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Relevant bibliographies by topics / Gastric organoid

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Academic literature on the topic 'Gastric organoid'

Author: Grafiati

Published: 14 March 2023

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Journal articles on the topic "Gastric organoid"

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Skubleny, Daniel, Saurabh Garg, Jim Wickware, Kieran Purich, Sunita Ghosh, Jennifer Spratlin, Dan Schiller, and Gina Rayat. "Murine and Human Gastric Tissue Establishes Organoids after 48 Hours of Cold Ischemia Time during Shipment." Biomedicines 11, no. 1 (January 6, 2023): 151. http://dx.doi.org/10.3390/biomedicines11010151.

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An inadequate supply of fresh tissue is a major limitation of three-dimensional patient-derived gastric organoid research. We propose that tissue procurement for organoid culture could be increased by developing a cold storage shipment protocol for fresh surgical tissues. Sixty stomach specimens from C57BL/6J mice were resected, of which forty-five were stored in Hank’s Balanced Salt (HBSS), University of Wisconsin (UW), or Histidine-Tryptophan-Ketoglutarate (HTK) solutions for subsequent organoid culture. Stomachs were dissociated and processed into gastric organoids as fresh tissue or after transport at 4 °C for 24 or 48 h. All gastric organoid cultures were established and maintained for 10 passages. Cold storage for 24 or 48 h did not significantly affect organoid viability. Although cold storage was associated with decreased organoid growth rate, there were no differences in viability, cytotoxic dose response, or LGR5 and TROY stem cell gene expression compared to organoids prepared from fresh tissue. As a proof of concept, six human gastric cancer organoids were established after 24 or 48 h of storage. Patient-derived gastric organoids from mouse and human gastric tissue can be established after 48 h of cold ischemia. Our method, which only requires ice packs, standard shipping containers, and HBSS is feasible and reliable. This method does not affect the reliability of downstream dose–response assays and maintains organoid viability for at least 10 passages. The shipment of fresh tissue for organoid procurement could serve to enhance multicenter collaboration and achieve more elaborate or controlled organoid experimentation.

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Seidlitz, Therese, Sebastian R. Merker, Alexander Rothe, Falk Zakrzewski, Cläre von Neubeck, Konrad Grützmann, Ulrich Sommer, et al. "Human gastric cancer modelling using organoids." Gut 68, no. 2 (April 27, 2018): 207–17. http://dx.doi.org/10.1136/gutjnl-2017-314549.

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ObjectiveGastric cancer is the second leading cause of cancer-related deaths and the fifth most common malignancy worldwide. In this study, human and mouse gastric cancer organoids were generated to model the disease and perform drug testing to delineate treatment strategies.DesignHuman gastric cancer organoid cultures were established, samples classified according to their molecular profile and their response to conventional chemotherapeutics tested. Targeted treatment was performed according to specific druggable mutations. Mouse gastric cancer organoid cultures were generated carrying molecular subtype-specific alterations.ResultsTwenty human gastric cancer organoid cultures were established and four selected for a comprehensive in-depth analysis. Organoids demonstrated divergent growth characteristics and morphologies. Immunohistochemistry showed similar characteristics to the corresponding primary tissue. A divergent response to 5-fluoruracil, oxaliplatin, irinotecan, epirubicin and docetaxel treatment was observed. Whole genome sequencing revealed a mutational spectrum that corresponded to the previously identified microsatellite instable, genomic stable and chromosomal instable subtypes of gastric cancer. The mutational landscape allowed targeted therapy with trastuzumab for ERBB2 alterations and palbociclib for CDKN2A loss. Mouse cancer organoids carrying Kras and Tp53 or Apc and Cdh1 mutations were characterised and serve as model system to study the signalling of induced pathways.ConclusionWe generated human and mouse gastric cancer organoids modelling typical characteristics and altered pathways of human gastric cancer. Successful interference with activated pathways demonstrates their potential usefulness as living biomarkers for therapy response testing.

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Caipa Garcia, Angela L., Jill E. Kucab, Halh Al-Serori, Rebekah S. S. Beck, Franziska Fischer, Matthias Hufnagel, Andrea Hartwig, et al. "Metabolic Activation of Benzo[a]pyrene by Human Tissue Organoid Cultures." International Journal of Molecular Sciences 24, no. 1 (December 29, 2022): 606. http://dx.doi.org/10.3390/ijms24010606.

