Patient-Derived Tumor Organoid and Fibroblast Assembloid Models for interrogation of the tumor microenvironment in Esophageal Adenocarcinoma
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ABSTRACT:
PROVIDER: PRJNA1160870 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30660768_1.fastq.gz | Fastqsanger.gz | |||
| SRR30660768_2.fastq.gz | Fastqsanger.gz | |||
| SRR30660769_1.fastq.gz | Fastqsanger.gz | |||
| SRR30660769_2.fastq.gz | Fastqsanger.gz | |||
| SRR30660770_1.fastq.gz | Fastqsanger.gz |
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Project description:The tumor microenvironment (TME) comprises all non-tumor elements of cancer and strongly influences disease progression and phenotype. To understand tumor biology and accurately test new therapeutic strategies, representative models should contain both tumor cells and normal cells of the TME. Here we describe and characterize co-culture tumor-derived organoids and cancer-associated fibroblasts (CAFs), a major component of the TME, in matrix-embedded assembloid models of esophageal adenocarcinoma (EAC). We demonstrate that the assembloid models faithfully recapitulate the differentiation status of EAC and different CAF phenotypes found in the EAC patient TME. We evaluate cell phenotypes by combining tissue clearing techniques with wholemount immunofluorescence and histology, providing a practical framework for characterization of cancer assembloids.
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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.
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Project description:A New Murine Esophageal Organoid Culture Method and Organoid-Driven Model of Esophageal Squamous Cell Neoplasia
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Project description:We used cDNA microarray to study the gene expression profile between the tumor and non-tumor tissue samples from patients with esophageal cancer Pooled RNA from 10 pairs of primary ESCCs and their corresponding non-tumor tissues were compared by Affymetrix microarrays.
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Project description:We used cDNA microarray to study the gene expression profile between the tumor and non-tumor tissue samples from patients with esophageal cancer
2011-11-19 | GSE33810 | GEO
Project description:We conducted a comprehensive genome-wide interrogation to identify gene targets regulated by PTTG1 using a bead-array platform. The raw data and normalized logarithmic data were included in this subset. Keywords: siRNA, esophageal cells
2007-07-01 | GSE7447 | GEO
Project description:Esophageal cancer is among the 10 most common malignancies and ranks as the 6th leading cause of death from cancer. It constitutes 7% of all gastrointestinal cancers and is one of the most lethal of all cancers. The large variation in the incidence of esophageal cancer in different geographic regions has often been thought to be due to variation in exposure to environmental factors; however, hereditary factors may also contribute to the variation in rates. A positive family history was found to be associated with an increased risk of esophageal cancer in several case-control and cohort studies in China. Familial aggregation also has been observed in Iran and Japan. The cancer data generated from six hospital based cancer registries in India under National Cancer Registry Programme (NCRP, Annual Report, 2003-2004) has revealed that the occurrence of esophageal cancer in Assam is highest in India. The aggregation of esophageal cancer in families is a long-observed and well-documented phenomenon in Assam of North-east part of India (AAR=32.6). In Assam high incidence of esophageal cancer with familial aggregation need investigation for etiology. The etiology of esophageal cancer in Northeast Indian population is different from other population at India due to wide variations in dietary habits or nutritional factors, tobacco chewing and alcohol habits. With in these high-risk regions, studies have shown a strong tendency toward familial aggregation, suggesting that genetic susceptibility, in conjunction with potential environmental exposures, may be involved in the etiology of esophageal cancer. Familial clustering of cancer has been one of the main avenues to the understanding of cancer etiology and the signal to the involvement of heritable genes. Familial clustering of cancer may be due to environmental factors shared by family members or due to shared genes. However, the familial aggregation of esophageal cancer among the population in northeast India may reflect the influence of environmental factors operating on individuals who are already genetically susceptible. Epidemiological studies indicate that tobacco smoking and alcohol consumption are the major factors for esophageal cancer, the role of genetic factors for familial aggregation has not been elucidated. In this study, tumor and matched normal tissue from esophageal squamous cell carcinoma patients with a family history of upper gastrointestinal cancer were analyzed using cDNA microarray containing 10,000genes to evaluate gene expression differences in esophageal squamous cell carcinoma patients with a family history of upper gastrointestinal cancer from a high- risk area in India. To identify alteration in genes and molecular functional pathways in esophageal cancer in a high incidence region of India where there is wide spread use of tobacco and betel quid with fermented areca nuts and familial aggregation cancer. Keywords: Gene Expression
