Single cell RNA sequencing of paired myelodysplastic syndrome and secondary acute myeloid leukemia bone marrow aspirate samples
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ABSTRACT:
PROVIDER: PRJNA847640 | ENA |
REPOSITORIES: ENA
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Project description:This experiment is designed to compare single cell gene expression in paired samples from two individuals who had MDS that progressed to sAML.
2022-06-14 | GSE205490 | GEO
Project description:Single cell RNA profiles of bone marrow aspirate concentrate
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Project description:Myelodysplastic syndromes (MDS) are a heterogenous group of hematopoietic stem cell disorders characterized by dysplastic blood cell formation and peripheral blood cytopenias. Up to 30% of patients with MDS will progress to a highly chemotherapy-resistant secondary acute myeloid leukemia (sAML). We identified mutations in U2AF1 in MDS patients and patients with U2AF1 mutations are at an increased risk of developing sAML.
2011-11-23 | GSE30195 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE21948: High Density custom Agilent 44K CGH array analysis of 7q and TET2 region in myelodysplastic/myeloproliferative neoplasms GSE21990: Affymetrix SNP 6.0 array data for myelodysplastic/myeloproliferative neoplasms Refer to individual Series
2010-06-30 | E-GEOD-21991 | biostudies-arrayexpress
Project description:Epigenetic therapy, using hypomethylating agents (HMA), is known to be effective in the treatment of high-risk myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) patients who are not suitable for intensive chemotherapy or allogeneic stem cell transplantation. However, response rates to HMA are low and there is an unmet need in finding prognostic and predictive biomarkers of treatment response. We performed global methylation analysis of 75 patients with high risk MDS and secondary AML (sAML) who were included in CETLAM MDS-09 protocol, in which patients received HMA or intensive treatment according to age, comorbidities and cytogenetics. At diagnosis, no global methylation pattern allowed us to differentiate patients according to the cytological subtype, cytogenetics or treatment response. But we found a methylation signature defined by 200 probes, which allowed us to distinguish between responding and non-responding patients to azacitidine (AZA) treatment. Studying follow-up samples, we have confirmed that AZA decreases global DNA methylation, but in our cohort the degree of methylation decrease did not correlate with the type of response. The methylation signature detected at diagnosis was not useful in treated samples to determine a methylation pattern predictive of progression or relapse. In conclusion, altered DNA methylation patterns at diagnosis, in a subset of determined CpGs, may serve as biomarker for predicting AZA response.
2021-01-27 | GSE152710 | GEO
Project description:We have demonstrated that DICER1 (a key enzyme of miRNA biogenesis) was underexpressed in myelodysplastic syndrome MSC. We hypothesize that those MSC harbored a deregulated pattern of miRNA versus healthy donors MSC.
2020-10-04 | GSE139471 | GEO
Project description:Background: There is a need to identify and quantify mesenchymal stromal cells (MSCs) in human bone marrow aspirate concentrate (BMAC) source tissues, but current methods to do so were established in cultured cell populations. Given that surface marker and gene expression change in cultured cells, it is doubtful that these strategies are valid to quantify MSCs in fresh BMAC. Purpose: To establish the presence, quantity, and heterogeneity of BMAC-derived MSCs in minimally manipulated BMAC using currently available strategies. Study Design: Descriptive Laboratory Study. Methods: Five published strategies to identify MSCs were compared for suitability and efficiency to quantify clinical-grade BMAC-MSCs and cultured MSCs at the single cell transcriptome level on BMAC samples being used clinically from fifteen orthopedic patients and on one cultured MSC sample. Strategies included: 1) the guidelines by the International Society for Cellular Therapy (ISCT), 2) CD271 expression, 3) the Ghazanfari et al. transcriptional profile, 4) the Jia et al. transcriptional profile, and 5) the Silva et al. transcriptional profile. Results: ISCT guidelines did not identify any MSCs in BMAC at the transcriptional level and only 1 in 9 million cells at the protein level. 9 of 12850 BMAC cells expressed the CD271 gene. Only 116 of 396 Ghazanfari genes were detected in BMAC, whereas no cells expressed all of them. No cells express all Jia genes, but 25 cells express at least 13 of 22. No cells express all Silva genes, but 19 cells express at least 8 of 23. Most importantly, the liberalized strategies tended to identify different cells and most of them clustered with immune cells. Conclusion: Currently available methods need to be liberalized to identify any MSCs in fresh human BMAC and lack consensus at the single cell transcriptome and protein expression levels. These different cells should be isolated and challenged to establish phenotypic differences. Clinical Relevance: This study demonstrated that improved strategies to quantify MSC concentrations in BMAC for clinical applications are urgently needed. Until then, injected minimally manipulated MSC doses should be reported as rough estimates or as unknown.
2021-03-12 | GSE162692 | GEO
Project description:Adult neural progenitor cells (aNPCs) are a potential source for cell based therapy for neurodegenerative diseases and traumatic brain injuries. We show that the ultrasonic aspirate samples that are typically considered as a waste after surgery are a great source for aHNPCs.
2017-08-15 | GSE89201 | GEO
Project description:Myelodysplastic syndromes (MDS) are a heterogenous group of hematopoietic stem cell disorders characterized by dysplastic blood cell formation and peripheral blood cytopenias. Up to 30% of patients with MDS will progress to a highly chemotherapy-resistant secondary acute myeloid leukemia (sAML). We identified mutations in U2AF1 in MDS patients and patients with U2AF1 mutations are at an increased risk of developing sAML. We identified mutations in U2AF1 in patients with MDS and hypothesized that U2AF1 mutations may represent a novel mechanism that could alter gene expression in MDS. To elucidate gene expression changes associated with U2AF1 mutations, we analyzed the global mRNA expression profile obtained from bone marrow CD34+ cells purified from 5 MDS patients with a U2AF1 mutation, 10 MDS patients without a mutation, and 4 normal donors.
2011-11-23 | E-GEOD-30195 | biostudies-arrayexpress
Project description:Control of oxidative stress in the bone marrow (BM) is key for maintaining the balance between self-renewal, proliferation, and differentiation of hematopoietic cells. Breakdown of this regulation can lead to diseases characterized by BM failure such as the myelodysplastic syndromes (MDS). To better understand the role of oxidative stress in MDS development, we compared protein carbonylation as an oxidative stress marker in BM of patients with MDS and control subjects, and also patients with MDS under treatment with the iron chelator deferasirox.
2019-10-30 | PXD013609 | Pride