Several colorectal cancer patient derived tumor organoid RNAseq data
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1021206 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26182964_1.fastq.gz | Fastqsanger.gz | |||
| SRR26182964_2.fastq.gz | Fastqsanger.gz | |||
| SRR26182965_1.fastq.gz | Fastqsanger.gz | |||
| SRR26182965_2.fastq.gz | Fastqsanger.gz | |||
| SRR26182966_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 28 |
Similar Datasets
Project description:Acquired drug resistance is a major challenge for cancer therapy and the leading cause of cancer mortality. However, the mechanisms of drug resistance are diverse and the strategy to specifically target drug resistant cancer cells remains an unmet clinical issue. We establisheda32 colorectal cancer (CRC) PDO biobank and induced acquired drug resistance by repeated low-level exposures of chemo-agents. Chemosensitivity profiling and transcriptomic analysis studies34 revealed that chemo-resistant PDOs exhibited elevated expression of LGR4 and activationof the35 Wnt signaling pathway. Further, we performed antibody screening against LGR4 and selecteda36 monoclonal antibody (LGR4-mAb) that potently inhibited the LGR4/Wnt signaling. In drug resistant PDOs and xenograft models, treatment with LGR4-mAb significantly sensitizeddrug- 38 induced ferroptosis. Mechanistically, LGR4 dependent Wnt signaling transcriptionally up-regulated SLC7A11, a key inhibitor of ferroptosis, to confer acquired drug resistance. Targeting40 Wnt signaling by LGR4-mAb and by other modulators augments ferroptosis when co-administrated with chemotherapeutic agents. Finally, LGR4-mAb therapy was effective against other cancers that express high levels of LGR4. Collectively, our results demonstrate a new strategy to selectively activate ferroptosis and provide a new opportunity to fight refractoryand44 recurrent cancers.
2023-09-25 | GSE244082 | GEO
Project description:Patient derived organoids (PDOs) have been established as a 3D culture model which closely recapitulates the in vivo tumor biology. However, one limitation of this culture model is the lack of tumor microenvironment which has a significant role in tumor progression and drug response. To address this, we established and molecularly characterized a novel 3D co-culture model of colorectal cancer (CRC) based on PDOs and patient matched fibroblasts. Both normal and cancer associated fibroblasts, NFs and CAFs respectively, were able to support organoid growth without addition of niche factors to the media. Additionally, co-cultures showed closer resemblance to primary patient material than organoid mono-cultures as evaluated by histology. Finally, RNA gene expression signatures of tumor cells and fibroblasts isolated from mono- or co-cultures demonstrated that co-cultures support greater cell type heterogeneity. In this proteomics dataset we compared pairs of NFs and CAFs derived from five patients. Collectively, we present a newly established human derived organoid-fibroblast model which, closely recapitulates in vivo tumor heterogeneity and involves the tumor microenvironment.
2023-03-14 | PXD032047 | Pride
Project description:In Rspondin-based 3D cultures, Lgr5 stem cells from multiple organs form ever-expanding epithelial organoids that retain their tissue identity. We report the establishment of tumor organoid cultures from 20 consecutive colorectal (CRC) patients. For most, organoids were also generated from adjacent normal tissue. The organoids closely resemble the original tumor. The spectrum of genetic changes observed within the 'living biobank' agrees well with previous large-scale mutational analyses of CRC. Gene expression analysis indicates that the major CRC molecular subtypes are represented. Tumor organoids are amenable to robotized, high-throughput drug screens allowing detection of gene-drug associations. As an example, a single organoid culture was exquisitely sensitive to Wnt secretion (porcupine) inhibitors and carried a mutation in the negative Wnt feedback regulator RNF43 (rather than in APC). Organoid technology may fill the gap between cancer genetics and patient trials, complement cell line- and xenograft-based drug studies and allow personalized therapy design. We generated organoids from healthy tissue and coloncarcinoma tissue. The organoids were trypsinized, plated in matrigel and overlaid with medium. After three days, RNA was isolated using Qiagen RNAeasy. Medium conditions are the same for all organoids, irrespective of their origin.
2015-05-07 | E-GEOD-64392 | biostudies-arrayexpress
Project description:We tested transcript profile of colorectal cancer (CRC) organoid from CRC patients. We compared the transcripts profile change between drug resistant organoid and drug sensitive organoid.
2022-11-29 | GSE218558 | GEO
Project description:Transcriptomic profiles of 6 commercially-available human patient-derived gastrointestinal organoid lines were obtained and compared to transcriptomic profile of a commercially available human iPSC-induced colon organoid line. Transcriptomic profile of iPSC-derived human colon organoid line was compared after culture in either Corning growth-factor-reduced Matrigel (Corning 356231) or MilliporeSigma growth-factor-reduced ECMGel (E6909)
2022-03-31 | E-MTAB-11557 | biostudies-arrayexpress
Project description:Patient-derived breast cancer organoid study
| PRJNA786253 | ENA
Project description:Patient-derived breast cancer organoid study
| PRJNA786254 | ENA
Project description:Patient-derived organoid fibroblast co-cultures closely mimic tumor cell heterogeneity of colorectal cancer
| PRJNA816490 | ENA
Project description:Fisetin suppresses colorectal cancer growth through AKAP12 in the patient-derived organoid xenograft model
| PRJNA883378 | ENA
Project description:In Rspondin-based three-dimensional cultures, Lgr5 stem cells from multiple organs form ever-expanding epithelial organoids that retain their tissue identity. Here we report the establishment of tumor organoid cultures from 20 consecutive colorectal carcinoma (CRC) patients. For most, organoids were also generated from adjacent normal tissue. Organoids closely resemble the original tumor. The spectrum of genetic changes within the 'living biobank' agrees well with previous large-scale mutational analyses of CRC. Gene expression analysis indicates that the major CRC molecular subtypes are represented. Tumor organoids are amenable to high-throughput drug screens allowing detection of gene-drug associations. As an example, a single organoid culture was exquisitely sensitive to Wnt secretion (porcupine) inhibitors and carried a mutation in the negative Wnt feedback regulator RNF43, rather than in APC. Organoid technology may fill the gap between cancer genetics and patient trials, complement cell line- and xenograft-based drug studies and allow personalized therapy design. Self-renewal of the intestinal epithelium is driven by Lgr5 stem cells located in crypts. We have recently developed a long-term culture system that maintains basic crypt physiology. Wnt signals are required for the maintenance of active crypt stem cells. Indeed, the Wnt agonist R-spondin1 induces dramatic crypt hyperplasia in vivo. R-spondin-1 is the ligand for Lgr5. Epidermal growth factor (EGF) signaling is associated with intestinal proliferation, while transgenic expression of Noggin induces a dramatic increase in crypt numbers. The combination of R-spondin-1, EGF, and Noggin in Matrigel sustains ever-expanding small intestinal organoids, which display all hallmarks of the original tissue in terms of architecture, cell type composition, and self-renewal dynamics. We adapted the culture condition for long-term expansion of human colonic epithelium and primary colonic adenocarcinoma, by adding nicotinamide, A83-01 (Alk inhibitor), Prostaglandin E2 and the p38 inhibitor SB202190. Of note, a two-dimensional culture method for cells from normal and malignant primary tissue has been described by Schlegel and colleagues. Here, we explore organoid technology to routinely establish and phenotypically annotate ‘paired organoids’ derived from adjacent tumor and healthy epithelium from CRC patients.
2015-05-07 | E-GEOD-65253 | biostudies-arrayexpress