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Repeat to gene expression ratios in leukemic blast cells can stratify risk prediction in acute myeloid leukemia

ABSTRACT: A high repeat to gene expression ratio identifies AML patient subgroups with a favorable prognosis, whereas a low repeat to gene expression is prevalent in AML patient subgroups with a poor prognosis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE175701 | GEO | 2021/05/28

REPOSITORIES: GEO

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Repeat to gene expression ratios in leukemic blast cells can stratify risk prediction in acute myeloid leukemia.

Project description: Not available

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Repeat to gene expression ratios in leukemic blast cells can stratify risk prediction in acute myeloid leukemia

Project description:Repeat to gene expression ratios in leukemic blast cells can stratify risk prediction in acute myeloid leukemia

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AML subtype is a major determinant of the association between prognostic gene expression signatures and their clinical significance.

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Friedreichâ??s Ataxia Induced Pluripotent Stem Cells Recapitulate GAAâ?¢TTC Triplet-Repeat Instability

Project description:The inherited neurodegenerative disease Friedreichâ??s ataxia (FRDA) is caused by hyperexpansion of GAAâ?¢TTC trinucleotide repeats within the first intron of the FXN gene, encoding the mitochondrial protein frataxin. Long GAAâ?¢TTC repeats causes heterochromatin-mediated silencing and loss of frataxin in affected individuals. We report the derivation of induced pluripotent stem cells (iPSCs) from FRDA patient fibroblasts through retroviral transduction of transcription factors. FXN gene repression is maintained in the iPSCs, as are the mRNA and miRNA global expression signatures reflecting the human disease. GAAâ?¢TTC repeats uniquely in FXN in the iPSCs exhibit repeat instability similar to patient families, where they expand and/or contract with discrete changes in length between generations. The mismatch repair enzyme Msh2, implicated in repeat instability in other triplet repeat diseases, is highly expressed in the iPSCs, occupies FXN intron 1, and shRNA silencing of Msh2 impedes repeat expansion, providing a possible molecular explanation for repeat expansion in FRDA. 65 samples from various number of tissue, primary cell lines undifferenatiated human embryonic stem cell lines, induces pluripotent stem cell lines have been run on Illumina HT12 v3 chips.

2010-07-30 | E-GEOD-22651 | biostudies-arrayexpress

Elevated acid ceramidase promotes acute myeloid leukemia blast survival through sphingolipid dysregulation and Mcl-1 upregulation

Project description:Gene expression of patient samples with acute myeloid leukemia (AML) were compared to normal controls to study dysregulated signalling pathways. Peripheral blood mononuclear cells (PBMCs) from primary AML patient samples were isolated using the Ficoll-Paque gradient separation method. RNA from CD34+ bone marrow cells of healthy donors were purchased from AllCells LLC (Alameda, CA; catalog number RNA-BM003C). Total RNA were harvested from patient samples using Trizol and subjected to microarray-based gene expression analysis.

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Proteomic and Genomic Signatures of Repeat-instability in Cancer and Adjacent Normal Tissues

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2020-06-02 | PXD012574 | Pride

Friedreich’s Ataxia Induced Pluripotent Stem Cells Recapitulate GAA•TTC Triplet-Repeat Instability

Project description:The inherited neurodegenerative disease Friedreich’s ataxia (FRDA) is caused by hyperexpansion of GAA•TTC trinucleotide repeats within the first intron of the FXN gene, encoding the mitochondrial protein frataxin. Long GAA•TTC repeats causes heterochromatin-mediated silencing and loss of frataxin in affected individuals. We report the derivation of induced pluripotent stem cells (iPSCs) from FRDA patient fibroblasts through retroviral transduction of transcription factors. FXN gene repression is maintained in the iPSCs, as are the mRNA and miRNA global expression signatures reflecting the human disease. GAA•TTC repeats uniquely in FXN in the iPSCs exhibit repeat instability similar to patient families, where they expand and/or contract with discrete changes in length between generations. The mismatch repair enzyme Msh2, implicated in repeat instability in other triplet repeat diseases, is highly expressed in the iPSCs, occupies FXN intron 1, and shRNA silencing of Msh2 impedes repeat expansion, providing a possible molecular explanation for repeat expansion in FRDA.

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Project description:Acute myeloid leukemia (AML) is an aggressive hematologic malignancy, often characterized by poor prognosis following standard induction therapy. The DNA methyltransferase inhibitor decitabine (DAC) is an alternative to intensive chemotherapy in elderly and relapsed/refractory AML patients. Despite some efficacy, DAC monotherapy does not promote complete remission and overall survival rates are very poor. Therefore, novel therapeutic regimens for AML are warranted. CD105 (endoglin), a receptor for the TGF-β superfamily, is expressed in various hematopoietic malignancies, including AML in which high expression correlates with poor prognosis. We have recently demonstrated that targeting CD105+ AML blasts with the TRC105 monoclonal antibody abrogates leukemogenesis in vivo. Based on these encouraging findings, here we investigated whether TRC105 in combination with DAC could represent a novel therapeutic option to treat relapsed/refractory AML. Treatment of leukemic mice with DAC in combination with TRC105 resulted in superior survival and significant reduction of leukemia burden in the bone marrow (BM) of AML xenografts compared to DAC monotherapy. To determine if TRC105 anti-leukemogenic effect is mediated by NK cells, we performed in vitro and in vivo studies. In the latter, we tested TRC105 in the context of NK depletion by injecting mice with an antibody to CD122. TRC105 treatment resulted in comparable reduction of leukemia burden in xenografts regardless of NK depletion, demonstrating that the anti-leukemogenic effect of TRC105 in AML is independent of NK cells. Altogether, our findings provide proof-of-principle for the clinical evaluation of TRC105 in combination with DAC in AML patients.

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2013-02-25 | E-GEOD-34157 | biostudies-arrayexpress

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