufficient to initiate myeloid leukemogenesis in mice, and this provides an in vivo system for biologic and preclinical studies.
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