Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA145771 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We detected changes in genes expression in patients with 5q- syndrome in CD14+ monocytes due to treatment with lenalidomide. Total RNA was obtained from CD14+ monocytes from peripheral blood of 6 controls, 6 patients before treatment, and 5 patients during treatment.
2011-09-11 | E-GEOD-31460 | biostudies-arrayexpress
Project description:We detected changes in genes expression in patients with 5q- syndrome in CD14+ monocytes due to treatment with lenalidomide.
2011-09-12 | GSE31460 | GEO
Project description:While del(5q) MDS patients comprise a well-defined hematological subgroup, the molecular basis underlying its origin and the reason behind the relapse to lenalidomide remains unknown. Using scRNAseq on CD34+ progenitor cells from patients with del(5q) MDS we were able to identify cells harboring the deletion, enabling us to deeply characterize the transcriptional impact of this genetic insult on disease pathogenesis and treatment response. We found, across all patients, an enrichment of del(5q) cells in GMP and megakaryocyte-erythroid progenitors not described to date. Interestingly, both del(5q) and non-del(5q) cells presented similar transcriptional lesions when compared to progenitors from healthy individuals, indicating that all cells, and not only those harboring the deletion, are altered in these patients and may contribute to aberrant hematopoietic differentiation. However, GRN analysis revealed a group of regulons with aberrant activity in del(5q) cells that could be responsible for triggering altered hematopoiesis, pointing to a more prominent role of these cells in the phenotype of these patients. An analysis of del(5q) MDS patients achieving hematological response upon lenalidomide treatment showed that the drug reverted several transcriptional alterations in both del(5q) and non-del(5q) cells, but other lesions remained, which may be responsible for potential future relapses. Moreover, lack of hematological response was associated with the inability of lenalidomide to reverse transcriptional alterations. Collectively, this study provides a deep characterization of del(5q) and non-del(5q) cells at single-cell resolution, revealing previously unknown transcriptional alterations that could contribute to disease pathogenesis, or lack of responsiveness to lenalidomide.
2024-04-18 | GSE245452 | GEO
Project description:Myelodysplastic syndromes (MDS) are uncommon entities, heterogeneous clinically and cytogenetically. Recently, a new drug, Lenalidomide, has demonstrated to be very effective in patients with MDS and 5q- reaching 70% of hematological responses whereas patients with MDS without 5q- has only 20-30% of hematological responses. The aim of the present study is to determine genetic alteration in this subset of patients, and describe candidate genes related with response or resistance to Lenalidomide. The aim of the present study is to determine genetic alteration in this subset of patients, and describe candidate genes related with response or resistance to Lenalidomide. Copy number analysis of Affymetrix GenomeWide SNP 6.0 arrays was performed for 2 patients with MDS an isolated 5q- by conventional cytogenetics. There are also 2 samples from separated CD3+ lymphocytes, which were used as references for copy number and LOH inference.
2014-10-07 | E-GEOD-59244 | biostudies-arrayexpress
Project description:Myelodysplastic syndromes (MDS) are uncommon entities, heterogeneous clinically and cytogenetically. Recently, a new drug, Lenalidomide, has demonstrated to be very effective in patients with MDS and 5q- reaching 70% of hematological responses whereas patients with MDS without 5q- has only 20-30% of hematological responses. The aim of the present study is to determine genetic alteration in this subset of patients, and describe candidate genes related with response or resistance to Lenalidomide.
2014-10-07 | GSE59244 | GEO
Project description:Diamond Blackfan anemia is a congenital bone marrow failure syndrome characterized by hypoproliferative anemia, often with associated physical abnormalities. Perturbations of the ribosome appear critically important to the development of DBA, as alterations in 9 different ribosomal protein genes have been identified in multiple unrelated families, along with rarer abnormalities of additional ribosomal proteins. However, presently only 50-60% of patients have an identifiable genetic lesion by ribosomal protein gene sequencing. Using genome-wide SNP array to evaluate for regions of recurrent copy variation, we identified 2 patients with mosaic loss in the region of the the chromosome 5-deleted region involved in somatically-acquired 5q- myelodysplastic syndrome. Samples were analyzed on Illumina HumanOmni1_Quad, HumanOmniExpress, or HumanOmniExpressExome Genotyping bead arrays; 1 patient was available for longitudinal study including assessment of mosaicism in lymphoid and myeloid-enriched cell populations before treatement with lenolidamide. Similar studies were performed while on lenoldamide therapy in peripheral blood at 3 months and in bone marrow at 20 months of treatment. One patient with mosaic deletion of 5q was available for longitudinal study including assessment of gene expression in bone marrow before and during treatment with lenalidomide.
