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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The effect of imatinib therapy on tumor associated macrophages (TAMs) in human gastrointestinal stromal tumor (GIST)

ABSTRACT: The gene expression profile of TAMs microbead isolated from freshly obtained human GISTs were compared in tumors that were untreated, responding to imatinib (sensitive), or resistant to imatinib (resistant) The Affymetrix Human Genome U133A 2.0 platform was used TAMs were microbead isolated from 12 untreated, 5 sensitive, and 4 resistant tumors. Tumors were obtained freshly from the operating room from consenting patients using an IRB approved protocol. Tumors were digested using collagenase and TAMs isolated using microbead negative selection for KIT, CD3, and CD56 followed by positive selection for CD14.

ORGANISM(S): Homo sapiens

SUBMITTER: Jeffrey Zhao

PROVIDER: E-GEOD-51697 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The effect of imatinib therapy on tumor associated macrophages (TAMs) in human gastrointestinal stromal tumor (GIST)

Project description:The gene expression profile of TAMs microbead isolated from freshly obtained human GISTs were compared in tumors that were untreated, responding to imatinib (sensitive), or resistant to imatinib (resistant) The Affymetrix Human Genome U133A 2.0 platform was used

2013-11-20 | GSE51697 | GEO

The effect of imatinib therapy on tumor associated macrophages (TAMs) in murine gastrointestinal stromal tumor (GIST)

Project description:The gene expression profile of TAMs sorted from vehicle control tumors in GIST mice (Sommer et al, PNAS 2003) was compared to TAMs sorted from mice after 2 weeks of imatinib therapy The Affymetrix Mouse Genome 430A 2.0 platform was used Each treatment group had 8 mice. After 2 weeks of treatment, mice were sacrificed and tumors digested with collagenase. TAMs were then FACS sorted and pooled by group. Pooled groups were run in duplicate for the gene expression array.

2013-11-20 | E-GEOD-51698 | biostudies-arrayexpress

Transcription profiling of human imatinib-sensitive and imatinib-resistant cells compared in the absence of imatinib

Project description:Both imatinib-sensitive and imatinib-resistant cells were compared in the absence of imatinib. The resistant cells in the presence of imatinib were compared to the sample in the absence of imatinib. The sample from the resistant cells in the presence of imatinib was labelled in duplicate to assess false-positive rates.

2003-11-30 | E-MEXP-21 | biostudies-arrayexpress

The effect of imatinib therapy on tumor associated macrophages (TAMs) in murine gastrointestinal stromal tumor (GIST)

2013-11-20 | GSE51698 | GEO

Genomic profiling of imatinib resistant and sensitive K562 cells to obtain insights into imatinib resistance

Project description:Chronic myeloid leukemia (CML) epitomizes successful targeted therapy, with 86% of patients in the chronic phase treated with tyrosine kinase inhibitors (TKIs) attaining remission. However, resistance to TKIs occurs during treatment, and patients with resistance to TKIs progress to the acute phase called Blast Crisis (BC), wherein the survival is restricted to 7-11 months. About 80 % of patients in BC are unresponsive to TKIs. This issue can be addressed by identifying a molecular signature which can predict resistance in CML-CP prior to treatment as well as by delineating the molecular mechanism underlying resistance. Herein, we report genomic analysis of CML patients and imatinib-resistant K562 cell line to achieve the same. WGS was performed on imatinib-sensitive and -resistant K562 cells. Library preparation was done by 30x WGS KAPA PCR-Free v2.1 kit, and Illumina HiSeq X sequencer was used for 2 x 150 bp paired-end sequencing. Our study identified accumulation of aberrations on chromosomes 1, 3, 7, 16 and 22 as predictive of occurrence of resistance. Further, recurrent amplification in chromosomal region 8q11.2-12.1 was detected in highly resistant K562 cells as well as CML patients. The genes present in this region were analyzed to understand molecular mechanism of imatinib resistance.

2024-01-01 | E-MTAB-11896 | biostudies-arrayexpress

Transcriptomic analysis of imatinib-resistant K562 cells with knocked down Pleomorphic Adenoma Gene 1 (PLAG1) to identify the targets

Project description:Genomic profiling of K562 cells resistant to imatinib as well as imatinib resistant CML patients harboured a recurrent chromosomal amplification in 8q11.2-12.1. Gene encoding PLAG1, a transcription factor associated with cancers and chemo resistance, resides on this locus and was found to be amplified in resistant cells. Upon PLAG1 knockdown we observed a decrease in imatinib resistance, and to understand the molecular events underlying PLAG1-mediated imatinib resistance, RNA sequencing was carried out. Imatinib-resistant K562 cells were transfected with lentiviral particles containing shRNA against PLAG1 and lentiviral particles containing pLKO.1-empty vectors. Monoclonal populations were established. Total RNA sequencing was performed. For QC, RNA samples were quantified using the Qubit RNA BR Assay kit (Invitrogen, Cat# Q10211). RNA purity was checked using QIAxpert, and RNA integrity was assessed on TapeStation using High Sensitivity RNA ScreenTape® (Agilent, Cat# 5067-5579). QC passed RNA samples were subjected to the library preparation, and NEB Ultra RNA-Seq Library Prep kit protocol (Cat# E7530L) was used and sequenced on Illumina NovaSeq 6000 instrument. Transcriptomic analysis identified several genes down-regulated upon PLAG1 knockdown which were further investigated.

