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Single cell RNA-seq analysis of the effects of idasanutlin and/or nilotinib on primary human CML cells engrafted into the bone marrow of immunocompromised mice

ABSTRACT: Single cell RNA-seq analysis of the effects of idasanutlin and/or nilotinib on primary human CML cells engrafted into the bone marrow of immunocompromised mice

PROVIDER: PRJNA902697 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22321148.fastq.gz	Fastqsanger.gz
	SRR22321149.fastq.gz	Fastqsanger.gz
	SRR22321150.fastq.gz	Fastqsanger.gz
	SRR22321151.fastq.gz	Fastqsanger.gz
	SRR22321152.fastq.gz	Fastqsanger.gz

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Single cell RNA-seq analysis of the effects of idasanutlin and/or nilotinib on primary human CML cells engrafted into the bone marrow of immunocompromised mice

Project description:Single cell RNA-seq was performed on primary human CML cells engrafted into the bone marrow of immunocompromised mice to understand the molecular consequences of treatment with the tyrosine kinase inhibitor nilotinib alone and in combination with the MDM2 inhibitor idasanutlin.

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Bulk RNA-seq analysis of primary CML CD34+ cells (n=3) treated with idasanutlin alone or in combination with nilotinib in vitro

Project description:Bulk RNA-seq was performed on primary human CML CD34+ cells to understand the molecular consequences of treatment with the MDM2 inhibitor idasanutlin alone and in combination with the tyrosine kinase inhibitor nilotinib for 24 hrs and 72 hrs.

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Bulk RNA-seq analysis of primary CML CD34+ cells (n=3) treated with idasanutlin alone or in combination with nilotinib in vitro

Project description:Bulk RNA-seq analysis of primary CML CD34+ cells (n=3) treated with idasanutlin alone or in combination with nilotinib in vitro

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Imatinib and Nilotinib induced molecular changes in Philadelphia chromosome-positive Chronic Myelogenous Leukemia

Project description:Chronic myelogenous leukemia (CML) is a malignant stem cell disease characterized by a reciprocal translocation between chromosome 9 and 22. The selective bcr-abl tyrosine-kinase inhibitor Imatinib has become the therapy of choice for patients with newly diagnosed CML including those previously considered candidates for allogeneic haematopoietic stem cell transplantation. The tyrosine-kinase inhibitor Nilotinib is a derivate of Imatinib with higher potency. To examine the molecular and functional effects of Nilotinib and Imatinib in chronic myelogenous leukemia, we performed gene expression and functional analyses in K562 cells following treatment with the two tyrosine kinase inhibitors.

2009-12-19 | GSE19567 | GEO

ChIP-seq analysis to determine p53 binding profiles in the BV173 cell line before and after treatment with the MDM2 inhibitor idasanutlin

Project description:We performed ChIP-seq analysis in order to determine the transcriptional targets of p53 in the CML cell line BV173 as a result of p53 activation using the MDM2 inhibitor idasanutlin.

2023-12-19 | GSE218182 | GEO

Transcription profiling of human K562 cells reveals Imatinib and Nilotinib induced molecular changes in Philadelphia chromosome-positive Chronic Myelogenous Leukemia

2010-01-19 | E-GEOD-19567 | biostudies-arrayexpress

Treatment of CML cells with RITA, CPI-203, the combination thereof and nilotinib.

Project description:CML CD34+ cells were treated with RITA, CPI-203, the combination thereof and nilotinib.

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Early and late TKI response of CML stem cells

Project description:Chronic myeloid leukaemia (CML) is a clonal haemopoietic stem cell (HSC) disorder associated with the BCR-ABL oncogene, which encodes a constitutively active tyrosine kinase. We have demonstrated the existence of CML HSC which are resistant to the tyrosine kinase inhibitors (TKI). We have hypothesised that CML stem cells are dependent on key survival pathways that are induced by TKI treatment. In order to elucidate these key survival pathways, we have investigated the transcriptional differences between CML stem/progenitor cells (CD34+38-) treated with TKIs (imatinib, dasatinib and nilotinib) at different time points (8 hours and 7 days, in the absence of growth factors) and by carrying out RNA profiling for the different populations. CD34+38- cells were isolated from chronic phase patient samples. >100ng of total RNA was amplified prior to analysis that was carried out with Affymetrix Human Gene 1.0 ST array.

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Idasanutlin differential expression in MOLM13 and OCIAML3

Project description:Targeting MDM2 is an attractive therapeutic approach for TP53 wild-type (WT) tumors, including the majority of de novo acute myeloid leukemia (AML) cases. However, patients with WT TP53 have shown variable responses to MDM2 inhibitors in clinical trials, highlighting the need to identify additional biomarkers to maximize the chances of clinical success. We performed CRISPR-Cas9 knockout screens to identify genes that confer resistance to an MDM2 inhibitor idasanutlin. We did not find recurrent sgRNA hits or mutations in p53 downstream targets, such as CDKN1A, BAX, PMIAP1, and BBC3, apart from TP53. This was consistent with the results of individual knockout validation experiments and exome sequencing data from idasanutlin resistant cell lines generated form long-term exposure to low doses of idasanutlin. RNA-seq differential expression analysis revealed that major p53 downstream targets were upregulated in both idasanutlin-sensitive MOLM13 and resistant OCIAML3 cell lines after idasanutlin treatment. These findings highlight the pleiotropic functions of TP53 and suggest that the loss of individual downstream targets of TP53 does not significantly contribute to MDM2 inhibitor resistance.

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Gene expression profiling of CD34/CD38 sorted CML cells

Project description:BACKGROUND: BCR-ABL1+ chronic myeloid leukemia (CML) is characterized by abnormal production of leukemic stem (LSC) and progenitor cells and their spread from the bone marrow into the blood resulting in extramedullary myeloproliferation. So far, little is known about specific markers and functions of LSC in CML. METHODS: We examined the phenotype and function of CD34+/CD38─/Lin─ CML LSC by a multi-parameter screen approach employing antibody-phenotyping, mRNA expression profiling, and functional studies, including LSC repopulation experiments in irradiated NOD-SCID-IL-2Rgamma-/- (NSG) mice, followed by marker-validation using diverse control-cohorts and follow-up samples of CML patients treated with imatinib. RESULTS: Of all LSC markers examined, dipeptidylpeptidase IV (DPPIV=CD26) was identified as specific and functionally relevant surface marker-enzyme on CD34+/CD38─ CML LSC. CD26 was not detected on normal CD34+/CD38─ stem cells or LSC in other hematopoietic malignancies. The percentage of CD26+ CML LSC decreased to undetectable levels during successful treatment with imatinib in all patients (p<0.001). Whereas the sorted CD26─ stem cells obtained from CML patients engrafted irradiated NSG mice with multilineage BCR-ABL1-negative hematopoiesis, CD26+ LSC engrafted NSG mice with BCR-ABL1+ cells. Functionally, CD26 was identified as target-enzyme disrupting the SDF-1alpha-CXCR4-axis by cleaving SDF-1alpha a chemotaxin for CXCR4+ stem cells. Whereas CD26 was found to inhibit SDF-1alpha-induced migration, CD26-targeting gliptins reverted this effect and blocked the mobilization of CML LSC in a stroma co-culture assay. CONCLUSIONS: CD26 is a robust biomarker of LSC and a useful tool for their quantification and isolation in patients with BCR/ABL1+ CML. Moreover, CD26 expression may explain the extramedullary spread of LSC in CML.

2014-04-17 | GSE40721 | GEO

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