Acute myeloid leukemia with the 8q22;21q22 translocation: secondary mutational events and alternative t(8;21) transcripts.
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Molecular mechanisms of ETS transcription factor-mediated tumorigenesisAML1/ETO proteins control POU4F1/BRN3A expression and function in t(8;21) acute myeloid leukemiaAccelerated leukemogenesis by truncated CBF beta-SMMHC defective in high-affinity binding with RUNX1t(8;21)(q22;q22) Fusion proteins preferentially bind to duplicated AML1/RUNX1 DNA-binding sequences to differentially regulate gene expression.Chromosomal minimal critical regions in therapy-related leukemia appear different from those of de novo leukemia by high-resolution aCGH.The leukemogenic t(8;21) fusion protein AML1-ETO controls rRNA genes and associates with nucleolar-organizing regions at mitotic chromosomes.Modeling interactions between leukemia-specific chromosomal changes, somatic mutations, and gene expression patterns during progression of core-binding factor leukemiasCharacterization of a t(5;8)(q31;q21) translocation in a patient with mental retardation and congenital heart disease: implications for involvement of RUNX1T1 in human brain and heart development.Advances in molecular genetics and treatment of core-binding factor acute myeloid leukemiaThe human SWI/SNF complex associates with RUNX1 to control transcription of hematopoietic target genesRUNX1 repression-independent mechanisms of leukemogenesis by fusion genes CBFB-MYH11 and AML1-ETO (RUNX1-RUNX1T1).Attenuation of AML1-ETO cellular dysregulation correlates with increased leukemogenic potential.Effector caspases and leukemiaCooperation between RUNX1-ETO9a and novel transcriptional partner KLF6 in upregulation of Alox5 in acute myeloid leukemia.Negative effects of GM-CSF signaling in a murine model of t(8;21)-induced leukemia.PRMT1 interacts with AML1-ETO to promote its transcriptional activation and progenitor cell proliferative potentialOverexpression and knockout of miR-126 both promote leukemogenesisRUNX1 and RUNX1-ETO: roles in hematopoiesis and leukemogenesis.MiR-495 is a tumor-suppressor microRNA down-regulated in MLL-rearranged leukemia.Integrative genetic analysis of mouse and human AML identifies cooperating disease alleles.Genetics of therapy-related myelodysplasia and acute myeloid leukemia.RUNX1/AML1 DNA-binding domain and ETO/MTG8 NHR2-dimerization domain are critical to AML1-ETO9a leukemogenesis.The role of aberrant transcription factor in the progression of chronic myeloid leukemia.Restoration of MYC-repressed targets mediates the negative effects of GM-CSF on RUNX1-ETO leukemogenicity.RUNX1-ETO induces a type I interferon response which negatively effects t(8;21)-induced increased self-renewal and leukemia development.JAK inhibitors suppress t(8;21) fusion protein-induced leukemia.Targeted therapy: The new lease on life for acute promyelocytic leukemia, and beyond.AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches.Prognosis and monitoring of core-binding factor acute myeloid leukemia: current and emerging factors.Single-nucleotide polymorphism-array improves detection rate of genomic alterations in core-binding factor leukemia.Epigenetic Silencing of Eyes Absent 4 Gene by Acute Myeloid Leukemia 1-Eight-twenty-one Oncoprotein Contributes to Leukemogenesis in t(8;21) Acute Myeloid Leukemia.Upregulation of CD200R1 in lineage-negative leukemic cells is characteristic of AML1-ETO-positive leukemia in mice.Multivalent binding of the ETO corepressor to E proteins facilitates dual repression controls targeting chromatin and the basal transcription machinery.Multi-sites cleavage of leukemogenic AML1-ETO fusion protein by caspase-3 and its contribution to increased apoptotic sensitivity.RUNX1/ETO blocks selectin-mediated adhesion via epigenetic silencing of PSGL-1.Synergistic suppression of t(8;21)-positive leukemia cell growth by combining oridonin and MAPK1/ERK2 inhibitors.Acute myeloid leukemia with the t(8;21) translocation: clinical consequences and biological implications.Two cell lines of t(8;21) acute myeloid leukemia with activating KIT exon 17 mutation: models for the 'second hit' hypothesis.Therapy-related acute myeloid leukemia with t(8;21) (q22;q22) shares many features with de novo acute myeloid leukemia with t(8;21)(q22;q22) but does not have a favorable outcome.Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5.
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Acute myeloid leukemia with the 8q22;21q22 translocation: secondary mutational events and alternative t(8;21) transcripts.
description
2007 nî lūn-bûn
@nan
2007 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
name
Acute myeloid leukemia with th ...... ional events and alternative t
@nl
Acute myeloid leukemia with th ...... ternative t(8;21) transcripts.
@ast
Acute myeloid leukemia with th ...... ternative t(8;21) transcripts.
@en
type
label
Acute myeloid leukemia with th ...... ional events and alternative t
@nl
Acute myeloid leukemia with th ...... ternative t(8;21) transcripts.
@ast
Acute myeloid leukemia with th ...... ternative t(8;21) transcripts.
@en
prefLabel
Acute myeloid leukemia with th ...... ional events and alternative t
@nl
Acute myeloid leukemia with th ...... ternative t(8;21) transcripts.
@ast
Acute myeloid leukemia with th ...... ternative t(8;21) transcripts.
@en
P2093
P2860
P1433
P1476
Acute myeloid leukemia with th ...... ternative t(8;21) transcripts.
@en
P2093
Akiko Joo Okumura
Anita Boyapati
Dong-Er Zhang
Eun-Young Ahn
Joseph R Biggs
Luke F Peterson
Miao-Chia Lo
P2860
P304
P356
10.1182/BLOOD-2006-11-019265
P407
P577
2007-04-05T00:00:00Z