Relevant bibliographies by topics / Tumour organoids

Academic literature on the topic 'Tumour organoids'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Tumour organoids"

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Munro, Matthew J., Swee T. Tan, and Clint Gray. "Applications for Colon Organoid Models in Cancer Research." Organoids 2, no. 1 (January 12, 2023): 37–49. http://dx.doi.org/10.3390/organoids2010003.

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Organoids are 3D organ-like structures grown from stem cells in vitro that mimic the organ or disease from which they are derived. Due to their stem cell origin, organoids contain a heterogeneous population of cells reflecting the diversity of cell types seen in vivo. Similarly, tumour organoids reflect intratumoural heterogeneity in a way that traditional 2D cell culture and cell lines do not, and, therefore, they show greater promise as a more relevant model for effective disease modelling and drug testing. Tumour organoids arise from cancer stem cells, which contribute to many of the greatest challenges to cancer treatment, including therapy resistance, tumour recurrence, and metastasis. In this review, we outline methods for generating colon organoids from patient-derived normal and tumour tissues. Furthermore, we discuss organoid biobanking, applications of organoids in disease modelling, and a range of platforms applicable to high-throughput drug testing, including apical-out/reverse-polarity colon organoids.
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LeBlanc, VG, D. Trinh, M. Hughes, I. Luthra, D. Livingstone, MD Blough, JG Cairncross, JJ Kelly, and MA Marra. "1450-1545 Young Investigator Awards & Presentations Basic/Translational Exploring cellular subpopulations in glioblastoma and matched organoids using single-cell RNA-seq 52." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, S3 (June 2018): S13—S14. http://dx.doi.org/10.1017/cjn.2018.297.

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Glioblastomas (GBMs) account for nearly half of all primary malignant brain tumours, and current therapies are often only marginally effective. Our understanding of the underlying biology of these tumours and the development of new therapies have been complicated in part by widespread inter- and intratumoural heterogeneity. To characterize this heterogeneity, we performed regional subsampling of primary glioblastomas and derived organoids from these tissue samples. We then performed single-cell RNA-sequencing (scRNA-seq) on these primary regional subsamples and 1-3 matched organoids per sample. We have profiled samples from six tumour sets to date and have obtained sequencing data for 21,234 primary tissue cells and 14,742 organoid cells. While the most apparent differences in gene expression appear to be between individual tumours, we were also able to identify similar cellular subpopulations across tissue samples and across organoids. Importantly, organoids derived from the same tissue sample appeared to be composed of similar cellular subpopulations and were highly comparable to each other, indicating that replicate organoids faithfully represent the original tumour tissue. Overall, our scRNA-seq approach will help evaluate the utility of tumour-derived organoids as model systems for GBM and will aid in identifying cellular subpopulations defined by gene expression patterns, both in primary GBM regional subsamples and their associated organoids. These analyses will allow for the characterization of clonal or subclonal populations that are likely to respond to different therapeutic approaches and may also uncover novel therapeutic targets previously unrevealed through bulk analyses.
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Pinho, Diana, Denis Santos, Ana Vila, and Sandra Carvalho. "Establishment of Colorectal Cancer Organoids in Microfluidic-Based System." Micromachines 12, no. 5 (April 28, 2021): 497. http://dx.doi.org/10.3390/mi12050497.

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Colorectal cancer is the second leading cause of cancer death worldwide. Significant advances in the molecular mechanisms underlying colorectal cancer have been made; however, the clinical approval of new drugs faces many challenges. Drug discovery is a lengthy process causing a rapid increase in global health care costs. Patient-derived tumour organoids are considered preclinical models with the potential for preclinical drug screening, prediction of patient outcomes, and guiding optimized therapy strategies at an individual level. Combining microfluidic technology with 3D tumour organoid models to recapitulate tumour organization and in vivo functions led to the development of an appropriate preclinical tumour model, organoid-on-a-chip, paving the way for personalized cancer medicine. Herein, a low-cost microfluidic device suitable for culturing and expanding organoids, OrganoidChip, was developed. Patient-derived colorectal cancer organoids were cultured within OrganoidChip, and their viability and proliferative activity increased significantly. No significant differences were verified in the organoids’ response to 5-fluorouracil (5-FU) treatment on-chip and on-plate. However, the culture within the OrganoidChip led to a significant increase in colorectal cancer organoid-forming efficiency and overall size compared with conventional culture on a 24-well plate. Interestingly, early-stage and late-stage organoids were predominantly observed on-plate and within the OrganoidChip, respectively. The OrganoidChip thus has the potential to generate in vivo-like organotypic structures for disease modelling and drug screening applications.
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M. Kholosy, Waleed, Marc Derieppe, Femke van den Ham, Kim Ober, Yan Su, Lars Custers, Linda Schild, et al. "Neuroblastoma and DIPG Organoid Coculture System for Personalized Assessment of Novel Anticancer Immunotherapies." Journal of Personalized Medicine 11, no. 9 (August 30, 2021): 869. http://dx.doi.org/10.3390/jpm11090869.