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Organoids are 3D cultures that to some extent reproduce the structure, composition and function of the mammalian tissues from which they derive, thereby creating in vitro systems with more in vivo-like characteristics than 2D monocultures. Here, the ability of human organoids derived from normal gastric, pancreas, liver, colon and kidney tissues to metabolise the environmental carcinogen benzo[a]pyrene (BaP) was investigated. While organoids from the different tissues showed varied cytotoxic responses to BaP, with gastric and colon organoids being the most susceptible, the xenobiotic-metabolising enzyme (XME) genes, CYP1A1 and NQO1, were highly upregulated in all organoid types, with kidney organoids having the highest levels. Furthermore, the presence of two key metabolites, BaP-t-7,8-dihydrodiol and BaP-tetrol-l-1, was detected in all organoid types, confirming their ability to metabolise BaP. BaP bioactivation was confirmed both by the activation of the DNA damage response pathway (induction of p-p53, pCHK2, p21 and γ-H2AX) and by DNA adduct formation. Overall, pancreatic and undifferentiated liver organoids formed the highest levels of DNA adducts. Colon organoids had the lowest responses in DNA adduct and metabolite formation, as well as XME expression. Additionally, high-throughput RT-qPCR explored differences in gene expression between organoid types after BaP treatment. The results demonstrate the potential usefulness of organoids for studying environmental carcinogenesis and genetic toxicology.

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Jeong, Haengdueng, and Ki Taek Nam. "Gastric stem cell research and gastric organoids." Organoid 2 (December 6, 2022): e27. http://dx.doi.org/10.51335/organoid.2022.2.e27.

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The stomach is a complex organ lined with ordered epithelium consisting of different adult stem cell (ASC) pools. In the previous decade, research into gastric epithelial stem cells has been performed using lineage tracing methods, and several putative ASC markers in the gastric gland have been identified, although their roles in homeostasis maintenance and the origin of cancer remain to be clarified. With advances in gastric stem cell research, 3-dimensional (3D) organoid culture has been developed on the basis of in-depth insights into the control of stem cell self-renewal, proliferation, and differentiation. Since the initial report that single intestinal stem cells have the ability to generate long-lived 3D structures that exhibit budding forms and self-renewal, tissue-specific adaptations of this method have been established in various organs, such as the small intestine, colon, liver, and stomach. In the murine stomach, putative ASCs isolated from the corpus and antrum generate gastric organoids that can simulate organ-specific cells to some extent. In addition, a few trials have been conducted to generate long-lived 3D organoids using human-derived ASCs and pluripotent stem cells. We hope that this review will provide comprehensive knowledge on gastric stem cell research and gastric organoids.

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Hashimi, Marziah, Thomas A. Seberll, Barkan Sidar, James N. Wilking, and Diane Bimczok. "Epithelial cell-derived chemokines induce DC recruitment to the gastric epithelium upon H. pylori infection." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 51.6. http://dx.doi.org/10.4049/jimmunol.202.supp.51.6.

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Abstract H. pylori is a non-invasive bacterial pathogen that infects the lumen of the stomach and interacts with epithelial cells. In tissues from H. pylori infected and non-infected patients, DCs are found in close association with the gastric epithelium, which likely promotes DC uptake of luminal H. pylori. We hypothesized that DCs are recruited to the gastric epithelium in a chemokine-dependent manner. The aim of this study was to identify the epithelial chemokines that recruit DCs under steady state conditions and upon H. pylori infection. In chemotaxis assays, supernatants from human gastric organoids microinjected with H. pylori induced a 2-fold higher recruitment of monocyte-derived DCs compared to mock-infected organoids. Microscopic analysis of DC organoid-co-cultures similarly revealed DC recruitment to the epithelium of non-infected organoids and significantly increased recruitment upon H. pylori infection. DCs showed only low chemotactic activity towards H. pylori or bacterial supernatants, pointing to a role for epithelial rather than bacterial factors. DC migration towards the supernatants of both mock-infected and H. pylori-infected organoids was abrogated by pertussis toxin, indicating that recruitment was chemokine dependent. Using a chemokine array, we showed that organoid gastric organoids secreted increased amounts CXCL1, 5, 8 and CCL20 upon H. pylori infection, while CXCL16 and 17 remained constant. Chemotaxis assays confirmed that human DCs show chemotactic responses to CXCL1, 5, 8, 16, 17 and CCL20. In summary, our study indicates that human gastric epithelial cells actively recruit DCs to the mucosal interface by secreting chemokines, with increased recruitment induced upon H. pylori infection.

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Alexander, Katie L., Carolina A. Serrano, Asmi Chakraborty, Marie Nearing, Leona N. Council, Arnoldo Riquelme, Marcelo Garrido, Susan L. Bellis, Lesley E. Smythies, and Phillip D. Smith. "Modulation of glycosyltransferase ST6Gal-I in gastric cancer-derived organoids disrupts homeostatic epithelial cell turnover." Journal of Biological Chemistry 295, no. 41 (August 6, 2020): 14153–63. http://dx.doi.org/10.1074/jbc.ra120.014887.

