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Global miRNA Expression of Bone Marrow Mesenchymal Stem/Stromal Cells in Fanconi Anemia Patients Before Transplantation and Unpaired Bone Marrow Donors

ABSTRACT: Global miRNA Expression of Bone Marrow Mesenchymal Stem/Stromal Cells in Fanconi Anemia Patients Before Transplantation and Unpaired Bone Marrow Donors

PROVIDER: PRJNA759641 | ENA |

REPOSITORIES: ENA

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

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Global miRNA Expression of Bone Marrow Mesenchymal Stem/Stromal Cells in Fanconi Anemia Patients Before Transplantation and Unpaired Bone Marrow Donors

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Global miRNA Expression of Bone Marrow Mesenchymal Stem/Stromal Cells in Fanconi Anemia Patients Before Transplantation and their Allogeneic Bone Marrow Donors

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Global miRNA Expression of Bone Marrow Mesenchymal Stem/Stromal Cells in Fanconi Anemia Patients Before and After Bone Marrow Transplantation, and their Allogeneic Bone Marrow Donors

Project description:Fanconi anemia (FA) is a rare genetic disorder characterized by genomic instability, developmental defects and bone marrow failure. Homeostasis of hematopoietic stem cells (HSCs) in the bone marrow partly relies on their direct or indirect interactions with the mesenchymal stem/stromal cells (MSCs). miRNAs can play a critical role during these interactions. There is no study available so far addressing the miRNA profile of bone marrow (BM-) MSCs in FA disease state. Non-coding RNA expression profiling was performed in BM-MSCs obtained from Donors (siblings of FA patients) as well as FA patients before (preBMT) and after bone marrow transplant (postBMT) using GeneChip miRNA 2.0 Array. Quality Control (QC) was performed via Normalized Unscaled Standard Errors (NUSE) and Relative Log Expression (RLE) before further analysis.

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Transcription profiling of human bone marrow cells from normal volunteers and from children and adults with Fanconi anemia

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MYC Promotes Bone Marrow Stem Cell Dysfunction in Fanconi Anemia

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In Fanconi Anemia, impaired accumulation of bone marrow neutrophils during emergency granulopoiesis induces hematopoietic stem cell stress

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