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Imetelstat is effective in Acute Myeloid Leukemia (AML) patient xenografts.

ABSTRACT: Imetelstat is effective in Acute Myeloid Leukemia (AML) patient xenografts.

PROVIDER: PRJNA736609 | ENA |

REPOSITORIES: ENA

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Acute Myeloid Leukemia (AML) patient xenografts

Project description:Acute Myeloid Leukemia (AML) patient xenografts

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Imetelstat is effective in Acute Myeloid Leukemia (AML) patient xenografts.

Project description:Imetelstat is a covalently lipidated 13-mer thiophosphoramidate oligonucleotide that competitively inhibits telomerase activity. Here, we show that imetelstat effectively diminishes AML burden and prolongs survival in a comprehensive, randomized Phase II-like preclinical trial in AML patient-derived xenografts (PDX).

2023-07-14 | GSE176523 | GEO

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The phosphoproteomic landscape of two FLT3+ Acute Myeloid Leukemia (AML) patient samples.

Project description:Acute myeloid leukemia (AML) is a clonal hematopoietic malignancy, characterized by expansion of immature leukemic blasts in the bone marrow. In AML, specific tyrosine kinases have been implicated in leukemogenesis, and are associated with poor treatment outcome. However, targeted therapy using kinase inhibitors (KIs) has had limited success, and may be improved by proper patient selection. We performed phosphotyrosine (pY) based, label-free phosphoproteomics to identify hyperphosphorylated, active kinases in two FLT3+ AML Pt samples.

2020-03-02 | PXD015639 | Pride

The phosphoproteomic landscape of two FLT3+ Acute Myeloid Leukemia (AML) patient samples-LYSATES.

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Adverse stem cell features in a single AML sample predict clinical outcome in AML patient cohorts

Project description:Patients with acute myeloid leukemia (AML) suffer dismal prognosis and the most adverse subpopulation within each tumor determines patient’s prognosis. To better understand challenging features in AML, we studied individual stem cells from a single AML sample, complementing genomic with in vivo functional studies. Primary tumor cells from an AML patient’s first and second relapse were transplanted into NSG mice to establish serially transplantable patient derived xenografts (PDX). In an innovative approach, twelve derivative PDX clones were generated thereof, each derived from a single AML stem cell as proven by molecular barcoding, and were color-marked to facilitate multiplex competitive in vivo assays. PDX clones consisted of four different genomic clusters; one cluster displayed resistance against Cytarabine treatment, while two other clusters harbored increased stem cell potential, indicating that stemness and treatment resistance had evolved independently in the sample. In vivo functional data correlated closely with the phylogenetic tree calculated from exome data. The Cytarabine-resistant cluster was characterized by a distinct gene expression profile, and a score thereof predicted outcome in large clinical patient data cohorts. Taken together, we provide proof of concept that intra-sample heterogeneity mimics inter-sample heterogeneity in AML. Stem cell disparities within a single sample allow insights into adverse characteristics of general importance for AML.

2022-04-04 | PXD026296 | Pride

Thoracic patient-derived xenografts

Project description:Thoracic patient-derived xenografts

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RNA sequencing of patient-derived AML xenografts treated with Selinexor (KPT-330)

Project description:RNA sequencing of patient-derived AML xenografts treated with Selinexor (KPT-330)

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Human AML patient samples, Method Optimization, LC-MSMS

Project description:We evaluated different in-solution and filter-aided sample preparation (FASP) proteomic workflows, and different enrichment strategies of phosphorylated peptides on acute myeloid leukemia (AML) patient samples. We also studied the effect of liquid nitrogen storage on the proteome and phosphoproteome of four AML patients.

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Gene expression patterns in response to IL-3 in human AML patient mononuclear cells

Project description:Aberrant activation of β-catenin is a common event in Acute Myeloid Leukemia (AML), and is recognized as an independent predictor of poor prognosis. Although increased β-catenin signaling in AML has been associated with AML1-ETO and PML-RARα translocation products, and activating mutations in the FLT3 receptor, it remains unclear which mechanisms activate β-catenin in AML more broadly. Here, we describe a novel link between interleukin-3 (IL-3) signaling and the regulation of β-catenin in myeloid transformation and AML. Using a murine model of HoxB8 and IL-3 cooperation we show that IL-3 modulates β-catenin protein levels, and Cre-induced deletion of β-catenin abolishes IL-3 dependent growth and colony formation. In the erythroleukemic cell line TF-1.8, we observed increased β-catenin protein levels and nuclear localization in response to IL-3, which correlated with transcriptional induction of β-catenin target genes. Furthermore, IL-3 promoted β-catenin accumulation in a subset of AML patient samples, and microarray gene expression analysis of these cells revealed induction of WNT/β-catenin and TCF4 transcriptional gene signatures in an IL-3 dependent manner. This study is the first to link β-catenin activation to IL-3 and suggests that targeting IL-3 signaling may be an effective approach for the inhibition of β-catenin activity in some patients with AML. AML patient samples (AML1-4) were cultured in the presence or absence of hIL-3 for 6 or 16h.

2014-02-13 | E-GEOD-51402 | biostudies-arrayexpress

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