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Programmed cell death promotes homeostatic cell turnover in the epithelium but is dysregulated in cancer. The glycosyltransferase ST6Gal-I is known to block homeostatic apoptosis through α2,6-linked sialylation of the death receptor TNFR1 in many cell types. However, its role has not been investigated in gastric epithelial cells or gastric tumorigenesis. We determined that human gastric antral epithelium rarely expressed ST6Gal-I, but the number of ST6Gal-I–expressing epithelial cells increased significantly with advancing premalignancy leading to cancer. The mRNA expression levels of ST6GAL-I and SOX9 in human gastric epithelial cells correlated positively with one another through the premalignancy cascade, indicating that increased epithelial cell expression of ST6Gal-I is associated with premalignant progression. To determine the functional impact of increased ST6Gal-I, we generated human gastric antral organoids from epithelial stem cells and differentiated epithelial monolayers from gastric organoids. Gastric epithelial stem cells strongly expressed ST6Gal-I, suggesting a novel biomarker of stemness. In contrast, organoid-derived epithelial monolayers expressed markedly reduced ST6Gal-I and underwent TNF-induced, caspase-mediated apoptosis, consistent with homeostasis. Conversely, epithelial monolayers generated from gastric cancer stem cells retained high levels of ST6Gal-I and resisted TNF-induced apoptosis, supporting prolonged survival. Protection from TNF-induced apoptosis depended on ST6Gal-I overexpression, because forced ST6Gal-I overexpression in normal gastric stem cell–differentiated monolayers inhibited TNF-induced apoptosis, and cleavage of α2,6-linked sialic acids from gastric cancer organoid-derived monolayers restored susceptibility to TNF-induced apoptosis. These findings implicate up-regulated ST6Gal-I expression in blocking homeostatic epithelial cell apoptosis in gastric cancer pathogenesis, suggesting a mechanism for prolonged epithelioid tumor cell survival.

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Li, Haixin, Hongkun Liu, and Kexin Chen. "Living biobank-based cancer organoids: prospects and challenges in cancer research." Cancer Biology & Medicine 19, no. 7 (July 21, 2022): 965–82. http://dx.doi.org/10.20892/j.issn.2095-3941.2021.0621.

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Biobanks bridge the gap between basic and translational research. Traditional cancer biobanks typically contain normal and tumor tissues, and matched blood. However, biospecimens in traditional biobanks are usually nonrenewable. In recent years, increased interest has focused on establishing living biobanks, including organoid biobanks, for the collection and storage of viable and functional tissues for long periods of time. The organoid model is based on a 3D in vitro cell culture system, is highly similar to primary tissues and organs in vivo, and can recapitulate the phenotypic and genetic characteristics of target organs. Publications on cancer organoids have recently increased, and many types of cancer organoids have been used for modeling cancer processes, as well as for drug discovery and screening. On the basis of the current research status, more exploration of cancer organoids through technical advancements is required to improve reproducibility and scalability. Moreover, given the natural characteristics of organoids, greater attention must be paid to ethical considerations. Here, we summarize recent advances in cancer organoid biobanking research, encompassing rectal, gastric, pancreatic, breast, and glioblastoma cancers. Living cancer biobanks that contain cancerous tissues and matched organoids with different genetic backgrounds, subtypes, and individualized characteristics will eventually contribute to the understanding of cancer and ultimately facilitate the development of innovative treatments.

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Chen, Wei, Jian Zhang, Huafeng Fu, Xun Hou, Qiao Su, Yulong He, and Dongjie Yang. "KLF5 Is Activated by Gene Amplification in Gastric Cancer and Is Essential for Gastric Cell Proliferation." Cells 10, no. 5 (April 24, 2021): 1002. http://dx.doi.org/10.3390/cells10051002.

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Gastric cancer is the third leading cause of cancer death worldwide. In this study, we tried to clarify the function of KLF5 in gastric cancer. Copy number variation (CNV) and the expression of KLF5 were interrogated in public datasets. The clinical significance of KLF5 amplification and gene expression in gastric cancer were evaluated. The function of KLF5 in cell proliferation was studied in gastric cancer cell lines and organoids. We found that KLF5 amplification mainly occurred in the chromosome instable tumors (CIN) and was significantly associated with TP53 mutation. In addition, higher KLF5 expression correlated with more locally invasive gastric cancer and higher T stage. Next, a KLF5 gene expression signature was curated. The genes in the signature were involved in cell development, cell cycle regulation, cell death, suggesting potential roles played by KLF5. Functional studies using siRNAs revealed that KLF5 was essential for the proliferation of gastric cancer cells. Finally, using gastric organoid models, we revealed that the proliferation of organoids was significantly inhibited after the down regulation of KLF5. Our study revealed that KLF5 was amplified and over-expressed in gastric cancer, and it may play an oncogene-like role in gastric cancer by supporting cell proliferation.