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Cancer immunotherapy has transformed the landscape of adult cancer treatment and holds a great promise to treat paediatric malignancies. However, in vitro test coculture systems to evaluate the efficacy of immunotherapies on representative paediatric tumour models are lacking. Here, we describe a detailed procedure for the establishment of an ex vivo test coculture system of paediatric tumour organoids and immune cells that enables assessment of different immunotherapy approaches in paediatric tumour organoids. We provide a step-by-step protocol for an efficient generation of patient-derived diffuse intrinsic pontine glioma (DIPG) and neuroblastoma organoids stably expressing eGFP-ffLuc transgenes using defined serum-free medium. In contrast to the chromium-release assay, the new platform allows for visualization, monitoring and robust quantification of tumour organoid cell cytotoxicity using a non-radioactive assay in real-time. To evaluate the utility of this system for drug testing in the paediatric immuno-oncology field, we tested our in vitro assay using a clinically used immunotherapy strategy for children with high-risk neuroblastoma, dinutuximab (anti-GD2 monoclonal antibody), on GD2 proficient and deficient patient-derived neuroblastoma organoids. We demonstrated the feasibility and sensitivity of our ex vivo coculture system using human immune cells and paediatric tumour organoids as ex vivo tumour models. Our study provides a novel platform for personalized testing of potential anticancer immunotherapies for aggressive paediatric cancers such as neuroblastoma and DIPG.
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van Tienderen, Groot Koerkamp, IJzermans, van der Laan, and Verstegen. "Recreating Tumour Complexity in a Dish: Organoid Models to Study Liver Cancer Cells and their Extracellular Environment." Cancers 11, no. 11 (November 1, 2019): 1706. http://dx.doi.org/10.3390/cancers11111706.

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Primary liver cancer, consisting predominantly of hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), remains one of the most lethal malignancies worldwide. This high malignancy is related to the complex and dynamic interactions between tumour cells, stromal cells and the extracellular environment. Novel in vitro models that can recapitulate the tumour are essential in increasing our understanding of liver cancer. Herein, primary liver cancer-derived organoids have opened up new avenues due to their patient-specificity, self-organizing ability and potential recapitulation of many of the tumour properties. Organoids are solely of epithelial origin, but incorporation into co-culture models can enable the investigation of the cellular component of the tumour microenvironment. However, the extracellular component also plays a vital role in cancer progression and representation is lacking within current in vitro models. In this review, organoid technology is discussed in the context of liver cancer models through comparisons to other cell culture systems. In addition, the role of the tumour extracellular environment in primary liver cancer will be highlighted with an emphasis on its importance in in vitro modelling. Converging novel organoid-based models with models incorporating the native tumour microenvironment could lead to experimental models that can better recapitulate liver tumours in vivo.
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Soto, Carolina Bizama, and Juan Carlos Roa. "Explorations in the development of novel early diagnosis and disease monitoring tools in digestive tract cancers." Impact 2018, no. 3 (June 15, 2018): 22–23. http://dx.doi.org/10.21820/23987073.2018.3.22.

