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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE202975 | GEO | 2024/05/31

REPOSITORIES: GEO

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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

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

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

| PRJNA837906 | ENA

Gain of Chromosome 1q is associated with early progression in multiple myeloma patients treated with lenalidomide, bortezomib, and dexamethasone.

Project description:Gain of chromosome 1q (+1q) is commonly identified in multiple myeloma and has been associated with inferior outcomes. However, the prognostic implication of +1q has not been evaluated in the setting of standard triplet regimens. We retrospectively analyzed 201 consecutive patients with newly diagnosed myeloma who received induction with lenalidomide, bortezomib, and dexamethasone (RVD) and were tested for +1q at diagnosis by fluorescent in-situ hybridization. Patients with +1q (n?=?94), compared to those without +1q (n?=?107), had shorter median progression-free survival (PFS) (41.9 months vs 65.1 months, p?=?0.002, HR?=?1.90) and overall survival (median not reached (NR) for either arm, p?=?0.003, HR 2.69). In subgroup analyses, patients with co-occurring +1q and t(4;14), t(14;16) or del(17p) or with 4 or more copies of 1q had significantly worse PFS (25.1 months and 34.6 months, p?<?0.001 and p?=?0.0063, respectively), whereas patients with three copies and no other high-risk cytogenetic abnormalities had no significant difference in PFS. These data suggest that when treated with RVD induction, patients with +1q should be considered at very high risk for early progression in multiple myeloma when ?4 copies are detected or in the context of other high-risk cytogenetic abnormalities.

| S-EPMC6877577 | biostudies-literature

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

An acquired high-risk chromosome instability phenotype in multiple myeloma: Jumping 1q Syndrome.

Project description:Patients with multiple myeloma (MM) accumulate adverse copy number aberrations (CNAs), gains of 1q21, and 17p deletions during disease progression. A subset of these patients develops heightened 1q12 pericentromeric instability and jumping translocations of 1q12 (JT1q12), evidenced by increased copy CNAs of 1q21 and losses in receptor chromosomes (RC). To understand the progression of these aberrations we analyzed metaphase cells of 50 patients with ≥4 CNAs of 1q21 by G-banding, locus specific FISH, and spectral karyotyping. In eight patients with ≥5 CNAs of 1q21 we identified a chromosome instability phenotype similar to that found in ICF syndrome (immunodeficiency, centromeric instability, and facial anomalies). Strikingly, the acquired instability phenotype identified in these patients demonstrates the same transient structural aberrations of 1q12 as those found in ICF syndrome, suggesting similar underlying pathological mechanisms. Four types of clonal aberrations characterize this phenotype including JT1q12s, RC deletions, 1q12-21 breakage-fusion-bridge cycle amplifications, and RC insertions. In addition, recurring transient aberrations include 1q12 decondensation and breakage, triradials, and 1q micronuclei. The acquired self-propagating mobile property of 1q12 satellite DNA drives the continuous regeneration of 1q12 duplication/deletion events. For patients demonstrating this instability phenotype, we propose the term "Jumping 1q Syndrome."

| S-EPMC6689064 | biostudies-literature

Clinical characteristics and treatment outcomes of newly diagnosed multiple myeloma with chromosome 1q abnormalities.

Project description:A gain in chromosome 1q (+1q) is among the most common cytogenetic abnormalities in multiple myeloma (MM). It is unclear whether +1q is independently associated with decreased overall survival (OS). The objective of this study was to evaluate the impact of +1q on clinical characteristics, treatment response, and survival outcomes. We included 1376 Mayo Clinic patients diagnosed with MM from 2005 to 2018 who underwent fluorescence in situ hybridization testing at diagnosis with a panel including the +1q probe. A gain in 1q was found in 391 patients (28%) and was associated with anemia, hypercalcemia, high tumor burden, International Staging System (ISS) stage 3, high-risk (HR) translocations, and chromosome 13 abnormalities. There was no difference in overall response or deeper responses to proteasome inhibitor (PI)-, immunomodulatory drug (iMiD)-, or PI plus IMiD-based induction. Time to next treatment was shorter in patients with +1q compared with those without +1q (19.9 vs 27.7 months; P < .001). On univariate analysis, +1q was associated with increased risk of death (risk ratio [RR], 1.9; P < .001), and decreased OS was seen in all treatment groups. +1q was independently associated with decreased OS on multivariate analysis when other HR cytogenetic abnormalities, ISS stage 3, and age ≥70 years were included (RR, 1.5; P < .001). Gain of >1 copy of 1q was not associated with worse OS compared with gain of 1 copy (4.9 vs 4.3 years; P = .21). +1q was associated with high tumor burden, advanced disease stage, and HR translocations. It is independently associated with decreased OS, even in the setting of novel therapy and transplant.

| S-EPMC7422105 | biostudies-literature

Feeder-free culture of human pluripotent stem cells drives MDM4-mediated gain of chromosome 1q.

Project description:Culture-acquired variants in human pluripotent stem cells (hPSCs) hinder their applications in research and clinic. However, the mechanisms that underpin selection of variants remain unclear. Here, through analysis of comprehensive karyotyping datasets from over 23,000 hPSC cultures of more than 1,500 lines, we explored how culture conditions shape variant selection. Strikingly, we identified an association of chromosome 1q gains with feeder-free cultures and noted a rise in its prevalence in recent years, coinciding with increased usage of feeder-free regimens. Competition experiments of multiple isogenic lines with and without a chromosome 1q gain confirmed that 1q variants have an advantage in feeder-free (E8/vitronectin), but not feeder-based, culture. Mechanistically, we show that overexpression of MDM4, located on chromosome 1q, drives variants' advantage in E8/vitronectin by alleviating genome damage-induced apoptosis, which is lower in feeder-based conditions. Our study explains condition-dependent patterns of hPSC aberrations and offers insights into the mechanisms of variant selection.

| S-EPMC11368687 | biostudies-literature

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