Pediatric AML and normal bone marrow
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE2191 | GEO | 2005/01/28
SECONDARY ACCESSION(S): PRJNA91251
REPOSITORIES: GEO
Similar Datasets
Project description:Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults and the second most common form of leukemia in children. Multiple lncRNAs participate in normal and may be implicated in malignant hematopoiesis associated with blood cell cancers, such as leukemia. Currently, the expression profile of lncRNAs in pediatric AML is unclear. In this study, we evaluated the lncRNA expression profile in the tissue of three pediatric AML patients with lncRNA microarray techniques. In order to gain insight into the function of targets of lncRNAs, GO term and KEGG pathway annotation were applied to the target gene pool. qPCR was performed to evaluate the expression patterns of dys-regulated lncRNAs. Bone marrow specimens were obtained at the time of diagnosis during routine clinical assessment of 3 pediatric patients with AML, who presented at the Department of Hematology and Oncology, Children's Hospital of Soochow University between 2000 and 2011. Additionally, bone marrow samples from 3 healthy donors were analyzed as controls. Human LncRNA Array analysis was performed by KangChen Bio-tech, Shanghai P.R. China. Total RNA from each sample was quantified by the NanoDrop ND-1000 and RNA integrity was assessed by standard denaturing agarose gel electrophoresis. For microarray analysis, Agilent Array platform was employed. The sample preparation and microarray hybridization were performed based on the manufacturerâs standard protocols with minor modifications. Briefly, mRNA was purified from total RNA after removal of rRNA (mRNA-ONLY⢠Eukaryotic mRNA Isolation Kit, Epicentre). Then, each sample was amplified and transcribed into fluorescent cRNA along the entire length of the transcripts without 3â bias utilizing a random priming method. The labeled cRNAs were hybridized onto the Human LncRNA Array v2.0 (8 x 60K, Arraystar). After having washed the slides, the arrays were scanned by the Agilent Scanner G2505C. Agilent Feature Extraction software (version 11.0.1.1) was used to analyze acquired array images. Quantile normalization and subsequent data processing were performed using the GeneSpring GX v12.0 software package (Agilent Technologies). After quantile normalization of the raw data, LncRNAs and mRNAs that at least 4 out of 6 samples have flags in Present or Marginal (âAll Targets Valueâ) were chosen for further data analysis. Differentially expressed LncRNAs and mRNAs with statistical significance between the two groups were identified through Volcano Plot filtering. Pathway analysis and GO analysis were applied to determine the roles of these differentially expressed mRNAs played in these biological pathways or GO terms. Finally, Hierarchical Clustering was performed to show the distinguishable LncRNAs and mRNAs expression pattern among samples.
2015-12-31 | E-GEOD-65263 | biostudies-arrayexpress
Project description:Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults and the second most common form of leukemia in children. Multiple lncRNAs participate in normal and may be implicated in malignant hematopoiesis associated with blood cell cancers, such as leukemia. Currently, the expression profile of lncRNAs in pediatric AML is unclear. In this study, we evaluated the lncRNA expression profile in the tissue of three pediatric AML patients with lncRNA microarray techniques. In order to gain insight into the function of targets of lncRNAs, GO term and KEGG pathway annotation were applied to the target gene pool. qPCR was performed to evaluate the expression patterns of dys-regulated lncRNAs.
2015-12-31 | GSE65263 | GEO
Project description:This series represents leukemic samples obtained from pediatric AML patients at diagnosis and control normal bone marrow samples.
2007-08-25 | E-GEOD-2191 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) play a pivotal role in the regulation of hematopoiesis and development of leukemia. Great interest emerged in modulating miRNA expression for therapeutic purposes. In order to identify miRNAs, which specifically suppress leukemic growth of AML with t(8;21), inv(16) or MLL-rearrangement by inducing differentiation, we conducted a miRNA expression profiling in a cohort of 90 cytogenetically characterized, de novo pediatric AML cases. Four miRNAs, specifically downregulated in MLL-rearranged, t(8;21) or inv(16) AMLs, were characterized by their tumor suppressive properties in cell lines representing those respective cytogenetic groups. Among those, forced expression of miR-9 reduced leukemic growth and induced monocytic differentiation of t(8;21) AML cell lines in vitro and in vivo. The tumor suppressive functions of miR-9 were specifically restricted to AML cell lines and primary leukemic blasts with t(8;21). On the other hand, these functions were not evident in AML blasts from patients with MLL-rearrangements. We showed that miR-9 exerts its effects through the cooperation with let-7 to repress the oncogenic LIN28B/HMGA2 axis. Thus, miR-9 is a tumor suppressor-miR which acts in a stringent cell context-dependent manner. In order to identify miRNAs, which specifically suppress leukemic growth of AML with t(8;21) (n=21), inv(16) (n=17) or MLL-rearrangement (n=35) by inducing differentiation, we conducted a miRNA expression profiling in a cohort of 90 cytogenetically characterized, de novo pediatric AML cases, which also included 12 t(15;17) and 5 t(7;12) samples.