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Exploring the possibility that genomic DNA (exoDNA) may represent a highly promising next-generation biomarker for early detection. The research team hope to validate the use of circulating exoDNA as a new generation biomarker using KRAS mutation status as a surrogate source of primary tumour information. This may be useful for early diagnosis in cases of pancreatic biliary cancer (PBC) and a valid tool for clinical decision making, disease monitoring and therapeutic stratification. Point mutations in KRAS are found in 50% of gallbladder cancers, thus the team will use an ultra-sensitive droplet digital PCR (ddPCR) platform to identify mutant KRAS in samples of circulating exoDNA isolated from 75 early stage pancreatic biliary cancer patients at the time of diagnosis. These samples will be matched with exoDNA from 'benign disease' controls that have been match on the basis of age and gender. Roa hopes to use exoDNA to query the 'actionable' exome in PBC using a head-to-head comparison using next generation sequencing. Bizama's main objective in investigating patient-derived organoids is to establish and characterise organoid cultures from GBC patients in order to evaluate the drug responses of these organoids both to standard treatments and to specific pathway inhibitors. Current human GBC research lacks in vitro models that can capture the pathophysiological traits of the original tumour and normal epithelia. The research team hope to demonstrate that organoid cultures can be successfully established from normal and tumour gallbladder tissues from Chilean patients and that these organoids will be representative of the primary specimens. The team plan to develop an organoid culture platform as a prototype for the prediction of prognosis and efficiency of standard and targeted therapy. This ex vivo organoids model project may help clinicians predict the response of particular patients to specific treatments, thus avoiding unnecessary therapies.
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Quinn, Jean A., Meera Patel, Kathryn AF Pennel, Dustin Flanagan, Paul G. Horgan, Donald C. McMillan, Simon MacKay, Owen Sansom, and Joanne Edwards. "IKKα as a potential novel target for treatment of colorectal cancer." Journal of Clinical Oncology 38, no. 4_suppl (February 1, 2020): 174. http://dx.doi.org/10.1200/jco.2020.38.4_suppl.174.

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174 Background: Colorectal cancer (CRC) is a heterogeneous disease leading to different survival outcomes for patients with the same stage of disease. The non-canonical NF-κB pathway has been shown to have a key role in tumorigenesis, and the aim of this study was to investigate the role of IKKα, the main catalytic component of this pathway in CRC. Methods: A tissue microarray was retrospectively constructed from a patient cohort (1033) with stage I-III CRC who underwent surgery. IHC was utilised to examine cytoplasmic and punctate IKKα expression and determine any association with clincopathological features and cancer specific survival (CSS). To assess IKKα inhibition, organoids were prepared from wild type (WT) mouse colon, mouse models of CRC (Apc and Apc.KRAS.pT53.TGFbR2 (AKPT)) and patient derived human organoids. These were treated with an IKKα inhibitor, SU1433 and organoid size and cell viability assessed. Results: High cytoplasmic expression of IKKα was associated with increasing T stage (p = 0.012), poor tumour differentiation (p = 0.010), tumour necrosis (p = 0.013) and low proliferation status (p = 0.013) but was not associated with CSS. High punctate IKKα expression associated with tumour differentiation (p = 0.001), necrosis (p = 0.004), proliferation (p = 0.044) and MMR competence (p < 0.001) and was also significantly associated with reduced CSS (HR1.20 95%CI 1.02-1.42, p < 0.001). SU1433 did not significantly impact on WT (C57/B16) organoid viability up to a concentration of 1 uM, however organoid size and cell viability was significantly reduced in a dose dependent manner in organoids from both Apc and AKPT mouse models. A similar reduction was observed in patient derived human organoids. Conclusions: Punctate IKKα expression was associated with poor cancer specific survival in CRC patients, and inhibition with SU1433, impacted on CRC mouse and patient derived human organoid size and cell viability. These results suggest that, following further investigation and confirmation, IKKα may be employed as a novel therapeutic target in CRC.
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Roelofs, Charlotte, Frédéric Hollande, Richard Redvers, Robin L. Anderson, and Delphine Merino. "Breast tumour organoids: promising models for the genomic and functional characterisation of breast cancer." Biochemical Society Transactions 47, no. 1 (January 9, 2019): 109–17. http://dx.doi.org/10.1042/bst20180375.

