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Addiction of t(8;21) and inv(16) AML to native RUNX1

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45748 | GEO | 2013/08/17

SECONDARY ACCESSION(S): PRJNA196158

REPOSITORIES: GEO

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Addiction of t(8;21) and inv(16) AML to native RUNX1

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-08-17 | E-GEOD-45748 | biostudies-arrayexpress

Addiction of t(8;21) and inv(16) AML to native RUNX1 [Gene Expression data]

2013-08-18 | GSE45743 | GEO

Addiction of t(8;21) and inv(16) AML to native RUNX1 [ChIP-Seq data]

2013-08-18 | GSE45738 | GEO

Addiction of t(8;21) and inv(16) AML to native RUNX1 [ChIP-Seq data]

Project description:Cancer cells maintain a sensitive balance between growth-promoting oncogenes and apoptosis inhibitors. We show that WT RUNX1 is required for survival of t(8;21)-Kasumi-1 and inv(16)-ME-1 AML cell lines. The malignant AML phenotype is sustained by a delicate AML1-ETO/RUNX1 balance that involves competition for common DNA binding sites regulating a subset of AML1-ETO/RUNX1 targets. Genomewide sequencing data is included herein: Transcription factors RUNX1 c-terminus and n-terminus which is shared with AML1-ETO were profiled independently), AML1-ETO and AP4 were profiled using ChIP-Seq in Kasumi-1 cells, as well as control ChIP-Seq experiments of non immune serum. Two replicates were performed for each transcription factor profiling and control experiment.

2013-08-18 | E-GEOD-45738 | biostudies-arrayexpress

Addiction of t(8;21) and inv(16) AML to native RUNX1 [Gene Expression data]

Project description:Cancer cells maintain a sensitive balance between growth-promoting oncogenes and apoptosis inhibitors. We show that WT RUNX1 is required for survival of t(8;21)-Kasumi-1 and inv(16)-ME-1 AML cell lines. The malignant AML phenotype is sustained by a delicate AML1-ETO/RUNX1 balance that involves competition for common DNA binding sites regulating a subset of AML1-ETO/RUNX1 targets. Genome expression was profiled after performing knockdown of RUNX1 and AML1-ETO in Kasumi-1 cells using specific siRNA-oligo nucleotides, and analyzed using Affymetrix Gene 1.0 ST arrays.

2013-08-18 | E-GEOD-45743 | biostudies-arrayexpress

Secondary cytogenetic abnormalities in core-binding factor AML harboring inv(16) vs t(8;21).

Project description:Patients with core-binding factor (CBF) acute myeloid leukemia (AML), caused by either t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), have higher complete remission rates and longer survival than patients with other subtypes of AML. However, ∼40% of patients relapse, and the literature suggests that patients with inv(16) fare differently from those with t(8;21). We retrospectively analyzed 537 patients with CBF-AML, focusing on additional cytogenetic aberrations to examine their impact on clinical outcomes. Trisomies of chromosomes 8, 21, or 22 were significantly more common in patients with inv(16)/t(16;16): 16% vs 7%, 6% vs 0%, and 17% vs 0%, respectively. In contrast, del(9q) and loss of a sex chromosome were more frequent in patients with t(8;21): 15% vs 0.4% for del(9q), 37% vs 0% for loss of X in females, and 44% vs 5% for loss of Y in males. Hyperdiploidy was more frequent in patients with inv(16) (25% vs 9%, whereas hypodiploidy was more frequent in patients with t(8;21) (37% vs 3%. In multivariable analyses (adjusted for age, white blood counts at diagnosis, and KIT mutation status), trisomy 8 was associated with improved overall survival (OS) in inv(16), whereas the presence of other chromosomal abnormalities (not trisomy 8) was associated with decreased OS. In patients with t(8;21), hypodiploidy was associated with improved disease-free survival; hyperdiploidy and del(9q) were associated with improved OS. KIT mutation (either positive or not tested, compared with negative) conferred poor prognoses in univariate analysis only in patients with t(8;21).

| S-EPMC8152510 | biostudies-literature

Outcome and prognostic factors of CBF pediatric AML patients with t(8;21) differ from patients with inv(16).

Project description:PurposeTo explore the outcome and prognostic factors between inv(16) and t(8;21) disrupt core binding factor (CBF) in acute myeloid leukemia (AML).MethodsThe clinical characteristic, probability of achieving complete remission (CR), overall survival (OS) and cumulative incidence of relapse (CIR) were compared between inv(16) and (8;21).ResultsThe CR rate was 95.2%, 10-year OS was 84.4% and CIR was 29.4%. Subgroup analysis showed that patients with t(8;21) had significant lower 10-year OS and CIR than patients with inv(16). Unexpectedly, there was a trend for pediatric AML receiving five courses cytarabine to have a lower CIR than four courses cytarabine (19.8% vs 29.3%, P = 0.06). Among the cohort of no-gemtuzumab ozogamicin(GO) treatment, inv (16) patients showed a similar 10-year OS (78.9% vs 83.5%; P = 0.69) and an inferior outcome on 10-year CIR (58.6% vs 28.9%, P = 0.01) than those patients with t(8;21). In contrast, inv (16) and t(8;21) patients receiving GO treatment had comparable OS (OS: 90.5% vs. 86.5%, P = 0.66) as well as CIR (40.4% vs. 21.4%, P = 0.13).ConclusionOur data demonstrated that more cumulative cytarabine exposure could improve the outcome of childhood patients with t(8;21), while GO treatment was beneficial to the pediatric patients with inv(16).

| S-EPMC10210276 | biostudies-literature

Somatic mutational landscape of AML with inv(16) or t(8;21) identifies patterns of clonal evolution in relapse leukemia.

Project description: Not available

| S-EPMC4679720 | biostudies-literature

The ATRA-21 gene-expression model predicts retinoid sensitivity in CEBPA double mutant, t(8;21) and inv(16) AML patients.

Project description: Not available

| S-EPMC6769013 | biostudies-literature

Expression profiling of Mouse inv(16):TET2ko and AML patient granulocyte macrophage progenitor (GMP) cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-28 | GSE161392 | GEO