2014-01-01 | E-GEOD-52541 | biostudies-arrayexpress
Project description:Gene expression data were obtained from 130 pediatric AML patients who were enrolled on the AML99 study conducted by the Japanese Childhood AML Cooperative Study Group. RNA samples obtained at the time of diagnosis were analyzed using GeneChip Human Genome U133 plus 2.0 array (Affymetrix).
2013-04-01 | E-GEOD-35784 | biostudies-arrayexpress
Project description:In high income countries 90% of the patients achieve complete remission after induction chemotherapy. However, 30-40% of these patients suffer from relapse. These patients face a dismal prognosis, as the majority (>60%) of relapsed patients die within 5 years. As a result, outcome for pediatric acute myeloid leukemia (AML) patients remains poor and has stabilized over the past 15 years. To prevent or better treat relapse of AML is the best option to improve outcome. Despite patient specific differences, most patients do respond to initial therapy. This suggests that at relapse, mechanisms are active that cause the altered response to chemotherapy. Detailed understanding of mechanisms that cause relapse remain largely elusive. To gain insight in the molecular pathways that characterize relapsed AML, we performed genome wide gene expression profiling on paired initial diagnosis and relapsed AML samples of 23 pediatric AML patients. We used pathway analysis to find which molecular pathways are involved in altered gene expression between diagnosis and relapse samples of individual AML patients. 23 paired diagnosis and relapse bone marrow or peripheral blood samples were collected and cryo-preserved. They were later thawed and processed for hybridization to Affymetrix U133 Plus 2.0 arrays.
2015-05-07 | E-GEOD-52891 | biostudies-arrayexpress
Project description:In high income countries 90% of the patients achieve complete remission after induction chemotherapy. However, 30-40% of these patients suffer from relapse. These patients face a dismal prognosis, as the majority (>60%) of relapsed patients die within 5 years. As a result, outcome for pediatric acute myeloid leukemia (AML) patients remains poor and has stabilized over the past 15 years. To prevent or better treat relapse of AML is the best option to improve outcome. Despite patient specific differences, most patients do respond to initial therapy. This suggests that at relapse, mechanisms are active that cause the altered response to chemotherapy. Detailed understanding of mechanisms that cause relapse remain largely elusive. To gain insight in the molecular pathways that characterize relapsed AML, we performed genome wide gene expression profiling on paired initial diagnosis and relapsed AML samples of 23 pediatric AML patients. We used pathway analysis to find which molecular pathways are involved in altered gene expression between diagnosis and relapse samples of individual AML patients.
2015-05-07 | GSE52891 | GEO
Project description:Pediatric acute myeloid leukemia (AML) is a heterogeneous disease characterized by non-random genetic aberrations related to outcome. Detecting these aberrations however still lead to failures or false negative results. Therefore, we focused on the potential of gene expression profiles (GEP) to classify pediatric AML. Gene expression microarray data of 237 children with AML were generated and cases were split into a discovery cohort (n=157) and an independent validation cohort (n=80). Next, a double-loop cross validation approach was used to generate a subtype-predictive GEP in the discovery cohort which was then tested for its true predictive value in the independent validation cohort. 237 bone marrow and peripheral blood samples were collected at diagnosis and frozen. They were later thawed and hybridized to Affymetrix U133 Plus 2.0 arrays.
2010-10-21 | E-GEOD-17855 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) play a pivotal role in the regulation of hematopoiesis and development of leukemia. Great interest emerged in modulating miRNA expression for therapeutic purposes. In order to identify miRNAs, which specifically suppress leukemic growth of AML with t(8;21), inv(16) or MLL-rearrangement by inducing differentiation, we conducted a miRNA expression profiling in a cohort of 90 cytogenetically characterized, de novo pediatric AML cases. Four miRNAs, specifically downregulated in MLL-rearranged, t(8;21) or inv(16) AMLs, were characterized by their tumor suppressive properties in cell lines representing those respective cytogenetic groups. Among those, forced expression of miR-9 reduced leukemic growth and induced monocytic differentiation of t(8;21) AML cell lines in vitro and in vivo. The tumor suppressive functions of miR-9 were specifically restricted to AML cell lines and primary leukemic blasts with t(8;21). On the other hand, these functions were not evident in AML blasts from patients with MLL-rearrangements. We showed that miR-9 exerts its effects through the cooperation with let-7 to repress the oncogenic LIN28B/HMGA2 axis. Thus, miR-9 is a tumor suppressor-miR which acts in a stringent cell context-dependent manner.
2014-01-01 | GSE52541 | GEO
Project description:Pediatric AML is an aggressive hematological malignancy associated with distinctive genomic features. We employed RNA-seq to study fusion genes and clinically relevant gene expression patterns in pediatric AML patients.
2023-05-02 | GSE222814 | GEO