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Abstract Until recently, established cancer cell lines have been used extensively in breast cancer research, due largely to the difficulties associated with the manipulation and long-term maintenance in culture of primary tumour cells from patients. The recent development of organoid cultures has provided new opportunities to model and analyse patient samples, allowing the propagation of malignant cells under conditions that resemble the three-dimensional growth of breast tumours. They have proved efficacious in preserving the heterogeneity of primary samples and are emerging as a new model to further characterise the molecular features of breast cancer. Organoids formed from patient-derived cells are now in use for the evaluation of drug sensitivity and to validate disease-causing genomic variations. Here, the advantages and limitations of organoid cultures will be discussed and compared with the parallel development of other two- and three-dimensional culture strategies and with patient-derived xenografts. In particular, we will focus on the molecular characterisation of breast cancer organoids and provide some examples of how they have been used in functional studies.
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Ramsay, Robert George. "Rapid in vitro evaluation of immune responses to tumor-derived organoids as an adjunct to immunotherapy trials." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): 3573. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.3573.

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3573 Background: Cancer immunotherapy has made rapid advances with the development of agents that subvert the negative arm of the immune system. This has been important because patients can mount anti-tumor immune responses. In the case of colorectal cancer (CRC), the presence of tumour infiltrating lymphocytes (TILs) appears to have predictive power regarding outcome. Nevertheless, assays that directly evaluate the quality, phenotype and anti-tumor activity of TILs are lacking. Here a novel immune assay platform is presented that measures the kinetics of TIL killing which correlates with pathological tumour response after treatment. Methods: Treatment naïve fresh cancer biopsies were processed to generate organoids and TILs from patients (n = 12) with pathological complete response (pCR) verses non-responding tumours (NRT). These were co-cultured with TILs to organoid ratios of 1:1, 5:1 and 10:1 for 48 hs and TILs function were measured by cytokine release and mean fluorescence intensity (MFI) based upon activated caspase activity. Additionally, TILs from patients with metastatic CRC (n = 20) have also been evaluated. Results: Ten thousand+ organoids are routinely cultured while millions of TILs are retrieved and expanded from biopsies. TIL-mediated killing of patient-matched tumor organoid confirm CD8+ve specific killing. At 24hrs MFI was significantly higher in pCR organoid indicative of immune-mediated cell death compared to NRT organoids at a ratio of 1:1. The efficiency of TIL killing was further enhanced as the ratio increased to 5:1 and 10:1. Gamma interferon production by cytotoxic (CD8+) T-cell is a robust measure of TIL activation state and was also significantly higher by pCR TILs compared to NRT TILs. Substantive differences in TIL subsets were also found in mCRC-derived samples compared to primary CRC. Conclusions: This is a novel functional immune assay and the first of its kind that successfully demonstrated the differences in patient-matched TIL killing between non-responding and responding CRC. This assay can be performed within in two weeks and thus it has translational potential that may change clinical management in the future and immunotherapy strategy design.
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Porter, Ross J., Graeme I. Murray, and Mairi H. McLean. "Current concepts in tumour-derived organoids." British Journal of Cancer 123, no. 8 (July 30, 2020): 1209–18. http://dx.doi.org/10.1038/s41416-020-0993-5.

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Dissertations / Theses on the topic "Tumour organoids"

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Sadiq, Barzan A. "A dissection of class I phosphoinositide 3-kinase signalling in mouse embryonic fibroblasts and prostate organoids." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/278056.

