E647b6d5-9848-4cdf-823b-7420702008cb - samples
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ABSTRACT:
PROVIDER: EGAD00001006996 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Copy number and LOH analysis was performed for 56 chronic myeloid leukemia cases obtained from 23 CML cases obtained atchronic phase, accelerated phase, blast crisis, or remission. All caseswere genotyped with Affymetrix 250k Sty and Nsp arrays. Keywords: Acute leukemia, BCR-ABL1, chronic myeloid leukemia, copy number analysis, loss-of-heterozygosity, genomics *** Due to privacy concerns, the primary SNP array data is no longer available with unrestricted access. Individuals wishing to obtain this data for research purposes may request access using the Web links below. ***
2009-09-02 | GSE9110 | GEO
Project description:The Bmi1 Polycomb protein is involved in the epigenetic repressive control of self renewal and survival of cancer initiating cells. In Chronic Myeloid Leukemia (CML), bmi1 expression increases gradually as the disease progresses from a chronic latent phase to a deadly blast crisis. We developped an inducible shRNA system to silence Bmi1 in the human K562 chronic myeloid leukemia (CML) cell line in order to identify new Bmi1-target genes.
2015-05-12 | GSE54262 | GEO
Project description:Blast crisis (BC) predicts dismal outcomes in patients with chronic myeloid leukaemia (CML). We comprehensively investigated genetic abnormalities in 112 BC and 71 chronic phase (CP) samples obtained from 216 CML patients using exome and targeted sequencing.
| EGAS00001005075 | EGA
Project description:Chronic myeloid leukemia (CML) is a hematopoetic stem cell disease with distinct biological and clinical features. The biological foundation of the stereotypical progression from chronic phase through accelerated phase to blast crisis is poorly understood. We used DNA microarrays to compare gene expression in 91 cases of CML in chronic (42 cases), accelerated (17 cases), and blast phases (32 cases). Three thousand genes were found to be significantly (p<10-10) associated with the progression from chronic to blast phase. A comparison of the gene signatures of chronic, accelerated, and blast phases suggest that the progression of chronic phase CML from chronic advanced phase (accelerated and blast crisis) CML is a two-step rather than a three-step process, with new gene expression changes occurring early in accelerated phase before the accumulation of increased leukemia blast cells. The genetic signature of advanced phase CML is similar to that of normal CD34+ cells; however, progression also involved novel genes not expressed in normal CD34+ cells. Especially noteworthy is deregulation of the WNT/b-catenin pathway, the decreased expression of both JunB and Fos, and dysregulation of genes under the control of MZF1 and delta EF1 zinc finger transcription factors. Studies of CML patients who relapsed after initially successful treatment with imatinib mesylate demonstrated a gene expression pattern closely related to advanced phase disease. Take together, these data suggest that CML progression begins relative early and before clinical and pathological detection, and features distinct genetic differences compared to normal hematpoetic cells that might provide diagnostic and therapeutic targets. Samples from different phases of CML were hybridized against the pool of chronic phases of samples.
2010-06-11 | E-GEOD-4170 | biostudies-arrayexpress
Project description:The Bmi1 Polycomb protein is involved in the epigenetic repressive control of self renewal and survival of cancer initiating cells. In Chronic Myeloid Leukemia (CML), bmi1 expression increases gradually as the disease progresses from a chronic latent phase to a deadly blast crisis. We developped an inducible shRNA system to silence Bmi1 in the human K562 chronic myeloid leukemia (CML) cell line in order to identify new Bmi1-target genes. Gene profiling was performed on inducible shBmi1-K562 cells incubated without (P3-K562+shBMI1) or with doxycycline for 96h (P4-K562+shBMI1+doxycycline) using HG-U133 Plus2 Affymetrix Arrays.
2015-05-12 | E-GEOD-54262 | biostudies-arrayexpress
Project description:Chronic myeloid leukemia (CML) is a hematopoetic stem cell disease with distinct biological and clinical features. The biological foundation of the stereotypical progression from chronic phase through accelerated phase to blast crisis is poorly understood. We used DNA microarrays to compare gene expression in 91 cases of CML in chronic (42 cases), accelerated (17 cases), and blast phases (32 cases). Three thousand genes were found to be significantly (p<10-10) associated with the progression from chronic to blast phase. A comparison of the gene signatures of chronic, accelerated, and blast phases suggest that the progression of chronic phase CML from chronic advanced phase (accelerated and blast crisis) CML is a two-step rather than a three-step process, with new gene expression changes occurring early in accelerated phase before the accumulation of increased leukemia blast cells. The genetic signature of advanced phase CML is similar to that of normal CD34+ cells; however, progression also involved novel genes not expressed in normal CD34+ cells. Especially noteworthy is deregulation of the WNT/b-catenin pathway, the decreased expression of both JunB and Fos, and dysregulation of genes under the control of MZF1 and delta EF1 zinc finger transcription factors. Studies of CML patients who relapsed after initially successful treatment with imatinib mesylate demonstrated a gene expression pattern closely related to advanced phase disease. Take together, these data suggest that CML progression begins relative early and before clinical and pathological detection, and features distinct genetic differences compared to normal hematpoetic cells that might provide diagnostic and therapeutic targets. Keywords: disease state analysis
2006-02-21 | GSE4170 | GEO
Project description:Title: Gene expression analysis of indolent and aggressive forms of Chronic Myeloid Leukaemia (CML). Description: Chronic Myeloid Leukaemia presents in chronic phase (CP) and terminates in 'blast crisis'. Despite a common abnormality, the duration of CP is variable. The aim is to compare the gene expression profiles of the indolent and aggressive forms of CML. All samples were taken within 3 months of first diagnosis. Indolent patients were defined by chronic phase CML, duration minimum 7 years. Aggressive patients were defined by chronic phase, duration maximum 3 years.
2013-01-30 | E-MIMR-17 | biostudies-arrayexpress
Project description:Profiling CD34+ BCR-ABL+ cells of CML patients in chronic phase or blast crisis to identify differentially expressed stage-specific genes.
2006-08-08 | E-MEXP-480 | biostudies-arrayexpress
Project description:This study compares the epigenetic signatures of CD34+ cells from chronic phase chronic myeloid leukemia (CML) samples and blast phase CML samples v.s. normal CD34+ cells from cord blood and adult bone marrow samples. H3K27me3 genomic loci were detected by ChIP-seq.
2021-11-08 | GSE188241 | GEO
Project description:Effect of Sdc1 knockout in mouse blast crisis chronic myeloid leukemia (bcCML) cells
| PRJNA667784 | ENA