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Seidlitz, Therese, and Daniel E. Stange. "Gastrointestinal cancer organoids—applications in basic and translational cancer research." Experimental & Molecular Medicine 53, no. 10 (October 2021): 1459–70. http://dx.doi.org/10.1038/s12276-021-00654-3.

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AbstractCancer is a major health problem and a leading cause of death worldwide. Early cancer detection and continuous changes in treatment strategies have improved overall patient survival. The recent development of targeted drugs offers new opportunities for personalized cancer treatment. Nevertheless, individualized treatment is accompanied by the need for biomarkers predicting the response of a patient to a certain drug. One of the most promising breakthroughs in recent years that might help to overcome this problem is the organoid technology. Organoid cultures exhibit self-renewal capacity, self-organization, and long-term proliferation, while recapitulating many aspects of their primary tissue. Generated patient-derived organoid (PDO) libraries constitute “living” biobanks, allowing the in-depth analysis of tissue function, development, tumor initiation, and cancer pathobiology. Organoids can be derived from all gastrointestinal tissues, including esophageal, gastric, liver, pancreatic, small intestinal and colorectal tissues, and cancers of these tissues. PDOs are amenable to various techniques, including sequencing analyses, drug screening, targeted therapy testing, tumor microenvironment studies, and genetic engineering capabilities. In this review, we discuss the different applications of gastrointestinal organoids in basic cancer biology and clinical translation.

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Idowu, Sulaimon, Paul P. Bertrand, and Anna K. Walduck. "Homeostasis and Cancer Initiation: Organoids as Models to Study the Initiation of Gastric Cancer." International Journal of Molecular Sciences 23, no. 5 (March 3, 2022): 2790. http://dx.doi.org/10.3390/ijms23052790.

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Gastric cancer represents a significant disease burden worldwide. The factors that initiate cancer are not well understood. Chronic inflammation such as that triggered by H. pylori infection is the most significant cause of gastric cancer. In recent years, organoid cultures developed from human and animal adult stem cells have facilitated great advances in our understanding of gastric homeostasis. Organoid models are now being exploited to investigate the role of host genetics and bacterial factors on proliferation and DNA damage in gastric stem cells. The impact of a chronic inflammatory state on gastric stem cells and the stroma has been less well addressed. This review discusses what we have learned from the use of organoid models to investigate cancer initiation, and highlights questions on the contribution of the microbiota, chronic inflammatory milieu, and stromal cells that can now be addressed by more complex coculture models.

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Dissertations / Theses on the topic "Gastric organoid"

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Engevik, Amy C. "The Regulation of Gastric Ulcer Repair." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1430749523.

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Sara, Peri. "Chemotherapy resistance-associated epithelial to endothelial transition in gastric cancer." Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1096074.

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Gastric cancer (GC) is the fifth most common malignancy worldwide and the third leading cause of cancer-related death. Despite decreased incidence in the last decades and progress in early detection of the disease, most of GC cases are still diagnosed at advanced stages. The only curative treatment remains surgery, but chemo- and radio-therapy are widely used to downstage, prevent metastasis and recurrence. Chemoresistance is a major problem in GC due to limited therapeutic options and it is responsible for treatment failure. We used a primary adenocarcinoma cell line (AGS) and made it resistant to three different chemotherapeutic drugs (5-fluorouracil, cisplatin and paclitaxel), separately. After evaluating the resistance of each line obtained to the different chemotherapy drugs and verifying that there was no cross-resistance, we tried to identify differences between resistant lines and the parental one that could be exploited to restore chemosensitivity. We evaluated factors associated with stemness and found an up-regulation in the resistant cell lines. This led us to investigate whether there was a greater propensity to vasculogenic mimicry in AGS resistant lines. The 5FU-resistant AGS cell line showed a marked capacity for vasculogenic mimicry, a phenomenon described and associated to bad prognosis in cancers like melanomas, but only recently discovered in gastric carcinoma. In addition, 5FU-resistant line acquired CD31 positivity, a marker that is normally associated with endothelial cells, demonstrating that 5FU-resistant AGS cells have undergone an epithelial-to-endothelial transition. We also tested an anti-angiogenic/anti-vasculogenic mimicry agent on 5FU-resistant AGS cells, that restored its chemosensitivity to 5-Fluorouracil. Preliminary studies also investigated metabolic alterations occurring in AGS-chemoresistant cell lines with respect to the chemosensitive AGS-wt cell line. We have detected alterations in AGS-chemoresistant cell lines that could possibly be exploited to revert chemoresistance. I also spent 8 months in the Netherlands, at the Hubrecht Institute, with the purpose of learning how to cultivate and manipulate stomach organoids derived from human biopsies. There I followed a project aimed to differentiate, in gastric organoids, endocrine cells (secreting somatostatin, ghrelin, serotonin, histamine and gastrin) that are found in the organ but only seldomly detected in organoid culture. For this purpose, it was necessary to transduce the pro-endocrine transcription factor Neurogenin 3 by lentivirus, which allowed a strong enrichment of the culture in endocrine cells but not for all lineages. New constructs were therefore cloned for the overexpression of other transcriptional factors that could be involved in endocrine differentiation. These were equally transduced into stomach organoid cultures. However, this approach did not lead to the desired result. Simultaneously, a gastric organoid line with an endogenous tagging for the gastrin gene was created by CRISPR/Cas9, so that when gastrin is expressed, the cell produces also a fluorescent protein that allows its easy identification. The realization of this cell line allowed a fast-screening of different culture conditions that could induce differentiation towards gastrin-secreting endocrine lineage. This led in a short time to the discovery of molecules that induced differentiation in gastrin-secreting cells, testifying the feasibility of the proposed method.