2024-01-01 | E-MTAB-11893 | biostudies-arrayexpress

Expression data from in vitro-induced non-hypoxic tumour associated macrophages (TAMs)

Project description:Active immunotherapy is a promising strategy for anti-angiogenic cancer therapy. Recently, we have reported that a vaccine using human umbilical vein endothelial cells (HUVECs) induced specific anti-endothelial immune responses in the most of immunized patients, and resulted in tumor regression in some patients with recurrent malignant brain tumors, whereas not in colorectal cancer patients. In this study, we hypothesized that non-hypoxic perivascular tumor associated macrophages (TAMs) in colorectal cancer, but not in glioblastoma, might negatively alter the therapeutic efficacy of anti-angiogenic active immunotherapy. To test this hypothesis, we examined global gene expression profiles of non-hypoxic macrophages stimulated in vitro by soluble factors released from tumor cells of human glioblastoma U-87MG (‘brain TAMs’) or colorectal adenocarcinoma HT-29 (‘colon TAMs’). Murine non-hypoxic TAMs were induced in vitro by incubation with soluble factors released from human cancer cell lines U-87MG ('brain TAMs') or HT-29 ('colon TAMs'), for RNA extraction and subsequent hybridization on Affymetrix microarrays. To evaluate homogeneous macrophage populations at different tumour developmental stages, RNA aliquots of control macrophages and TAMs obtained at five different time-points, i.e. 8h, 16h, 24h, 32h and 40h, were pooled and used for screening of differentially expressed genes. The experiments for TAMs as well as for control unstimulated macrophages were performed in triplicates.

2012-03-31 | E-GEOD-18804 | biostudies-arrayexpress

Transcriptome sequencing analysis of CSF-1Rhigh TAMs and CSF-1Rlow TAMs in colon adenocarcinoma.

Project description:Tumor-associated macrophages (TAMs) are a major component of the leukocyte and a heterogenous population in tumors. Recent reports have increasingly suggested that manipulating the function of TAMs may serve as a promising therapeutic strategy against advanced tumors. Our present work indicates that CSF-1R+ TAMs are abundantly found in a significant proportion of COAD specimens. Therefore，to determine the role of the CSF-1Rhigh TAMs in COAD, we sorted the CSF-1Rhigh TAMs and the CSF-1R low TAMs from the colon adenocarcinomas for Smart-seq2. We found that CSF-1Rhigh TAM infiltration involved in multiple tumor immune signaling pathways. CSF-1Rhigh TAMs mostly exhibited a immunosuppressive phenotypes, and were associated with enhanced levels of Treg cells. CSF-1R high TAMs promotes COAD progression by modulating tumor immunity environment

2022-03-31 | GSE193814 | GEO

Genomic profiling of immature hematopoietic cells to obtain insights into imatinib resistance

Project description:Chronic myeloid leukemia (CML) epitomizes successful targeted therapy, with 86% of patients in the chronic phase treated with tyrosine kinase inhibitors (TKIs) attaining remission. However, resistance to TKIs occurs during treatment, and patients with resistance to TKIs progress to the acute phase called Blast Crisis (BC), wherein the survival is restricted to 7-11 months. About 80 % of patients in BC are unresponsive to TKIs. This issue can be addressed by identifying a molecular signature which can predict resistance in CML-CP prior to treatment as well as by delineating the molecular mechanism underlying resistance. Herein, we report genomic analysis of CML patients and imatinib-resistant K562 cell line to achieve the same. Thirteen CML patients (sensitive and resistant to TKIs) and 2 BMT donors (as control) were recruited for the study. DNA was isolated from an enriched CD34+ fraction for each sample as well as from K562 cells made resistant to imatinib which provided a model system for further molecular investigations. DNA was subjected to Cytoscan HD array (Affymatrix) analysis from patient samples and cell lines. Affymetrix CytoScan™ HD array (Applied Biosystems™, Cat# 901835) chip consists of 2.6 M oligonucleotide probes across the genome, including 1953K unique non-polymorphic probes and 750K bi-allelic SNP (single nucleotide polymorphism) probes. Our study identified accumulation of aberrations on chromosomes 1, 3, 7, 16 and 22 as predictive of occurrence of resistance. Further, recurrent amplification in chromosomal region 8q11.2-12.1 was detected in highly resistant K562 cells as well as CML patients. The genes present in this region were analyzed to understand molecular mechanism of imatinib resistance.

2024-01-01 | E-MTAB-11899 | biostudies-arrayexpress

Gene expression profiles of tumor-associated macrophages (TAMs) overexpressing miR-511-3p

Project description:Hematopoietic stem/progenitor cells (HS/PCs) were transduced with lentiviral vectors overexpressing OFP and either miR-511-3p or a control, mutated miRNA sequence (miR-511-3p-mut). The transduced HS/PCs were then transplanted in recipient C57BL/6 mice. Tumors (Lewis lung carcinomas, LLC) were injected s.c. 4 weeks after HS/PC transplant. Lentiviral vector-transduced (OFP+), tumor-associated macrophages (TAMs) were isolated 4 weeks after LLC injection by fluorescence-activated cell sorting. Gene expression profiles of TAMs overexpressing either miR-511-3p or miR-511-3p-mut were obtained from 3 independent biological samples/each. Gene expression profiles of miRNA-overexpressing TAMs were then compared with the gene expression profiles of wild-type TAMs isolated from LLCs grown in nontransplanted C57BL/6 mice; the latter TAMs were subfractioned into MRC1+CD11c(low) or CD11c+MRC1(low) subsets before RNA isolation and analysis. Comparison of gene expression profiles of TAMs revealed that miR-511-3p overexpression tunes down the expression of multiple genes that are classically upregulated in protumoral MRC1+CD11c(low) TAMs. TAMs were isolated from Lewis lung carcinomas grown s.c. in C57BL/6 mice.

2012-04-01 | E-GEOD-34903 | biostudies-arrayexpress

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