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Expression profiles of cell populations purified from human CRC (3 ways)

ABSTRACT: The survival of isolated metastatic cells and expansion into macroscopic tumour has been recognized as a limiting step for metastasis formation in several cancer types yet the determinants of this process remain largely uncharacterized. In colorectal cancer (CRC), we identify a transcriptional programme in tumour-associated stromal cells, which is intimately linked to a high risk of developing recurrent disease after therapy. A large proportion of CRCs display mutational inactivation of the TGF-beta pathway but paradoxically they are characterized by high TGF-beta production. In these tumours, TGF-beta instructs a transcriptional programme in stromal cells, which confers a high risk of developing metastatic disease. We purified by FACS [CD45(+),Epcam(-)], [CD45(-) Epcam(+)] and [CD45(-) Epcam(-)] cell populations from fresh CRC samples and assessed their gene expression profiles

ORGANISM(S): Homo sapiens

PROVIDER: GSE39395 | GEO | 2013/01/17

SECONDARY ACCESSION(S): PRJNA170773

REPOSITORIES: GEO

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Expression profiles of cell populations purified from human CRC (3 ways)

Project description:The survival of isolated metastatic cells and expansion into macroscopic tumour has been recognized as a limiting step for metastasis formation in several cancer types yet the determinants of this process remain largely uncharacterized. In colorectal cancer (CRC), we identify a transcriptional programme in tumour-associated stromal cells, which is intimately linked to a high risk of developing recurrent disease after therapy. A large proportion of CRCs display mutational inactivation of the TGF-beta pathway but paradoxically they are characterized by high TGF-beta production. In these tumours, TGF-beta instructs a transcriptional programme in stromal cells, which confers a high risk of developing metastatic disease. We purified by FACS [CD45(+),Epcam(-)], [CD45(-) Epcam(+)] and [CD45(-) Epcam(-)] cell populations from fresh CRC samples and assessed their gene expression profiles Freshly obtained tumors from CRC patients (n=8) treated at Hospital del Mar (Barcelona, Spain) were minced and incubated with 0.1% Hyaluronidase and 0.1% Collagenase 1A. Pieces were then homogenized. Enzymatic reaction was stopped by adding 10% FBS and single cells were collected by sequential filtering. Cells were resuspended in Ammonium Chloride (0.15M) to lyse erythrocytes. Cells were stained with anti-hEpcam/TROP1-APC and anti-CD45-PE conjugated antibody. Dead cells were labeled with Propidium Iodide. Fluorescence Activated Cell Sorting (FACS) was used to separate cells.

2013-01-17 | E-GEOD-39395 | biostudies-arrayexpress

Expression profiles of cell populations purified from human CRC (4 ways)

Project description:The survival of isolated metastatic cells and expansion into macroscopic tumour has been recognized as a limiting step for metastasis formation in several cancer types yet the determinants of this process remain largely uncharacterized. In colorectal cancer (CRC), we identify a transcriptional programme in tumour-associated stromal cells, which is intimately linked to a high risk of developing recurrent disease after therapy. A large proportion of CRCs display mutational inactivation of the TGF-beta pathway but paradoxically they are characterized by high TGF-beta production. In these tumours, TGF-beta instructs a transcriptional programme in stromal cells, which confers a high risk of developing metastatic disease. We purified by FACS CD31(+), CD45(+), FAP(+) and Epcam(+) populations from fresh CRC samples and assessed their gene expression profiles Freshly obtained tumours from 6 CRC patients treated at Hospital del Mar or Hospital Clinic (Barcelona, Spain) were minced and incubated with Collagenase IV (100 U mL-1). Enzymatic reaction was stopped by adding 10% FBS, single cells were collected by sequential filtering and resuspended in ammonium chloride (0.15M) to lyse erythrocytes. Cells were stained with FAP unconjugated rabbit antibody. After two washes with HBSS, cells were stained with an APC conjugated anti-rabbit antibody; anti-hEPCAM/TROP1-FITC, anti-CD31-PE and anti-CD45-PE-Cy7 conjugated antibody. Dead cells were labelled with Propidium Iodide. Fluorescence Activated Cell Sorting (FACS) was used to separate 2000 cells from each population; [CD45(+), EPCAM(-), CD31(-), FAP(-)], [CD45(-) EPCAM(+), CD31(-), FAP(-)], [CD45(-), EPCAM(-), CD31(+),FAP(-)] and [CD45(-), EPCAM(-), CD31(-), FAP(+)].

2013-01-17 | E-GEOD-39396 | biostudies-arrayexpress

Expression profiles of cell populations purified from human CRC (4 ways)

2013-01-17 | GSE39396 | GEO

Expression data from fibroblasts treated with TGF-Beta

Project description:The survival of isolated metastatic cells and expansion into macroscopic tumour has been recognized as a limiting step for metastasis formation in several cancer types yet the determinants of this process remain largely uncharacterized. In colorectal cancer (CRC), we identify a transcriptional programme in tumour-associated stromal cells, which is intimately linked to a high risk of developing recurrent disease after therapy. A large proportion of CRCs display mutational inactivation of the TGF-beta pathway but paradoxically they are characterized by high TGF-beta production. In these tumours, TGF-beta instructs a transcriptional programme in stromal cells, which confers a high risk of developing metastatic disease. We quantified the association of TGF-beta-activated fibroblasts with disease progression. To this end, we used as surrogates the gene expression programme upregulated by addition of TGF-beta to normal colon mucosa-derived fibroblasts (CCD-Co-18) in culture. CCD-Co-18 were seeded at 60% confluence and treated with TGF-Î²1. Gene expression profiles were measured in duplicate using HG-U133 plus 2.0. We used RMA background correction, quantile normalization and RMA summarization (Gautier et al., 2004). A TGF-Î² response signature was obtained by selecting genes with limma P-value < 0.05 and at least two fold up-regulation in TGF-Î² treated fibroblasts.