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Schumacher, Michael A. "Hedgehog Signaling is a Mediator of the Gastric Immune Response to Helicobacter pylori Infection." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1394725492.

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Kumar, Sacheen. "Mass spectrometric analysis of volatile organic compounds in oesophago-gastric cancer." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24837.

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In the UK, oesophago-gastric (OG) cancer remains a disease with poor patient outcomes and only 35% of patients are suitable for potentially curative treatment at first presentation. Early detection of these cancers is necessary with Volatile Organic Compound (VOC) analysis being a promising area to explore for new endogenous biomarkers. In this research, the application of Selected-Ion Flow Tube Mass Spectrometry (SIFT-MS), a real-time technique, for the analysis of VOCs in biofluids and exhaled breath has been investigated. The primary aim of this research was to identify potential VOC biomarkers in oesophago-gastric cancer; the long-term application being the translational development of VOCs as non-invasive diagnostic tests. A total of 13 VOCs emitted from gastric content were investigated in the first study; acetone, formaldehyde, acetaldehyde, hexanoic acid, hydrogen sulphide, acetic acid, hydrogen cyanide and methyl phenol were found to be significantly different between oesophago-gastric cancer and healthy groups. In a study on the headspace of urine, acetaldehyde, acetone, acetic acid, hexanoic acid, hydrogen sulphide, methanol and phenol were found to be at significantly different concentrations between oesophago-gastric cancer, positive control and healthy groups. Methodology experiments including the optimisation of VOC sampling techniques with evaluation of exogenous contamination and variability measures have also been conducted. Investigation of reference ranges for C3-C10 aldehydes in healthy subjects using SIFT-MS have been undertaken for the first time; C4-C10 aldehydes were present in the exhaled breath of healthy persons at concentrations < 3 ppbv. In a study on 210 consecutive patients, increased concentrations of fatty acids, phenols and aldehydes were observed in the exhaled breath of patients with oesophageal and gastric adenocarcinoma. The potential effects of clinical confounding factors have been also assessed and possible explanations for the observed differences have been discussed. The results of the pilot study on acute infection demonstrated minimal influence on the cancer-linked VOCs in OG cancer, except for butanal. The analysis of gastric content, urine and exhaled breath have proven that trace compounds are more influential than abundant metabolites in upper gastro-intestinal malignancy. It is also demonstrated that VOC profiles rather than individual compounds are more accurate in the molecular-orientated diagnosis of oesophago-gastric cancer.

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Bertaux-Skeirik, Nina. "The Role of CD44 Variant Isoforms in Gastric Regeneration and Disease." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1504879114818203.

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Wilcockson, John Brooke. "Gastro-intestinal magnification and dietary bioavailability of chlorinated organic contaminants/xenobiotics, implications for biomagnification." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ37664.pdf.

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Rodrigues, Florence Ana Carolina. "Réponses physiologiques de bifidobactéries soumises aux stress acide, froid et gastro-intestinal en laits biologique et conventionnel." Phd thesis, AgroParisTech, 2013. http://pastel.archives-ouvertes.fr/pastel-01053733.