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Class I PI3Ks are a family (α, β, δ and γ) of ubiquitous lipid kinases that can be activated by cell surface receptors to 3-phosphorylate PI(4,5)P2 (phosphatidylinositol(4,5)-bisphosphate) and generate the signalling lipid PI(3,4,5)P3. The PI(3,4,5)P3 signal then activates a diverse collection of effector proteins involved in regulation of cell migration, metabolism and growth. The importance of this network is evidenced by the relatively high frequency with which cancers acquire gain-of-function mutations in this pathway and huge efforts to make PI3K inhibitors to treat cancer. The canonical model describing these events suggests class I PI3Ks are activated at the plasma membrane and generate PI(3,4,5)P3 in the inner leaflet of the plasma membrane where its effectors are activated. The PI(3,4,5)P3 signal can be terminated directly, by the tumour-suppressor and PI(3,4,5)P3-3-phosphatase PTEN, or modified to a distinct PI(3,4)P2 signal, by SHIP-family 5-phosphatases. The PI(3,4)P2 is removed by INPP4-family 4-phosphatases. Published work has shown that PI(3,4,5)P3 signalling can also occur in endosomes and nuclei, however, there is very little data defining the intracellular distribution of endogenous class I PI3Ks that supports these ideas; this is as a result of technical problems such as; their very low abundance, poor antibody-based tools and artefacts generated by overexpression of PI3Ks. Past work has indicated that, in PTEN-null mouse models of prostate tumour progression, either PI3Kβ or PI3Ks α and β, have important roles. Furthermore, the cell types and mechanism involved remained unclear. Recent published work in the host laboratory had indicated that there is an unexpectedly large accumulation of PI(3,4)P2 in PTEN-null cells that might be an important part of its status as a major tumour suppressor. The explanation and prevalence of this observation was unclear but potentially a result of PTEN also acting as a PI(3,4)P2 3-phosphatase in vivo. MEFs were derived from genetically-modified mice expressing endogenous, AviTagged class I PI3K subunits and used in experiments to define the subcellular localisation of class I PI3Ks. We found that following stimulation with PDGF, class IA PI3K subunits were unexpectedly depleted from the adherent basal membrane, in contrast, p85α and p110α, but not p85β and p110β, accumulated transiently in the nucleus. Interestingly, p110β, but none of the other subunits, was constitutively localised in the nucleus. These results support the idea that class I PI3K and PI(3,4,5)P3 signalling occurs in the nucleus. In organoids derived from WT, PI3Kγ-null or PTEN-null mouse prostate, application of PI3K-selective inhibitors revealed that PI3Kα had a dominant role in generating PI(3,4,5)P3 in prostate epithelial cells. The levels of PI(3,4)P2 were also elevated substantially in PTEN-null, compared to WT prostate organoids, use of PI3K-selective inhibitors suggested that it was also generated by PI3Kα. These data were consistent with the idea that PTEN can act as a PI(3,4)P2 3-phosphatase. Surprisingly, raising the pH of the organoids medium dramatically increased accumulation of PI(3,4,5)P3 and PI(3,4)P2, although the cause of this effect was unclear, we hypothesised the pH of the local environment may influence signalling via class I PI3Ks.
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Muta, Yu. "Composite regulation of ERK activity dynamics underlying tumour-specific traits in the intestine." Kyoto University, 2018. http://hdl.handle.net/2433/235061.

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Morice, Pierre-Marie. "Evaluation de la déficience de la recombinaison homologue et de la réponse des tumeurs ovariennes aux inhibiteurs de PARP grâce à l'utilisation de modèles de culture 3D en vue du développement d'un test prédictif Identifying eligible patients to PARP inhibitors: from NGS-based tests to promising 3D functional assays Automated scoring for assessment of RAD51-mediated homologous recombination in patient-derived tumor organoids of ovarian cancers Risk of myelodysplastic syndrome and acute myeloid leukemia related to PARP inhibitors: a combined approach using a safety meta-analysis of placebo randomized controlled trials and the World Health Organization's pharmacovigilance database The long non-coding RNA ‘UCA1’ modulates the response to chemotherapy of ovarian cancer through direct binding to miR-27a-5p and control of UBE2N levels." Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC414.

