Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA272531 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature
| PRJNA272423 | ENA
Project description:Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [Agilent]
| PRJNA272429 | ENA
Project description:Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [ChIP-Seq]
| PRJNA272428 | ENA
Project description:Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [DNAse-Seq]
| PRJNA272427 | ENA
Project description:The microarray gene expression pattern was studied using 798 different cancer cell lines. The cancer cell lines are obtained from different centers. Annotation information were provided in the supplementary file. golub-00327 Assay Type: Gene Expression Provider: Affymetrix Array Designs: HT_HG-U133A Organism: Homo sapiens (ncbitax) Tissue Sites: leukemia, Urinary tract, Lung, BiliaryTract, Autonomic Ganglion, Thyroid gland, Stomach, Breast, Pancreas, Head and Neck, Lymphoma, Colorectal, Placenta, Liver, Brain, Bone, pleura, Skin, endometrium, Ovary, cervix, Oesophagus, Connective and Soft Tissue, Muscle, Kidney, Prostate, Adrenal Gland, Eye, Testis, Smooth Muscle Tissue, Vulva, Unknow Material Types: cell, synthetic_RNA, whole_organism, total_RNA, BVG Disease States: M3 acute myeloid leukemia, hairy cell leukemia, transitional cell carcinoma, Adenocarcinoma, B cell lymphoma unspecified, Acute Lymphoblastic Leukemia, blast phase chronic myeloid leukemia, Carcinoma, M6 acute myeloid leukemia, Neuroblastoma, follicular carcinoma, ductal carcinoma, Burkitt Lymphoma, Squamous Cell Carcinoma, M5 acute myeloid leukemia, Mycosis Fungoides and Sezary Syndrome, Acute T-Cell Lymphoblastic Leukemia, Adult T-Cell Leukemia/Lymphoma, M2 Therapy-Related Myeloid Neoplasm, Choriocarcinoma, Plasma Cell Myeloma, Hepatocellular Carcinoma, anaplastic large cell lymphoma, primitive neuroectodermal tumor-medulloblastoma, M4 acute myeloid leukemia, B Acute Lymphoblastic Leukemia, Acute Leukemia of Ambiguous Lineage, Osteosarcoma, Hodgkin Lymphoma, Mesothelioma, chondrosarcoma, Glioblastoma Multiforme, Malignant Melanoma, carcinosarcoma-malignant mesodermal mixed tumor, bronchioloalveolar adenocarcinoma, chronic lymphocytic leukemia-small lymphocytic lymphoma, micropapillary carcinoma, diffuse large B cell lymphoma, myelodysplastic syndrome, giant cell carcinoma, teratoma, multipotential sarcoma, Small Cell Carcinoma, ASTROCYTOMA, Fibrosarcoma, mucoepidermoid carcinoma, Rhabdomyosarcoma, L1 Acute T-Cell Lymphoblastic Leukemia, Glioma, Anaplastic Astrocytoma, Non-small cell carcinoma, Large Cell Carcinoma, mucinous carcinoma, Acute Myeloid Leukemia, malignant fibrous histiocytoma-pleomorphic sarcoma, clear cell carcinoma, B cell lymphoma unspecified, Anaplastic Carcinoma, Ewings sarcoma-peripheral primitive neuroectodermal tumor, undifferentiated carcinoma, Sarcoma, Embryonal Rhabdomyosarcoma, epithelioid sarcoma, renal cell carcinoma, carcinoid-endocrine tumor, Synovial Sarcoma, lymphoid neoplasm, rhabdoid tumor, Refractory Anemia with Excess Blasts, Liposarcoma, biphasic mesothelioma, adrenal cortical carcinoma, adenosquamous carcinoma, L2 Acute T-Cell Lymphoblastic Leukemia, chronic myeloid leukemia, Micropapillary Serous Carcinoma, desmoplastic, acute leukemia, Retinoblastoma, teratocarcinoma, clear cell renal cell carcinoma, Follicular Lymphoma, Wilms Tumor, M7 acute myeloid leukemia, gliosarcoma, embryonal carcinoma, Leiomyosarcoma, medullary carcinoma, granulosa cell tumor, papillary carcinoma, NS Acute Lymphoblastic Leukemia, papillary transitional cell carcinoma, small cell adenocarcinoma, epithelial dysplasia, hyperplasia, tubular adenocarcinoma, metaplasia, papillary ductal carcinoma, chronic eosinophilic leukemia-hypereosinophilic syndrome, #N/A, malignant trichilemmal cyst, Medullary Breast Carcinoma, L2 Acute Lymphoblastic Leukemia, Osteoblastic Osteosarcoma
2015-05-16 | E-GEOD-68950 | biostudies-arrayexpress
