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Studies in an early development window unveils a severe HSC defect in both murine and human Fanconi anemia [human]

ABSTRACT: Studies in an early development window unveils a severe HSC defect in both murine and human Fanconi anemia [human]

PROVIDER: PRJNA491830 | ENA |

REPOSITORIES: ENA

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Studies in an early development window unveils a severe HSC defect in both murine and human Fanconi anemia

Project description:Studies in an early development window unveils a severe HSC defect in both murine and human Fanconi anemia

| PRJNA491828 | ENA

Studies in an early development window unveils a severe HSC defect in both murine and human Fanconi anemia [mouse]

Project description:Studies in an early development window unveils a severe HSC defect in both murine and human Fanconi anemia [mouse]

| PRJNA491829 | ENA

Studies in an early development window unveils a severe HSC defect in both murine and human Fanconi anemia [human]

Project description:We performed a unique kinetics study of hematopoiesis in Fancg-/- mouse embryos, between E12.5 and E14.5 developmental window. We also report for the first time that a deep HSC defect is also observed during human FA development, and that human FA FL HSCs present a transcriptome profile similar to that of mouse E12.5 Fancg-/- FL HSCs.

2018-11-30 | GSE120168 | GEO

Studies in an early development window unveils a severe HSC defect in both murine and human Fanconi anemia [mouse]

2018-11-30 | GSE120167 | GEO

Studies in an Early Development Window Unveils a Severe HSC Defect in both Murine and Human Fanconi Anemia.

Project description:Fanconi anemia (FA) causes bone marrow failure early during childhood, and recent studies indicate that a hematopoietic defect could begin in utero. We performed a unique kinetics study of hematopoiesis in Fancg-/- mouse embryos, between the early embryonic day 11.5 (E11.5) to E12.5 developmental window (when the highest level of hematopoietic stem cells [HSC] amplification takes place) and E14.5. This study reveals a deep HSC defect with exhaustion of proliferative and self-renewal capacities very early during development, together with severe FA clinical and biological manifestations, which are mitigated at E14.5 due to compensatory mechanisms that help to ensure survival of Fancg-/- embryos. It also reports that a deep HSC defect is also observed during human FA development, and that human FA fetal liver (FL) HSCs present a transcriptome profile similar to that of mouse E12.5 Fancg-/- FL HSCs. Altogether, our results highlight that early mouse FL could represent a good alternative model for studying Fanconi pathology.

| S-EPMC6234961 | biostudies-literature

Modeling clonal evolution in Fanconi anemia

Project description:Transcriptomic comparison of stages of clonal evolution of Fanconi anemia modeled using induced pluripotent stem cells.

2024-04-17 | GSE205844 | GEO

BM clonal evolution in Fanconi anemia patients

Project description:Arrays-CGH and/or SNP-array data from n=57 Fanconi anemia BM and n=36 paired fibroblasts

2011-07-28 | E-MTAB-529 | biostudies-arrayexpress

Studies in an early development window unveils a severe HSC defect in both murine and human Fanconi anemia

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

2018-11-30 | GSE120169 | GEO

Expression data from normal and Fanconi anemia low density bone marrow cells

Project description:Fanconi anemia (FA) is a rare inherited disease complicated by aplastic anemia. There is evidence that hematopoietic stem cells have lost self replicative capacity and undergo apoptosis when exposed to inhibitory cytokines including interferon gamma and tumor necrosis factor-alpha. We used gene expression microarrays to identify transcriptomal differences between bone marrow cells from normal volunteers and from children and adults with Fanconi anemia

2009-09-15 | GSE16334 | GEO

Gene expression based identification of potential genes involved in Fanconi anemia

Project description:Fanconi anemia is a rare inherited hematological disorder which commonly presents with bone marrow failure, developmental abnormalities and susceptibility to cancer with high rates of prevalence in ethnic populations. The objective of this study was to identify potential genes that aid in the progression of the disease or produce its principal symptoms and to hypothesize enabling roles for certain genes that are not part of the central molecular machinery causing the disease. A total of 2 Fanconi anemia samples were collected from patients who displayed characteristic FA features. All of them gave positive results for the DNA breakage test after mitomycin C treatment. Samples were referred by Dr. Sheila Mohan of REFAIN (Registry for Fanconi anemia in India). Whole genome microarray analysis of peripheral blood from 2 patient samples and one normal individual. Sequential analysis of microarray data was carried out using gene ontology and pathway analysis to identify candidate genes.

2010-06-24 | E-GEOD-17233 | biostudies-arrayexpress

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