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Chaque année, plus de 150 000 décès sont associés aux cancers épithéliaux de l’ovaire dans le monde, notamment en raison du développement d’une résistance à la chimiothérapie. Environ la moitié de ces cancers présentent des altérations moléculaires provoquant une déficience de la réparation de l’ADN par recombinaison homologue (HRD) qui les sensibilise à l’action des inhibiteurs de la protéine PARP (PARPi). A ce jour, il n’existe pas de test capable d’appréhender le phénotype HRD dans sa globalité, limitant ainsi l’accès à ces traitements. Dans ce contexte, nous avons entrepris de mettre au point des tests fonctionnels basés sur l’utilisation d’explants tumoraux tranchés puis sur l’utilisation d’organoïdes tumoraux dérivés de tumeurs ovariennes de patientes chimio-naïves ou antérieurement traitées. La culture d’explants s’est révélée inappropriée pour la réalisation de ces tests et nous avons alors focalisé nos travaux sur les organoïdes tumoraux. Ces derniers ont été exposés au carboplatine (traitement de 1e ligne) et à deux inhibiteurs de PARP (l’olaparib et le niraparib) utilisés en traitement d’entretien. En parallèle, nous avons collecté les données cliniques des patientes (survie, intervalle sans platine, RECIST, traitements) afin d’évaluer le potentiel prédictif de ces modèles. Les organoïdes tumoraux établis ont répondu de façon hétérogène aux différents médicaments testés, et nos résultats montrent que les tests réalisés sur les organoïdes sont capables d’identifier des patientes présentant un niveau de résistance élevé au carboplatine, suggérant que ce test fonctionnel pourrait présenter un intérêt prédictif vis-à-vis de ce médicament. Concernant le potentiel prédictif des organoïdes vis-à-vis des PARPi, des profils de sensibilité variés ont été identifiés, mais la corrélation avec la réponse clinique reste à établir par des études menées sur des échantillons de tumeurs issus de patientes traitées par ces médicaments
Worldwide each year, more than 150 000 women die from epithelial ovarian cancer largely due to emergence of resistance to chemotherapy. Approximately half of these cancers display molecular alterations that cause deficiency of DNA repair via homologous recombination (HRD), which confer sensitivity to PARP protein inhibitors (PARPi). To date, there is no test capable of fully identifying the HRD phenotype, thus limiting access to these treatments. In this context, we are developing functional assays based on the use of tumor explant slices and then, on the use of tumor organoids derived from ovarian tumors of chemotherapy-naive or previously treated patients. The culture of explants was unsuitable for this application and we then focused our work on tumor organoids. Tumor organoids were exposed to carboplatin (first-line treatment) and two PARP inhibitors (olaparib and niraparib) used for maintenance therapy. In parallel, we collected clinical data from patients (survival, platinum-free interval, RECIST, treatments) to evaluate the predictive potential of these models. The established tumor organoids responded heterogeneously to different drugs, and our results show that the organoid-based assay is capable of identifying patients highly resistant to carboplatin, suggesting that this functional assay could have a predictive value for patients treated with carboplatin. Regarding the potential of organoids in predicting PARPi response, multiple sensitivity profiles have been identified, but the correlation with clinical response has yet to be determined by studies conducted on tumor samples from patients treated with these drugs
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Neef, Sylvia Karin [Verfasser]. "Entwicklung und Anwendung von Methoden zur metabolischen Phänotypisierung von Formalin-fixiertem, Paraffin-eingebettetem Gewebe und Tumor-Organoiden / Sylvia Karin Neef." Tübingen : Universitätsbibliothek Tübingen, 2023. http://d-nb.info/1237684536/34.

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Pérez, lanzón María. "Modeling Hormone Receptor Positive Breast Cancer in Immunocompetent Mice Blocking tumor-educated MSC paracrine activity halts osteosarcoma progression Organoids for Modeling Genetic Diseases. In: International Review of Cell and Molecular Biology A preclinical mouse model of osteosarcoma to define the extracellular vesicle-mediated communication between tumor and mesenchymal stem cells Failure of immunosurveillance accelerates aging The metabolomic signature of extreme longevity: Naked mole rats versus mice Lurbinectedin synergizes with immune checkpoint blockade to generate anticancer immunity Laminin-binding integrins are essential for the maintenance of functional mammary secretory epithelium in lactation Immunoprophylactic and immunotherapeutic control of hormone receptor-positive breast cancer." Thesis, université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL019.

