TP53 suppression promotes erythropoiesis in del(5q) MDS, suggesting a targeted therapeutic strategy in lenalidomide-resistant patients.
Caceres, Gisela; McGraw, Kathy; Yip, Bon Ham; Pellagatti, Andrea; Johnson, Joseph; Zhang, Ling; Liu, Kenian; Zhang, Lan Min; Fulp, William J; Lee, Ji-Hyun; Al Ali, Najla H; Basiorka, Ashley; Smith, Larry J; Daugherty, F Joseph; Littleton, Neil; Wells, Richard A; Sokol, Lubomir; Wei, Sheng; Komrokji, Rami S; Boultwood, Jacqueline; List, Alan F.
Proc Natl Acad Sci U S A
; 110(40): 16127-32, 2013 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-24043769
Analysis of clinical and molecular features of MDS patients with complex karyotype in China.
TP53 overexpression is an independent adverse prognostic factor in de novo myelodysplastic syndromes with fibrosis.
Myelodysplastic syndromes with 5q deletion: pathophysiology and role of lenalidomide.
Favorable impact of allogeneic stem cell transplantation in patients with therapy-related myelodysplasia regardless of <i>TP53</i> mutational status.
Characterization of TP53 mutations in low-grade myelodysplastic syndromes and myelodysplastic syndromes with a non-complex karyotype.
Clinical effect of increasing doses of lenalidomide in high-risk myelodysplastic syndrome and acute myeloid leukemia with chromosome 5 abnormalities.
Lenalidomide promotes p53 degradation by inhibiting MDM2 auto-ubiquitination in myelodysplastic syndrome with chromosome 5q deletion.
Clonal heterogeneity in the 5q- syndrome: p53 expressing progenitors prevail during lenalidomide treatment and expand at disease progression.
Jumping translocations: Short telomeres or pathogenic TP53 variants as underlying mechanism in acute myeloid leukemia and myelodysplastic syndrome?
Short- and long-term benefits of lenalidomide treatment in patients with lower-risk del(5q) myelodysplastic syndromes.