2008-02-09 | GSE10127 | GEO
Project description:Esophageal cancer is among the 10 most common malignancies and ranks as the 6th leading cause of death from cancer. It constitutes 7% of all gastrointestinal cancers and is one of the most lethal of all cancers. The large variation in the incidence of esophageal cancer in different geographic regions has often been thought to be due to variation in exposure to environmental factors; however, hereditary factors may also contribute to the variation in rates. A positive family history was found to be associated with an increased risk of esophageal cancer in several case-control and cohort studies in China. Familial aggregation also has been observed in Iran and Japan. The cancer data generated from six hospital based cancer registries in India under National Cancer Registry Programme (NCRP, Annual Report, 2003-2004) has revealed that the occurrence of esophageal cancer in Assam is highest in India. The aggregation of esophageal cancer in families is a long-observed and well-documented phenomenon in Assam of North-east part of India (AAR=32.6). In Assam high incidence of esophageal cancer with familial aggregation need investigation for etiology. The etiology of esophageal cancer in Northeast Indian population is different from other population at India due to wide variations in dietary habits or nutritional factors, tobacco chewing and alcohol habits. With in these high-risk regions, studies have shown a strong tendency toward familial aggregation, suggesting that genetic susceptibility, in conjunction with potential environmental exposures, may be involved in the etiology of esophageal cancer. Familial clustering of cancer has been one of the main avenues to the understanding of cancer etiology and the signal to the involvement of heritable genes. Familial clustering of cancer may be due to environmental factors shared by family members or due to shared genes. However, the familial aggregation of esophageal cancer among the population in northeast India may reflect the influence of environmental factors operating on individuals who are already genetically susceptible. Epidemiological studies indicate that tobacco smoking and alcohol consumption are the major factors for esophageal cancer, the role of genetic factors for familial aggregation has not been elucidated. In this study, tumor and matched normal tissue from esophageal squamous cell carcinoma patients with a family history of upper gastrointestinal cancer were analyzed using cDNA microarray containing 10,000genes to evaluate gene expression differences in esophageal squamous cell carcinoma patients with a family history of upper gastrointestinal cancer from a high- risk area in India. To identify alteration in genes and molecular functional pathways in esophageal cancer in a high incidence region of India where there is wide spread use of tobacco and betel quid with fermented areca nuts and familial aggregation cancer. Low RNA Input Fluorescent Linear Amplification Kit (Agilent, Santa Clara, CA) was used for labeling. Briefly, both first and second strand cDNA were synthesized by incubating 500ng of total RNA with 1.2ul of oligo dT-T7 Promoter Primer in nuclease-free water at 65 â¦C for 10 min followed by incubation with 4.0ul of 5à First strand buffer, 2ul of 0.1M DTT, 1 ul of 10mM dNTP mix, 1ul of 200 U/ul MMLV-RT, and 0.5ul of 40U/ul RNaseOUT, at 40 â¦C for 2 hour. Immediately following cDNA synthesis, the reaction mixture was incubated with 2.4 ul of 10 mM Cyanine-3-CTP or 2.4 ul of 10 mM Cyanine-5-CTP (Perkin-Elmer, Boston, MA), 20ul of 4X Transcription buffer, 8 ul of NTP mixture, 6 ul of 0.1M DTT, 0.5 ul of RNaseOUT, 0.6ul of Inorganic pyrophosphatase, 0.8 ul of T7 RNA polymerase, and 15.3ul of nuclease-free water at 40 â¦C for 2 hour. Qiagenâs RNeasy mini spin columns were used for purifying amplified aRNA samples. The quantity and specific activity of cRNA was determined by using NanoDrop ND-1000 UV-VIS Spectrophotometer version3.2.1. Samples with specific activity >8 were used for hybridization. 825ng of each Cyanine 3 or Cyanine 5 labeled cRNA in a volume of 41.8ul were combined with 11ul of 10x Blocking agent and 2.2ul of 25x Fragmentation buffer (Agilent), and incubated at 60deg C for 30 minutes in dark. The fragmented cRNA were mixed with 55ul of 2x Hybridization Buffer (Agilent). About 110ul of the resulting mixture was applied to the Microarray and hybridized at 65degC for 17 hours in an Agilent Microarray Hybridization Chamber (SureHyb: G2534A) with Hybridization Oven. After hybridization, slides were washed with Agilent Gene expression Wash Buffer I for 1 minute at room temperature followed by a 1 min wash with Agilent Gene expression Wash Buffer II for 37C. Slides were finally rinsed with Acetonitrile for cleaning up and drying. Microarrays were scanned on an Agilent scanner (G2565AA) at 100% laser power, 30% PMT.Data extraction was carried out with Agilent Feature Extraction software (version 9.1), and normalization was done using linear per array algorithm according to the manufacturerâs protocol. The data was analysed by GeneSpring GX and Biointerpreter software from Genotypic Technology, Bangalore. The differential expression was considered if the Log 2 mean of at least -1 for the down regulated genes and +1 for the upregulated genes. We considered only the genes that were reproducible from all replicates.
2010-06-25 | E-GEOD-10127 | biostudies-arrayexpress