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Les bifidobactéries sont exposées à de nombreux stress, liés aux conditions environnementales rencontrées lors de la production, du stockage au froid, et pendant la digestion des laits fermentés. Afin d'améliorer leur survie, cette étude vise la compréhension des mécanismes de dégradation de l'état physiologique de différentes souches de Bifidobacterium soumises aux stress froid et acide et au stress gastro-intestinal simulé in vitro. Elle ambitionne également d'établir des relations entre la résistance aux différents stress et la teneur en acides gras membranaires et des laits biologiques et conventionnels. Les résultats montrent que l'activité acidifiante des bifidobactéries est souche-dépendante et qu'elle augmente lorsque les bactéries sont associées aux bactéries lactiques du yaourt, avec du lait biologique et lorsque la température d'incubation est fixée à 42°C au lieu de 37°C. La cultivabilité et la survie des souches ont été déterminées après fermentation, après stockage à 4°C pendant 7 à 28 jours, et pendant un processus de digestion simulé in-vitro dans un digesteur dynamique reproduisant le tractus gastro-intestinal. Ces caractéristiques sont améliorées dans les laits fermentés biologiques par rapport aux produits conventionnels, lorsque la fermentation est effectuée à 42°C jusqu'à pH 4,4, et lorsque les laits fermentés sont maintenus à 28°C pendant 12 heures avant d'être refroidi à 4°C. Ces procédures de fabrication spécifiques génèrent ainsi une adaptation physiologique des bifidobactéries aux stress. Pendant la digestion in-vitro, la cultivabilité des bifidobactéries se dégrade moins lorsque la fermentation se déroule en lait biologique plutôt qu'en lait conventionnel et, dans une moindre mesure, lorsque les procédures d'adaptation sont appliquées pendant la fabrication du lait fermenté. Ces résultats sont liés aux teneurs plus élevées en acides gras insaturés, en particulier en acides trans-vaccénique, linoléique conjugué et α-linolénique, qui caractérisent les produits biologiques. Ces profils d'acides gras particuliers aux laits biologiques permettent aux bifidobactéries de modifier leur composition en acides gras membranaires, en augmentant leur teneur en acides gras insaturés et en raccourcissant la longueur moyenne des chaînes d'acides gras saturés, adaptant ainsi leur fluidité membranaire. Lorsque les procédures de fabrication spécifiques sont mises en oeuvre pour induire une adaptation physiologique des bifidobactéries, la composition en acides gras des membranes se modifie différemment de ce qui est observé en lait biologique. Cette différence indique ainsi que d'autres mécanismes biologiques d'adaptation sont probablement impliqués, en particulier au niveau protéomique. Finalement, cette étude démontre que les modifications au niveau de la membrane contribuent à moduler la résistance aux stress technologique et gastro-intestinal de souches de Bifidobacterium.

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Garrido-Utrilla, Anna. "Conversion des cellules D productrices de somatostatine en cellules productrices d'insuline par l’expression ectopique de Pax4." Electronic Thesis or Diss., Université Côte d'Azur, 2020. http://theses.univ-cotedazur.fr/2020COAZ6032.

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Le diabète est l'une des maladies métaboliques les plus répandues dans le monde. Différents types de diabète ont été décrits comme le diabète de type 1, de type 2 et monogénique. Le diabète de type 1 résulte de la perte auto-immune des cellules β productrices d'insuline. Il est important de souligner que malgré les thérapies actuelles, les personnes diabétiques de type 1 présentent encore une qualité de vie considérablement altérée et une espérance de vie réduite. Il subsiste donc un fort besoin en thérapies alternatives. Une piste de recherche d'un grand intérêt est la régénération des cellules β par conversion de cellules endogènes en cellules productrices d'insuline.Des résultats antérieurs de notre laboratoire ont démontré que l'expression ectopique de Pax4 dans les cellules β pancréatiques productrices de somatostatine induit leur néo-genèse et leur conversion en cellules β. Fait intéressant, le tractus gastro-intestinal contient un grand nombre de cellules D exprimant la somatostatine. L’on pourrait donc se demander si telle conversion médiée par Pax4 pourrait également déclencher la transformation des cellules D intestinales en cellules β.Dans ce but, nous avons généré des souris transgéniques exprimant Pax4 dans les cellules productrices de somatostatine et nous avons analysé le duodénum et l'estomac. De plus, nous avons également mis en œuvre une approche ex vivo basée sur des organoïdes intestinaux dérivés de souris.Nos résultats démontrent la présence de cellules insuline+ dans les tissus gastro-intestinaux analysés, et par le traçage de lignage, il apparait que ces cellules proviennent de cellules D. Une caractérisation plus poussée des cellules productrices d’insuline résultantes montre qu'elles expriment plusieurs marqueurs de cellules β. De plus, nous avons évalué la fonctionnalité de ces cellules néo-générées au moyen d'organoïdes intestinaux. Les résultats obtenus prouvent la capacité des organoïdes transgéniques à libérer de l'insuline en réponse à une stimulation par le glucose.Ainsi, nos résultats suggèrent que la seule expression ectopique de Pax4 dans les cellules D les convertit en cellules de type β. De plus, ces cellules d'insuline+ néo-générées sont fonctionnelles, ce qui ouvre la porte vers de nouvelles recherches d’intérêt pour le diabète de type 1
Diabetes is one of the most common metabolic diseases worldwide. Different types of diabetes have been described such as type 1, type 2 and monogenic diabetes. Type 1 diabetes results from the autoimmune-mediated loss of insulin-producing β-cells. Importantly, despite currently available therapies, type 1 diabetic individuals still exhibit a significantly altered quality of life and a shortened life expectancy. There is therefore a need for the establishment of alternative therapies. One research avenue of great interest is the regeneration of lost β-cells by converting endogenous cells into insulin-producing cells.Previous results from our laboratory demonstrated that the ectopic expression of Pax4 in pancreatic somatostatin-producing β-cells triggers their neogenesis and subsequent conversion into β-like cells. Interestingly, the gastrointestinal tract contains a great number of somatostatin-expressing D cells. One could therefore wonder whether such Pax4-mediated conversion could also trigger D cells to be turned into β-like cells. Towards this goal, we generated transgenic mice misexpressing Pax4 in somatostatin cells and we analysed the duodenum and the stomach. Moreover, we also implemented an ex vivo approach based on mice-derived gut organoids.Our results outlined the presence of insulin+ cells in the gastrointestinal tissues analysed, and by lineage tracing, we proved that these cells arose from D cells. Further characterisation of the insulin-converted cells demonstrated that they expressed several β-cell markers. Additionally, we assessed the functionality of these neo-generated β-like cells by means of gut organoids. The results obtained proved the capacity of transgenic organoids to release insulin upon glucose stimulation.Hence, our results suggest that the sole misexpression of Pax4 in D cells converts these into β-like cells. Further, we confirmed that these gastrointestinal neo-generated insulin+ cells are functional, thus opening new research avenues in the context of diabetes research