2013-01-17 | E-GEOD-39394 | biostudies-arrayexpress

Expression data from fibroblasts treated with TGF-Beta

2013-01-17 | GSE39394 | GEO

68Ga-FAPI PET imaging assesses tumor immunity and guides TGF-β inhibition to sensitize metastatic colorectal cancer to immunotherapy

Project description:BACKGROUND. Improving and predicting tumor response to immunotherapy remains challenging. Combination therapy with a transforming growth factor β (TGF-β) inhibitor that targets cancer associated fibroblasts (CAFs) is promising to enhance efficacy of cancer immunotherapies. However, the effect of this approach in clinical trials is limited, requiring in vivo methods to better assess tumor responses to combination therapy. METHODS. We measure CAFs in vivo using gallium 68-labeled fibroblast activation protein inhibitor (68Ga-FAPI) for PET/CT imaging to guide TGF-β inhibition and sensitize metastatic colorectal cancer (CRC) to immunotherapy. A total of 131 patients with metastatic CRC underwent 68Ga-FAPI and 18F-fludeoxyglucose (18F-FDG) PET/CT imaging. Fourteen patients underwent surgery after the imaging. Relationship between uptake of 68Ga-FAPI and tumor immunity was analyzed. Mouse cohorts of metastatic CRC were treated with TGF-β receptor (TGF-βR) inhibitor combined with KN046 which blocks PD-L1 and CTLA4, followed with 68Ga-FAPI and 18F-FDG micro-PET/CT imaging to assess tumor responses. RESULTS. Patients with metastatic CRC demonstrated high uptakes of 68Ga-FAPI, along with suppressive tumor immunity and poor prognosis. TGF-βR inhibitor enhanced tumor infiltrating T cells and significantly sensitized metastatic CRC to KN046. 68Ga-FAPI PET/CT imaging accurately monitored the dynamical changes of CAFs and tumor response to combined TGF-βR inhibitor with immunotherapy. CONCLUSION. 68Ga-FAPI PET/CT imaging is powerful in assessing tumor immunity and response to immunotherapy in metastatic CRC. This study supports future clinical application of 68Ga-FAPI PET/CT to stratify and guide patients with CRC for precise TGF-β inhibition plus immunotherapy, recommending 68Ga-FAPI and 18F-FDG dual PET/CT for CRC management.

2023-12-19 | GSE247303 | GEO

LAKTP_MTO orthotopic primary caecum tumours from Galunisertib-treated C57BL/6J mice

Project description:Mouse tumour organoids (MTOs) derived from a compound mutant (LAKTP) intestinal cancer model were orthoptopically transplanted into syngeneic C57BL/6J mice. Tumour-bearing mice were treated with TGF-beta inhibitor Galunisertib or vehicle control. Whole tumour mRNA was extracted from primary tumours and expression profiling was performed with the objective to characterize the tumour microenvironment (TME). As a TGF-beta-activated TME has been associated to a poor prognosis and the CRC consensum molecular subtype CMS4, and the mouse model was found to have such an activated TME, we used the array data to classify these tumours in this mouse model system as CMS4-like. Furthermore, treatment with TGF-beta inhibitor reduced the fibroblast- and T cell-specific TGF-beta response signatures, also associated to poor prognosis in human CRC. This treatment was associated to a strong reduction/prevention of liver metastasis, as well as a reduction of primary tumour (and local carcinomatosis) size.

2018-02-12 | GSE103562 | GEO

Single cell analysis of Villin-Cre;Apc min;Lef1 fl/fl (VApcMinL) and ApcMin Epcam- cells and CD45-Epcam- stromal cells from lamina propria at the age of 11 wks.

Project description:Comparison of Villin-Cre;Apc min;Lef1 fl/fl (VApcMinL) and ApcMin Epcam- cells and CD45-Epcam- stromal cells from lamina propria at the age of 11 wks. Two male mice per group was used in the experiment.

2021-12-10 | GSE173565 | GEO

RNA-seq profiling of gene expression in Ezh2-deficient and control murine lung epithelial and stromal cell populations at day E16.5

Project description:Epithelial (CD31-CD45-EpCAM+) and stromal (CD31-CD45-EpCAM-) lung cells were derived by FACS from ShhCre;Ezh2fl/fl and control ShhCre;Ezh2fl/+ mouse embryos at day E16.5 (3 biological replicates per genotype-tissue combination). Total RNA extracted from the samples was subjected to NGS library preparation using TruSeq Stranded Total RNA with Ribo-Zero (Illumina). Completed libraries from different samples were sequenced on HiSeq 2000 TruSeq with SBS Kit v3 - HS reagents (Illumina) as 100 bp single end reads at the Australian Genome Research Facility. RNA-seq gene expression profiles from Ezh2 deficient and control lung epithelial and stromal cell populations at day E16.5 (3 replicates per genotype-tissue combination).

2015-05-11 | E-GEOD-57391 | biostudies-arrayexpress

RNA-seq profiling of gene expression in Ezh2-deficient and control murine lung epithelial and stromal cell populations at day E16.5

2015-05-11 | GSE57391 | GEO

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