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Whole exome sequencing (WES) of previously untreated AML samples

ABSTRACT: MNC were isolated from bone of 95 AML patients at initial diagnosis via Ficoll gradient. WES has been performed on all 95 samples.

PROVIDER: EGAS00001007223 | EGA |

REPOSITORIES: EGA

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41c5322c-c1e3-40f1-b6ea-e2602510f45f - samples

Project description:MNC were isolated from bone of 95 AML patients at initial diagnosis via Ficoll gradient. WES has been performed on all 95 samples. Paired exome sequencing was done on a NovaSeq 6000 sequencer with Twist human core exome plus kit.

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Project description:2014 AML WES study contains 51 paired WES samples which were collected from SNUH. The study was designed to examine the molecular abnormalities from leukemic patients at initial diagnosis in comparison with corresponding germ line control (saliva samples). The results of WXS were analyzed by Mutect for ranking cancer variants and creating mutational matrix.

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Phosphoproteomics of primary human FLT3-ITD+ AML cells treated with gilteritinib

Project description:Primary human AML cells (newly diagnosed, prior to treatment initation) were obtained from donor after consent and AML blasts were isolated by standard Ficoll centrifugation. AML blasts were treated with FLT3 inhibitor gilteritinib (or DMSO vehicle control) at 10 nM concentration for 6 h, followed by harvest for LC/MS.

2022-08-25 | PXD034080 | Pride

DNR pulse treatment of primary AML

Project description:Primary human AML bone marrow sample (newly diagnosed, prior to treatment initation) was obtained from donor after consent and AML blasts were isolated by standard Ficoll centrifugation. AML blasts were pulse-treated with daunorubicine (100 nM, 200 nM, 400 nM) or DMSO control for 1 hour, followed by wash-out and short-term cell culture to allow cellular responses to develop. 20,000 cells were analysed by LC-MS3, and 5,000 cells were subjected to flow cytometry apoptosis assay.

2022-10-15 | PXD030280 | Pride

Acquired TET2 mutation-linked clonal hematopoiesis in FPD/AML patient led to the development of pre-leukemic clone resulting independently in T2-ALL and AML-M0.

Project description:Germline RUNX1 mutations are found in familial platelet disorders with predisposition to acute myelogenous leukemia (FPD/AML). This very rare disease is characterized by thrombocytopenia, platelet dysfunction and a 35% lifetime risk of developing MDS/AML and in rare cases also T-ALL. Here, we focus on a case of a man with a familial history of RUNX1 R174Q mutation who developed at the age of 42 years an EGIL T2-ALL and two years after remission an AML-M0. To investigate whether initial and relapsed leukemic blasts originated from the same clone, we performed CGH array and WES on both blasts populations. In both T2-ALL and AML-M0 samples, CGH array revealed loss of 1p36.32-23 and 17q11.2 and nine other small deletions. Both AML-M0 and T2-ALL demonstrated clonal rearrangements of both TCR (V9-J1-1) and TCR (D2-J1 and D2-J3). 18 genes were found by WES to be mutated in the original clone at a frequency of more than 40%. Additional variants were identified only in T2-ALL or in AML-M0 evoking the existence of a common original clone. MiSeq technology performed on peripheral blood-derived CD34+ cells five years prior T2-ALL development revealed only missense TET2 P1962T mutation at a frequency of 1% suggesting that this mutation in association with germline RUNX1 R174Q mutation led to amplification of a hematopoietic clone susceptible to acquire other transforming alterations. Identification of clonal hematopoiesis with acquired mutations at low frequency in hematopoietic progenitors before leukemia development could clearly serve as a marker of pre-leukemic state and might be helpful in patient care.

2017-07-05 | E-MTAB-4679 | biostudies-arrayexpress

Acquired TET2 mutation-linked clonal hematopoiesis in FPD/AML patient led to the development of pre-leukemic clone resulting independently in T2-ALL and AML-M0

Project description:Germline RUNX1 mutations are found in familial platelet disorders with predisposition to acute myelogenous leukemia (FPD/AML). This very rare disease is characterized by thrombocytopenia, platelet dysfunction and a 35% lifetime risk of developing MDS/AML and in rare cases also T-ALL. Here, we focus on a case of a man with a familial history of RUNX1 R174Q mutation who developed at the age of 42 years an EGIL T2-ALL and, two years after remission, an AML-M0. To investigate whether initial and relapsed leukemic blasts originated from the same clone, we performed CGH array and WES on both blasts populations. In both T2-ALL and AML-M0 samples, CGH array revealed loss of 1p36.32-23 and 17q11.2 and nine other small deletions. Both AML-M0 and T2-ALL blasts demonstrated clonal rearrangements of both TCRÎ³ (VÎ³9-JÎ³1-1) and TCRÎ´ (DÎ´2-JÎ´1 and DÎ´2-JÎ´3). 18 genes were found by WES to be mutated in both blasts at a frequency of more than 40%. Additional variants were identified only in T2-ALL or in AML-M0 evoking the existence of a common original clone, which gave rise to subclonal populations. MiSeq technology performed on peripheral blood-derived CD34+ cells five years prior T2-ALL development revealed only missense TET2 P1962T mutation at a frequency of 1% (which reaches a frequency of 50 % in fully transformed leukemic clone) suggesting that this mutation in association with germline RUNX1 R174Q mutation led to amplification of a hematopoietic clone susceptible to acquire other transforming alterations. Identification of clonal hematopoiesis with acquired mutations at low frequency in hematopoietic progenitors before leukemia development could clearly serve as a marker of pre-leukemic state and be helpful in patient care.

2017-06-29 | E-MTAB-4623 | biostudies-arrayexpress

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Project description:Primary human AML cells (newly diagnosed, prior to treatment initation) was obtained from donor after consent and AML blasts were isolated by standard Ficoll centrifugation. Cells were treated ex vivo with DMSO vehicle control or 10 nM FLT3 inhibitors quizartinib, crenolanib, gilteritinib for 6 hours in SILAC medium and processed for LC/MS.

2022-08-25 | PXD034081 | Pride

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.

2017-06-19 | GSE65409 | GEO

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Project description:Blood samples from patients with myeloid malignancies were analyzed using whole exome sequencing (WES). Data set from genotyping by microarray of the same samples has been deposited in ArrayExpress under accession number E-MTAB-1845 (https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1845/).

2013-11-01 | E-MTAB-1850 | biostudies-arrayexpress

Impaired B-lymphocyte immunity in acute myeloid leukemia patients after chemotherapy

Project description:We analyzed via microarray gene expression profiles in de-identified, clinically annotated samples from Ficoll-purified peripheral blood samples from 10 acute myeloid leukemia (AML) patients in remission and 10 healthy donors collected under IRB-approved protocols.

2017-08-11 | GSE97485 | GEO

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