Project description:Acute Myeloid Leukemia (AML) is a heterogeneous disease from the molecular and biological standpoints, and even patients with a specific gene expression profile may present clinical and molecular heterogeneity. We studied the epigenetic profiles of a cohort of patients that shared a common gene expression profile but differed in that only half of them harbored mutations of the CEBPA locus, while the rest presented with silencing of this gene and co-expression of certain T cell markers. DNA methylation studies revealed that these two groups of patients could be readily segregated in an unsupervised fashion based on their DNA methylation profiles alone. Furthermore, CEBPA silencing was associated with the presence of an aberrant DNA hypermethylation signature, which was not present in the CEBPA mutant group. This aberrant hypermethylation occurred more frequently at sites within CpG islands. CEBPA silenced leukemias also displayed marked hypermethylation when compared with normal CD34+ hematopoietic cells, while CEBPA mutant cases showed only mild changes in DNA methylation when compared to these normal progenitors. Biologically, CEBPA silenced leukemias presented with a decreased response to myeloid growth factors in vitro. Keywords: DNA methylation profiling Direct comparison of DNA methylation in leukemic blasts from 8 patients with Acute Myeloid Leukemia (AML) carrying a CEBPA mutation and 8 patients with AML without CEBPA mutation but with silencing of CEBPA expression. Two control groups are included: 8 CD34+ bone marrow samples from healthy donors and 9 samples of T Acute Lymphoblastic Leukemia (T-ALL) patients.
2010-05-07 | E-GEOD-14417 | biostudies-arrayexpress
Project description:Acute Myeloid Leukemia (AML) is a heterogeneous disease from the molecular and biological standpoints, and even patients with a specific gene expression profile may present clinical and molecular heterogeneity. We studied the epigenetic profiles of a cohort of patients that shared a common gene expression profile but differed in that only half of them harbored mutations of the CEBPA locus, while the rest presented with silencing of this gene and co-expression of certain T cell markers. DNA methylation studies revealed that these two groups of patients could be readily segregated in an unsupervised fashion based on their DNA methylation profiles alone. Furthermore, CEBPA silencing was associated with the presence of an aberrant DNA hypermethylation signature, which was not present in the CEBPA mutant group. This aberrant hypermethylation occurred more frequently at sites within CpG islands. CEBPA silenced leukemias also displayed marked hypermethylation when compared with normal CD34+ hematopoietic cells, while CEBPA mutant cases showed only mild changes in DNA methylation when compared to these normal progenitors. Biologically, CEBPA silenced leukemias presented with a decreased response to myeloid growth factors in vitro. Experiment Overall Design: Direct comparison of gene expression in leukemic blasts from 8 patients with Acute Myeloid Leukemia (AML) carrying a CEBPA mutation and 8 patients with AML without CEBPA mutation but with silencing of CEBPA expression, and with 9 samples of T Acute Lymphoblastic Leukemia (T-ALL) patients.
2009-01-24 | E-GEOD-14479 | biostudies-arrayexpress
Project description:Neutrophil production and function are primarily determined by granulocyte colony stimulating factor receptor (G-CSFR). G-CSFRs associated mutations (mostly localized in the transmembrane and cytoplasmic domains of the receptor) have been reported with several distinct hematological abnormalities as well as malignancies, e.g. severe congenital neutropenia (SCN), acute myeloid leukemia (AML) and chronic neutrophilic leukemia (CNL). Ibrutinib, a small molecule Bruton’s tyrosine kinase (BTK) inhibitor, is FDA approved and clinically used against B-cell related leukemia. In our previous published work (Dwivedi et al., Leukemia.2019;33:75–87), we have shown ibrutinib’s efficacy in the mutated G-CSFRs based leukemia model systems (mouse and human). However, the signaling mechanism of ibrutinib’s efficacy is not explored yet. Here, we present a unique SWATH-based label free quantitative proteomics analysis of the normal and mutated G-CSFRs signaling post ibrutinib treatment, using 32D cell-line-based in vitro model system.
2020-04-27 | PXD013402 | Pride
Project description:RIZ1 repression is associated with insulin-like growth factor-1 signaling activation in chronic myeloid leukemia...
| PRJNA91511 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE31941: Prognostic DNA Methylation Patterns in Cytogenetically Normal Acute Myeloid Leukemia are predefined by Stem Cell Chromatin Marks [gene expression] GSE32251: Prognostic DNA Methylation Patterns in Cytogenetically Normal Acute Myeloid Leukemia are predefined by Stem Cell Chromatin Marks [methylation] Refer to individual Series
2011-09-20 | E-GEOD-32252 | biostudies-arrayexpress