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SETD2 Mutations Do Not Contribute to Clonal Fitness in Response to Chemotherapy in Childhood B Acute Lymphoblastic Leukemia (ATAC-Seq)

ABSTRACT: To investigate the impact of SETD2 mutations on clonal fitness in B actue lymphoblastic leukemia we generated cells lines with SETD KO using CRISPR/Cas9 system. We then performed phenotypic based assays as well as gene expression profiling, mutation burden, and chromtain accessibilty analysis using data obtained from RNA-seq, Whole exom sequencing following drug traetment, and ATAC-seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE231721 | GEO | 2024/05/01

REPOSITORIES: GEO

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SETD2 Mutations Do Not Contribute to Clonal Fitness in Response to Chemotherapy in Childhood B Acute Lymphoblastic Leukemia (WES)

Project description:To investigate the impact of SETD2 mutations on clonal fitness in B actue lymphoblastic leukemia we generated cells lines with SETD KO using CRISPR/Cas9 system. We then performed phenotypic based assays as well as gene expression profiling, mutation burden, and chromtain accessibilty analysis using data obtained from RNA-seq, Whole exom sequencing following drug traetment, and ATAC-seq.

2024-05-01 | GSE231723 | GEO

SETD2 Mutations Do Not Contribute to Clonal Fitness in Response to Chemotherapy in Childhood B Acute Lymphoblastic Leukemia (RNA-Seq)

2024-05-01 | GSE231720 | GEO

SETD2 Mutations Do Not Contribute to Clonal Fitness in Response to Chemotherapy in Childhood B Acute Lymphoblastic Leukemia

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

2024-05-01 | GSE231724 | GEO

Setd2 knockdown.

Project description:Setd2 knockdown.

| PRJNA612891 | ENA

Proteomics analysis on SETD2 loss induced ccRCC formation

Project description:Patients with polycystic kidney disease (PKD) encounter a high risk of clear cell renal cell carcinoma (ccRCC), a malignant tumor with dysregulated lipid metabolism. SET domain–containing 2 (SETD2) has been identified as an important tumor suppressor gene in ccRCC. However, the role of SETD2 in tumorigenesis during the transition from PKD to ccRCC remains largely unexplored. Herein, we performed metabolomics, lipidomics, transcriptomics and proteomics with SETD2 loss induced PKD-ccRCC transition mouse model. To characterize biological responses triggered by SETD2 deletion during PKD-ccRCC transition at the protein level, we conducted global proteomics studies.

2023-10-31 | PXD038966 | Pride

RNA sequencing of SETD2 isogenic renal cell carcinoma cell lines

Project description:RNA sequencing of SETD2 isogenic renal cell carcinoma cell lines. Examination of RNA expression in SETD2 isogenic cell lines

2015-06-17 | E-GEOD-66879 | biostudies-arrayexpress

Comparison of gene expression pattern between Wild-type and Setd2 knockout mESCs [Affymetrix]

Project description:SETD2/HYPB has been known as a histone H3K36 specific methyltransferase. However, its roles in physiology such as development and cellular function remain unclear. In this study, using mESCs as cellular model, we show that Setd2 mainly regulates differentiation of murine embryonic stem cells (mESCs) towards primitive endoderm. This study aimed at exploring how did Setd2 regulate primitive endoderm. differentiation. We used microarrays to detail the global programme of gene expression controled by setd2, which is required for endoderm differentiation. Wild type and Setd2 knockout mESCs were selected for RNA extraction and hybridization on Affymetrix GeneChip® mouse genome 430 2.0 arrays. We sought to obtain some deregulated genes, which were required for primitive endoderm differentiation. For comparison, three biological repeats of each were performed.

2014-10-14 | E-GEOD-54931 | biostudies-arrayexpress

Setd2 knockdown.

Project description:Setd2 knockdown leads to subtle but significant changes in gene expression and alternative splicing.

2020-06-18 | GSE147077 | GEO

Quantitative Analysis of Wild Type(wt) and Setd2 knockout(ko) mESCs Transcriptomes [RNA-Seq]

Project description:Purpose: This study aimed at exploring the deregulated genes in setd2 knockout mESCs compared with wt, more particularly to find the mechanism controlled by setd2,which was required for endoderm differentiation. Methods: Setd2 wt and ko mESCs were generated by deep sequencing, using Illumina GAIIx. Using Avadis NGS (version:1.3) software to analyze the sequence reads that passed quality filter to acquire the expression level of all genes. qRT–PCR validation was performed usingSYBR Green assays. Results: Using an optimized data analysis workflow, we mapped about 80 million sequence reads per sample to the mouse genome (build mm9) and identified 17,827 transcripts in the sted2 wt and ko mESCs. About 2,516 genes were deregulated in setd2 ko mESCs, more than 10 genes were validated using qRT-PCR. Conclusions: Through RNA-seq,we noticed that a subset of genes that related to MAPK signaling pathways were down-regulated in ko mESCs. This provided a bridge to connect setd2 and mESCs endoderm differentiation. One wt and one ko mESCs were generated by deep sequencing, using Illumina GAIIx.

2014-10-14 | E-GEOD-54932 | biostudies-arrayexpress

RNA-sequencing of renal cells from Setd2-wildtype PKD and Setd2-knlckout ccRCC mice.

Project description:To explore potential role of SETD2 in PKD-ccRCC transition in vivo, we generated a PKD mouse model by overexpressing oncogene c-MYC under the control of the Ksp promoter (KM mice), and knockout Setd2 gene using the same Ksp promoter in this PKD mice (KMs mice) to establish a ccRCC mouse model. To further characterize biological responses trigered by SETD2 deletion during PKD-ccRCC transition at the mRNA level, we next conducted global transcriptomics studies.

2022-12-26 | GSE221136 | GEO

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