KAT6B gene deletion in small cell lung cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE62773 | GEO | 2015/10/07
SECONDARY ACCESSION(S): PRJNA265100
REPOSITORIES: GEO
Similar Datasets
Project description:KAT6B gene deletion as a predictive biomarker to Irinotecan response in small cell lung cancer
| PRJNA265094 | ENA
Project description:The histone lysine acetyltransferase KAT6B (MYST4, MORF, QKF) is the target of recurrent chromosomal translocations causing haematological malignancies with poor prognosis. Using Kat6b germline deletion and overexpression in mice, we determined the role of KAT6B in the haematopoietic system. We found that KAT6B sustained the fetal haematopoietic stem cell pool but did not affect viability or differentiation. KAT6B was essential for normal levels of histone H3 lysine 9 (H3K9) acetylation but not for a previously proposed target, H3K23. Compound heterozygosity of Kat6b and the closely related gene, Kat6a, abolished haematopoietic reconstitution after transplantation. KAT6B and KAT6A cooperatively promoted transcription of genes regulating haematopoiesis, including the Hoxa cluster, Pbx1, Meis1, Gata family, Erg and Flt3. In conclusion, we identified the haematopoietic processes requiring Kat6b and showed that KAT6B and KAT6A synergistically promoted HSC development, function and transcription. Our findings are pertinent to current clinical trials testing KAT6A/B inhibitors as cancer therapeutics.
2024-02-25 | GSE256039 | GEO
Project description:To develop our gene expression experiment, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentially regulated by the transcriptional coactivator KAT6B. Expression of KAT6B gene was downregulated in two human SCLC cell lines using two different short hairpin RNAs. RNAs from these modified cell lines were hybridized in Agilent platform.
2015-10-07 | GSE59136 | GEO
Project description:The RNA sequencing data are part of a study reporting and investigating a mouse model of the Say-Barber-Biesecker-Young-Simpson (SBBYS) syndrome (OMIM:603736) and demonstrating proof-of-principle efficacy of postnatal treatment with sodium valproate (VPA) or acetyl-carnitine (ALCAR). The KAT6B gene encodes a histone lysine acetyltransferase. The RNA sequencing experiments identified genes that are differentially expressed between Vehicle treated Kat6b+/– and Kat6b+/+ cortical neurons and the subset genes that are restored to normal expression after treatment with ALCAR or VPA. Cortical neurons were isolated from four Kat6b+/– and four Kat6b+/+ E16.5 mouse cerebral cortex. Cells from each cortical neuron isolate were cultured with 1 mM ALCAR, 1 mM VPA or untreated medium (Vehicle) for 4 days.
2024-01-28 | GSE249964 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE28571: Gene Copy Number Aberrations are Associated with Survival in Histological Subgroups of Non-Small Cell Lung Cancer (expression data) GSE28572: Gene Copy Number Aberrations are Associated with Survival in Histological Subgroups of Non-Small Cell Lung Cancer (copy number data) Refer to individual Series
2011-11-01 | E-GEOD-28582 | biostudies-arrayexpress
Project description:Microarray gene expression analysis of genes that showed a gene copy number difference in non small cell lung cancer samples. Only data for a subset of the genes on the array chip are shown here.
2008-05-11 | E-TABM-270 | biostudies-arrayexpress
Project description:Small cell lung cancer (SCLC) is an aggressive cancer often diagnosed only after it has metastasized to distant sites (Meuwissen and Berns 2005; Cooper and Spiro 2006). Despite the need to better understand this disease, SCLC remains poorly characterized at the molecular and genomic levels (Forgacs et al. 2001; Pleasance et al. 2010). Using a genetically-engineered mouse model of SCLC driven by conditional deletion of Trp53 and Rb1 in the lung (Jonkers et al. 2001; Vooijs et al. 2002; Meuwissen et al. 2003; Sage et al. 2003), we identified several frequent, high-magnitude focal DNA copy number alterations in SCLC. We uncovered amplification of a novel, oncogenic transcription factor, Nuclear Factor I/B (Nfib) in the mouse SCLC model and in human SCLC. Functional studies indicate that NFIB regulates cell viability and proliferation during transformation. Gene expression analysis of two replicates each of two independent mSCLC cell lines (3583T3 and 3151T4) stably expressing Nfib, Mycl1 or both Nfib and Mycl1
2011-12-08 | E-GEOD-29533 | biostudies-arrayexpress
Project description:Small cell lung cancer (SCLC) is an aggressive cancer often diagnosed only after it has metastasized to distant sites (Meuwissen and Berns 2005; Cooper and Spiro 2006). Despite the need to better understand this disease, SCLC remains poorly characterized at the molecular and genomic levels (Forgacs et al. 2001; Pleasance et al. 2010). Using a genetically-engineered mouse model of SCLC driven by conditional deletion of Trp53 and Rb1 in the lung (Jonkers et al. 2001; Vooijs et al. 2002; Meuwissen et al. 2003; Sage et al. 2003), we identified several frequent, high-magnitude focal DNA copy number alterations in SCLC. We uncovered amplification of a novel, oncogenic transcription factor, Nuclear Factor I/B (Nfib) in the mouse SCLC model and in human SCLC. Functional studies indicate that NFIB regulates cell viability and proliferation during transformation.
2011-12-08 | GSE29533 | GEO
Project description:Hypothesis: Non-small cell lung cancer (NSCLC) is characterized by a multitude of genetic aberrations with unknown clinical impact. In this study, we aimed to identify gene copy number changes that correlate with clinical outcome in NSCLC. To maximize the chance to identify clinically relevant events, we applied a strategy involving two prognostically extreme patient groups. Results: Genetic aberrations were strongly associated with tumor histology. In adenocarcinoma (n=50), gene copy number gains on chromosome 8q21-q24.3 (177 genes) were more frequent in long-term survivors. In squamous cell carcinoma (n=28), gains on chromosome 14q23.1-24.3 (133 genes) were associated with shorter survival, whereas losses in a neighboring region, 14q31.1-32.33 (110 genes), correlated with favorable outcome. In accordance with copy number gains and losses, mRNA expression levels of corresponding genes were increased or decreased, respectively. Conclusion: Comprehensive tumor profiling permits the integration of genomic, histologic and clinical data. We identified gene copy number gains and losses, with corresponding changes in mRNA levels, that were associated with prognosis in adenocarcinoma and squamous cell carcinoma of the lung.
2011-10-28 | GSE28571 | GEO