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Les progrès de la recherche sur le cancer du sein dépendent de la disponibilité d’outils appropriés, comme les lignées cellulaires qui peuvent être implantées chez des souris immunocompétentes. La souche de souris C57Bl/6 est la plus étudiée et c’est la seule pour laquelle certaines variantes génétiques sont disponibles. Étant donné qu'aucune lignée cellulaire de carcinome mammaire à récepteurs hormonaux positifs de souche C57Bl/6 n'est disponible, nous avons décidé d'établir des lignées cellulaires de ce type. Nous avons induit des cancers du sein chez des souris C57BL/6 femelles en utilisant un analogue synthétique de la progestérone combiné à un agent endommageant l'ADN. Des lignées cellulaires ont été établies à partir de ces tumeurs et sélectionnées pour leur positivité au niveau du double récepteur (estrogène + progestérone), ainsi que pour leur transplantabilité chez les femelles C57BL/6. Parmi plusieurs lignées, une lignée cellulaire, que nous avons appelée MD5, remplissait ces critères et a permis l'établissement de tumeurs mal différenciées et très prolifératives. Ces tumeurs ont réduit leur croissance (sans toutefois régresser) lors du traitement par des antagonistes des récepteurs d’œstrogènes, ainsi que par une chimiothérapie à base d'anthracylines. Cependant, ce dernier effet n'a pas été influencé par la déplétion des lymphocytes T et, en outre, ces tumeurs n'ont pas répondu au blocage de PD-1, ce qui suggère que les tumeurs MD5 sont immunologiquement froides. En conclusion, les cellules MD5, dérivées des animaux C57BL/6, constituent un modèle de cancer du sein à récepteurs hormonaux positifs de mauvais pronostic
Progress in breast cancer research relies on the availability of suitable cell lines that can be implanted in immunocompetent laboratory mice. The best explored mouse strain, C57Bl/6, is also the only one for which multiple genetic variants are available. Driven by the fact that no hormone receptor-positive C57Bl/6-derived mammary carcinoma cell lines are available, we decided to establish such cell lines. Breast cancers were induced in female C57BL/6 mice using a synthetic progesterone analogue combined with a DNA damaging agent. Cell lines were established from these tumors and selected for dual (estrogen + progesterone) receptor positivity, as well as transplantability into C57BL/6 females. One cell line, which we called MD5,fulfilled these criteria and allowed for the establishment of poorly differentiated, highly proliferative, immune cold tumors. Such tumors reduced their growth (though did not regress) upon treatment with estrogen receptor antagonists, as well as with anthracyline-based chemotherapy. However, the latter effect was not influenced by T cell depletion and MD tumors failed to respond to PD-1 blockade, suggesting that they are immunologically cold. In conclusion, C57BL/6-derived MD5 cells constitute a model of poor prognosis hormone receptor-positive breast cancer
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Gieniec, Krystyna Anna. "Investigating the Contribution of Specific Cancer-Associated Fibroblast Subsets to Colorectal Tumourigenesis." Thesis, 2020. http://hdl.handle.net/2440/130896.

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Despite colorectal cancer (CRC) remaining a prominent cause of cancer death worldwide, there is little known about how the surrounding connective tissue ‘stroma’ specifically encourages poorer prognosis. While many studies have attempted to interrogate the molecular cross-talk between the tumour and stromal cancer-associated fibroblasts (CAFs), the most important tumour-promoting interactions remain ill-defined. We are yet to adequately exploit these pathways for the prevention and treatment of CRC. In this thesis I aimed to identify and test specific CAF subsets for their putative ability to promote CRC, both in vitro and in vivo. Through RNA-sequencing, prognostic analyses and immunohistochemistry, I identified Melanoma cell adhesion molecule (MCAM) as a candidate CRC-promoting stromal factor that was significantly associated with worse patient prognosis. MCAM expression was significantly upregulated in mouse and human CRC compared to normal colon tissue and marked proliferative tumour-associated stroma comprised of both endothelial and fibroblast cell populations in vivo. Upon overexpression in primary mouse colon fibroblasts in vitro, MCAM significantly reduced contractile activity and enhanced migration. I also developed immunocompetent mouse models of primary and metastatic CRC to examine the efficacy of an inhibitor of a known CRC-promoting stromal factor, Gremlin1 (GREM1). These mouse models involved the implantation of mouse colorectal tumour organoids directly into the colon wall via colonoscope or into the liver via the portal vein, and the tumours generated represented human disease both genetically and pathologically. If we can better understand CAF biology and heterogeneity, and identify specific tumour-promoting CAF subtypes, then we can develop more targeted therapeutic strategies that inhibit both the cancer and its enhancing stroma to ultimately improve CRC patient survival.
Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2021
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Books on the topic "Tumour organoids"

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Soker, Shay, and Aleksander Skardal, eds. Tumor Organoids. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-60511-1.

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Soker, Shay, and Aleksander Skardal. Tumor Organoids. Humana, 2017.

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Soker, Shay, and Aleksander Skardal. Tumor Organoids. Humana, 2018.

