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IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way [CLIP-seq]

ABSTRACT: IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way [CLIP-seq]

PROVIDER: PRJNA837906 | ENA |

REPOSITORIES: ENA

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IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way

Project description:IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way

| PRJNA837903 | ENA

IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way [RNA-seq]

Project description:IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way [RNA-seq]

| PRJNA837905 | ENA

IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way [CLIP-seq]

Project description:Combination analysis of m6A-seq, IGF2BP1-KD RNA-seq, IGF2BP1 CLIP-seq in H929 cells

2024-05-31 | GSE202973 | GEO

IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way [RNA-seq]

Project description:Combination analysis of m6A-seq, IGF2BP1-KD RNA-seq, IGF2BP1 CLIP-seq in H929 cells

2024-05-31 | GSE202974 | GEO

Gain and/or amplification of chromosome 1q are frequently found in Multiple Myeloma (MM).

Project description:Background: Gain and/or amplification of chromosome 1q are frequently found in Multiple Myeloma (MM). The number of 1q copies correlates with a poor prognosis. The aim of this work is to study the impact on the clinical outcome and the trascriptomic changes induced by Gain1q (3 copies of 1q, 3X) and amplification 1q (Amp1q, ≥4 copies of 1q, 4X) in MM patients enrolled in the CoMMpass study (NCT145429). Methods: Fluorescence in situ hybridization (FISH) in CD138+ purified bone marrow plasma cells was centralized and performed at baseline. The cut-off level for Gain1q was 10% of nuclei with ≥3 copies of 1q (3X), while Amp1q was defined as ≥ 20% of nuclei with ≥4 copies of 1q (4X). Transcriptome data from patients were used to find differentially expressed genes (DEGs) in gain (3X) and amp1q (4X) patients.

2023-01-16 | GSE193427 | GEO

Single cell RNA-seq of seizure-affected brain tissue with mosaic copy number gain of chromosome 1q

Project description:Somatic mosaicism is a known cause of neurological disorders, including developmental brain malformations and epilepsy. Brain mosaic copy number gain of chromosome 1q is associated with cortical malformations, early-onset epilepsy, and developmental delay. Pathogenic brain mosaicism is traditionally attributed to post-zygotic genetic alterations arising in a neural progenitor cell during fetal development. However, in our cohort, in at least five of six patients with brain mosaic copy number gain of chromosome 1q, the alteration occurred pre-conception. We observed a third non-constitutive, but parentally-derived, haplotype for chromosome 1q in patient brain tissue, demonstrating that the copy number alteration occurred in a gamete pre-conception. The altered cells had no representation in parental buccal or proband blood or buccal samples, but were prominently observed in proband brain tissue, suggesting the copy number gain was lost in most cell lineages during embryonic development. Single-nuclei genotyping coupled with gene expression profiling revealed a strong enrichment of the chromosome 1q gain in astrocytes, which correlated with the unusual finding of hyaline astrocytic inclusions in all six cases.

2023-09-08 | GSE221849 | GEO

IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way

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

2024-05-31 | GSE202975 | GEO

Characterization of Two Novel Ependymoma Cell Lines with Chromosome 1q gain derived from Posterior Fossa Tumors of Childhood

Project description:Introduction: Ependymoma (EPN) studies have revealed certain genetic markers, such as gain of chromosome 1q (1q+), as indicators of poor survival and high rate of recurrence. Development of novel therapeutics for EPN has been hampered by a lack of in vivo and in vivo models. We describe two unique 1q+ cell lines (811 and 928) derived from two children with metastatic, recurrent EPN. Both cell lines were characterized using histological, karyotypic and transcriptomic methods Transcriptomic analysis revealed that both lines, when cultured in 3D format, clustered closer to primary EPN tumors than monolayer format and with better fidelity of EPN-specific transcripts, namely those related to cilia function. Additionally, 3D culture histology revealed striking ependymal rosette formation, similar to primary tumors. Transcriptional enrichment of extracellular matrix, however, was a common signature of EPN primary tumor and cell lines in both monolayer and 3D formats.

2016-09-09 | GSE86574 | GEO

m6A modification profile in primary microglia with/without Igf2bp1 knockdown

Project description:Our study demonstrated that the expression of Igf2bp1 in activated microglia was significantly up-regulated, implying a role of Igf2bp1 in LPS-induced m6A modifications in microglia. To understand the roles of Igf2bp1 on LPS-induced m6A modification in microglia, we performed Igf2bp1 loss-of-function (LOF) approach. Microglia stimulated by LPS were transfected with either scrambled siRNA control or Igf2bp1 siRNA for 48 hours. To m6A modification profiles in control and Igf2bp1 LOF microglia were determined by MeRIP-seq analysis.

2022-12-31 | E-MTAB-11411 | biostudies-arrayexpress