Myeloid-specific inactivation of p15Ink4b results in monocytosis and predisposition to myeloid leukemia
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چکیده
منابع مشابه
MYELOID NEOPLASIA Myeloid-specific inactivation of p15Ink4b results in monocytosis and predisposition to myeloid leukemia
1Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD; 2Laboratory of Molecular Oncology, Cancer Research Institute, Slovak Academy of Sciences, Bratislava, Slovakia; 3Department of Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, Washington, DC; and 4Centre for Biologics Research,...
متن کاملMyeloid-specific inactivation of p15Ink4b results in monocytosis and predisposition to myeloid leukemia.
Inactivation of p15INK4b, an inhibitor of cyclin-dependent kinases, through DNA methylation is one of the most common epigenetic abnormalities in myeloid leukemia. Although this suggests a key role for this protein in myeloid disease suppression, experimental evidence to support this has not been reported. To address whether this event is critical for premalignant myeloid disorders and leukemia...
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Germline testing for familial predisposition to myeloid malignancies is becoming more common with the recognition of multiple familial syndromes. Currently, Clinical Laboratory Improvement Amendments-approved testing exists for the following: familial platelet disorder with propensity to acute myeloid leukemia, caused by mutations in RUNX1; familial myelodysplastic syndrome/acute myeloid leukem...
متن کاملInherited predisposition to myeloid neoplasms
Myeloid neoplasms include myelodysplastic/ myeloproliferative neoplasms (MDS/MPN) and acute myeloid leukemia (AML). While majority of these disorders are still sporadic, it is becoming clear that a subset of them have a germline predisposition and is familial in nature. With the advancement and integration of molecular studies, it has been recognized that approximately 5-10% of hematological ma...
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ژورنال
عنوان ژورنال: Blood
سال: 2010
ISSN: 0006-4971,1528-0020
DOI: 10.1182/blood-2009-08-238360