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立松, 英純, and Hidezumi Tatematsu. "Correlation between Magnifying Narrow-band Imaging Endoscopy Results and Organoid Differentiation Indicated by Cancer Cell Differentiation and its Distribution in Depressed-Type Early Gastric Carcinoma." Thesis, 2013. http://hdl.handle.net/2237/18977.

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Fried, Sabrina Liora. "Drug screening in gastro-esophageal adenocarcinoma and the advantages of the organoid model: a literature review." Thesis, 2020. https://hdl.handle.net/2144/41236.

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Abstract:

Gastro-esophageal adenocarcinomas (GEA) are among the fastest rising malignancies in North America. Despite advances in cancer prevention and treatment for other cancers, the number of GEA cases continues to rise and prognosis remains bleak with five-year survival rates of only 20%. Additionally, many GEA patients won’t respond to first line therapy, many may develop therapeutic resistance, or will show disease recurrence. Previous drug screen models failed clinical trials due to the failure of the model to adequately recapitulate the primary sample. A new model, the patient-derived organoid (PDO), has become the newest method of investigating and testing numerous characteristics of the in vivo tumor. Initial studies have demonstrated the organoid’s advantages: PDOs are highly heterogeneous, may be maintained in culture indefinitely, and have the capability to model carcinogenesis and therapeutic response. However, limitations exist and questions remain that have yet to be addressed. Indeed, one of the challenges of using organoids is knowing whether the organoids are recapitulating normal or tumor tissue. Additionally, there seem to be limits on immortality of the organoids and the heterogeneity. Finally, without the stroma and Tumor Microenvironment (TME) in culture, the model is limited in its ability to test the response to immunotherapy-based drugs. Current research aims to develop a clinical pipeline utilizing organoids regularly as a diagnostic tool to evaluate therapeutic response, identify emergence of chemoresistance and perform targeted drug screens. Overall, PDOs are a burgeoning method of investigating GEA and are a powerful translational tool from bench to bedside.

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Book chapters on the topic "Gastric organoid"

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Chakrabarti, Jayati, Loryn Holokai, LiJyun Syu, Nina Steele, Julie Chang, Andrzej Dlugosz, and Yana Zavros. "Mouse-Derived Gastric Organoid and Immune Cell Co-culture for the Study of the Tumor Microenvironment." In Methods in Molecular Biology, 157–68. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8600-2_16.

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Bertaux-Skeirik, Nina, Jomaris Centeno, Jian Gao, Joel Gabre, and Yana Zavros. "Oncogenic Transformation of Human-Derived Gastric Organoids." In Methods in Molecular Biology, 205–13. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/7651_2016_4.

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Bertaux-Skeirik, Nina, Jomaris Centeno, Rui Feng, Michael A. Schumacher, Ramesh A. Shivdasani, and Yana Zavros. "Co-culture of Gastric Organoids and Immortalized Stomach Mesenchymal Cells." In Methods in Molecular Biology, 23–31. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3603-8_3.

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Pompaiah, Malvika, and Sina Bartfeld. "Gastric Organoids: An Emerging Model System to Study Helicobacter pylori Pathogenesis." In Current Topics in Microbiology and Immunology, 149–68. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-50520-6_7.

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Teal, Emma, Nina Bertaux-Skeirik, Jayati Chakrabarti, Loryn Holokai, and Yana Zavros. "Establishment of Human- and Mouse-Derived Gastric Primary Epithelial Cell Monolayers from Organoids." In Methods in Molecular Biology, 145–55. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8600-2_15.