2013-11-05 | E-GEOD-42570 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of monocytes from healthy donors, systemic inflammatory response syndrome (SIRS) and septic patients. The Illumina Infinium MethylationEPIC Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpGs in CD14+CD66bneg monocytes isolated from PBMCs of 11 healthy donors, 4 SIRS and 14 septic patients.
2019-10-03 | GSE138074 | GEO
Project description:Previous studies suggest that monocytes are an important contributor to tuberculosis (TB)-specific immune signatures in blood. Here we carried out single-cell profiling of classical CD14+CD16- and intermediate CD14+CD16+ monocytes in paired blood samples of active TB (ATB) patients at diagnosis and end-treatment. At diagnosis, ATB patients displayed upregulation of interferon signaling genes that significantly overlapped with previously reported blood TB signatures in both CD14+ subsets. In ATB diagnosis, we identified additional transcriptomic and functional changes in intermediate CD14+CD16+ monocytes, such as the upregulation of inflammatory and MHC-II genes, and increased capacity to activate T cells, reflecting overall increased activation in this population. Single-cell transcriptomics revealed that distinct subsets of intermediate CD14+CD16+ monocytes were responsible for each gene signature, indicating significant functional heterogeneity within this population. Finally, we observed that transcriptomic changes in CD14+ monocytes were transient, as they were no longer observed in the same ATB patients mid-treatment, suggesting they are associated with disease resolution.
2023-01-02 | GSE214237 | GEO
Project description:Clever-1 is a scavenger receptor expressed on a subset of immunosuppressive macrophages and monocytes. We analyzed the gene expression profiles of CD14+ monocytes isolated from cancer patients treated with a humanized anti-Clever-1 antibody (FP-1305) in a phase I/II clinical trial (MATINS; NCT03733990) to understand how anti-Clever-1 treatment changes the phenotype and activation of circulating monocytes.
2021-06-03 | GSE151085 | GEO
Project description:Lenalidome is a drug especially effective in low risk myelodysplastic syndromes (MDS) with isolated 5q deletion. However, 25% of the patients did not respond. TP53 mutations have been described to play a role in the disease progression, and karyotypic complexity also has an important impact in the outcome. We selected 53 MDS patients with 5q deletion and treated with lenalidomide and we studied by the following techniques: conventional G-banding cytogenetics (CC), single nucleotide polymorphism arrays (SNP-A) and sequencing, in order to assess their impact on treatment response and disease progression. Low karyotypic complexity (by CC), a high baseline platelet count (>280x103/L) and TP53 unmutated gene status are associated with the achievement of hematological response (P=0.005, P=0.008 and P=0.057, respectively). In a multivariate model, the most important predictors for lenalidomide failure are karyotypic complexity (P=0.014) and a platelet count below 280x103/L (P=0.042). Additionally, none of the TP53 mutated cases achieved complete cytogenetics response. Nevertheless, inclusion of defects by SNP-A did not allow for a better separation of responders and non responders. These findings constitute a useful reference data to be considered before lenalidomide treatment enrollment. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from bone marrow or peripheral blood and, in some cases, also lymphocytes CD3 isolated from peripheral blood samples. Copy number analyses of Affymetrix 250K and 6.0 SNP arrays were performed for 53 MDS with 5q deletion samples. There are also 30 samples from lymphocytes CD3 isolated from peripheral blood, which were used as germ-line DNA (control).
2013-07-01 | E-GEOD-35656 | biostudies-arrayexpress