MYELOID NEOPLASIA Reduced ribosomal protein gene dosage and p53 activation in low-risk myelodysplastic syndrome
نویسندگان
چکیده
Departments of 1Genetics and 2Pathology, and 3Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, CA; 4Departments of Pathology and Clinical Laboratories, Memorial Sloan-Kettering Cancer Center, New York, NY; 5Department of Pediatrics, Stanford University, Stanford, CA; 6Department of Basic Medical Sciences, Purdue University, West Lafayette, IN; and 7Hudson Alpha Institute for Biotechnology, Huntsville, AL
منابع مشابه
Reduced ribosomal protein gene dosage and p53 activation in low-risk myelodysplastic syndrome.
Reduced gene dosage of ribosomal protein subunits has been implicated in 5q- myelodysplastic syndrome and Diamond Blackfan anemia, but the cellular and pathophysiologic defects associated with these conditions are enigmatic. Using conditional inactivation of the ribosomal protein S6 gene in laboratory mice, we found that reduced ribosomal protein gene dosage recapitulates cardinal features of t...
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Myelodysplastic syndrome (MDS) with interstitial deletion of a segment of the long arm of chromosome 5q [del(5q)] is characterized by bone marrow erythroid hyperplasia, atypical megakaryocytes, thrombocythemia, refractory anemia, and low risk of progression to acute myeloid leukemia (AML) compared with other types of MDS. The long arm of chromosome 5 contains two distinct commonly deleted regio...
متن کاملHaploinsufficiency for ribosomal protein genes causes selective activation of p53 in human erythroid progenitor cells.
Haploinsufficiency for ribosomal protein genes has been implicated in the pathophysiology of Diamond-Blackfan anemia (DBA) and the 5q-syndrome, a subtype of myelodysplastic syndrome. The p53 pathway is activated by ribosome dysfunction, but the molecular basis for selective impairment of the erythroid lineage in disorders of ribosome function has not been determined. We found that p53 accumulat...
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تاریخ انتشار 2011