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Flanagan, Dustin J., Renate H. M. Schwab, Bang M. Tran, Toby J. Phesse, and Elizabeth Vincan. "Isolation and Culture of Adult Intestinal, Gastric, and Liver Organoids for Cre-recombinase-Mediated Gene Deletion." In Methods in Molecular Biology, 123–33. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/7651_2016_14.

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Zhang, Yixia, and Daxiang Cui. "Identification of Volatile Organic Compound Biomarkers Associated with Gastric Cancer Cells and Their Ultrasensitive Electrochemical Detection." In Translational Medicine Research, 105–14. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-0951-2_6.

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Ueda, S., T. Yoshikawa, S. Takahashi, Y. Naito, H. Oyamada, T. Takemura, Y. Morita, T. Tanigawa, S. Sugino, and M. Kondo. "Protection by Seleno-Organic Compound, Ebselen, Against Acute Gastric Mucosal Injury Induced by Ischemia-Reperfusion in Rats." In Advances in Experimental Medicine and Biology, 187–91. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5730-8_30.

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Blackaby, Andrew, Michael J. Dawson, Richard M. Hall, Carol A. Jones, Andrew R. Knaggs, Peter S. Marshall, Nick L. Taylor, Philip Sidebottom, and Graham Webb. "Production of novel derivatives of a gastrin antagonist (GW1) using biotransformation." In Studies in Organic Chemistry, 173–76. Elsevier, 1998. http://dx.doi.org/10.1016/s0165-3253(98)80021-7.

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Chakrabarti, Jayati, and Yana Zavros. "Generation and use of gastric organoids for the study of Helicobacter pylori pathogenesis." In Methods in Cell Biology, 23–46. Elsevier, 2020. http://dx.doi.org/10.1016/bs.mcb.2020.04.011.

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Conference papers on the topic "Gastric organoid"

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Yue, Sarah Siu Kuen, Helen Hoi Ning Yan, Hoi Cheong Siu, Siu Lun Ho, Wai Yin Tsui, Dessy Chan, Annie Shuk Yee Chan, Bernard Chi Hang Lee, Anthony Kin Wang Chan, and Suet Yi Leung. "Abstract 4378: Gastric cancer organoid culture shows preserved genomic stability in long-term passage." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4378.

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Chen, Jiamin, Noemi Andor, Susan M. Grimes, Billy Lau, and Hanlee P. Ji. "Abstract 4339: Single cell RNA sequencing dissects cellular growth factor dependencies and oncogenic driver effects in an organoid model of gastric cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4339.

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Lo, Yuan-Hung, Kevin S. Kolahi, Yuhong Du, Chiung-Ying Chang, Andrey Krokhotin, Ajay Nair, Walter D. Sobba, et al. "Abstract 123: A CRISPR/Cas9-engineered ARID1A-deficient human gastric cancer organoid model reveals essential and non-essential modes of oncogenic transformation." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-123.

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Sakamoto, Naoya, Kazuhito Naka, Shoichi Ukai, Ririno Honma, Daiki Taniyama, Tsuyoshi Takashima, Ryota Maruyama, Kazuaki Tanabe, Hideki Ohdan, and Wataru Yasui. "Abstract 4762: Metabolome in 5-FU resistant gastric cancer organoids." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4762.

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Gao, Mei, Miranda Lin, Wesam M. Frandah, Moamen Gabr, Houssam E. Mardini, Michael Cavnar, and Joseph Kim. "Abstract A21: Utilizing endoscopic-derived gastric cancer organoids for personalized neoadjuvant chemotherapy." In Abstracts: AACR Special Conference on the Evolving Landscape of Cancer Modeling; March 2-5, 2020; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.camodels2020-a21.

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Jones, Brendan, Giovanni Giobbe, Francesca Sgualdino, and Paolo De Coppi. "127 Modelling human stomach development in vitro with the use of gastric organoids." In GOSH Conference 2019, Care of the Complex Child. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-gosh.127.

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Zhao, Yi, Mingle Huang, Yuefan Zhu, Lixia Xu, Xiaoxing Li, and Jun Yu. "IDDF2022-ABS-0105 Patient-derived organoids can predict chemotherapy response of gastric cancers and analysis of its molecular characteristics." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 2–4 September 2022. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2022. http://dx.doi.org/10.1136/gutjnl-2022-iddf.51.

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Kang, Sun Kyoung, Hyun Joo Bae, Woo Sun Kwon, Tae Soo Kim, Sujin Lee, Sang Woo Cho, Hyun Cheol Chung, and Sun Young Rha. "Abstract 2973: Establishment of organoids and patient derived cancer cell lines from gastric cancer body fluids as preclinical models for personalized therapy." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2973.

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