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Book chapters on the topic "Tumour organoids"

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Smits, Daan, and Antoine A. Khalil. "Multimodal Techniques to Study Tumor Growth, Basement Membrane Breaching, and Invasion in 3D Matrices." In Cell Migration in Three Dimensions, 281–303. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_17.

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AbstractCancer-derived organoids and three-dimensional (3D) extracellular matrix (ECM) are taking center stage as in vitro models to study neoplastic cell behavior, since they recapitulate the heterogeneous cellular composition of tumors and their extracellular environment. In combination with imaging and molecular/biochemical techniques, 3D organoid models have contributed substantially to our knowledge about the cellular and molecular mechanisms that regulate the growth of tumors and invasion into the surrounding tissue. We here outline a set of protocols that describe culturing of cancer-derived organoids in 3D matrices and various strategies that allow modeling of tumor growth, tumor cell penetration into basement membranes, and invasion into Collagen I-rich ECM. Furthermore, we specify protocols for subsequent handling of organoids cultured in 3D ECM for confocal microscopy and analysis of gene expression at the protein and mRNA level. Although we here use breast cancer-derived organoids, these protocols can be directly applied or adapted for organoids derived from other cancer types or healthy tissues. Thus, in addition to investigating cell behavior of multiple cancer types, the combination of protocols described here may be used to study processes such as cell differentiation and migration during homeostasis and normal development.
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Hammes, Stefan. "Benign Tumors and Organoid Nevi." In Laser and IPL Technology in Dermatology and Aesthetic Medicine, 43–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03438-1_4.

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Pontius, W. Dean, Lisa C. Wallace, Katrina Fife, and Christopher G. Hubert. "Human Glioblastoma Organoids to Model Brain Tumor Heterogeneity Ex Vivo." In Brain Tumors, 133–58. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0856-2_7.

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Shelkey, Ethan, Anthony Dominijanni, Steven Forsythe, David Oommen, and Shay Soker. "Chapter 11. Modeling of the Tumor Microenvironment in Tumor Organoids." In Biomaterials Science Series, 279–303. Cambridge: Royal Society of Chemistry, 2022. http://dx.doi.org/10.1039/9781839166013-00279.

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Yamanishi, Cameron, Kimberly Jen, and Shuichi Takayama. "Techniques to Produce and Culture Lung Tumor Organoids." In Cancer Drug Discovery and Development, 1–15. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60511-1_1.

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Karolak, Aleksandra, and Katarzyna A. Rejniak. "Mathematical Modeling of Tumor Organoids: Toward Personalized Medicine." In Cancer Drug Discovery and Development, 193–213. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60511-1_10.

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Li, Linbo, and Shan Bian. "Modeling Brain Tumors Using Genetically Edited Brain Organoids." In Neuromethods, 159–71. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2720-4_9.

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Shirure, Venktesh S., Mary Kathryn Sewell-Loftin, Sandra F. Lam, Tyson D. Todd, Priscilla Y. Hwang, and Steven C. George. "Building Better Tumor Models: Organoid Systems to Investigate Angiogenesis." In Cancer Drug Discovery and Development, 117–48. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60511-1_7.

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Baker, Lindsey A., Hervé Tiriac, and David A. Tuveson. "Generation and Culture of Human Pancreatic Ductal Adenocarcinoma Organoids from Resected Tumor Specimens." In Methods in Molecular Biology, 97–115. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8879-2_9.

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Baker, Lindsey A., and David A. Tuveson. "Generation and Culture of Tumor and Metastatic Organoids from Murine Models of Pancreatic Ductal Adenocarcinoma." In Methods in Molecular Biology, 117–33. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8879-2_10.

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Conference papers on the topic "Tumour organoids"

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Verduin, M., A. Hoeben, L. Ackermans, D. Eekers, C. Hubert, J. Rich, V. Tjan-Heijnen, and M. Vooijs. "PO-340 Tumour heterogeneity in patient-derived glioblastoma organoids." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.852.

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Wang, Bowen, Peyton J. Tebon, Alexander L. Markowitz, Graeme F. Murray, Huyen Thi Lam Nguyen, Nasrin Tavanaie, Thang L. Nguyen, Paul C. Boutros, Alice Soragni, and Michael A. Teitell. "Functional Drug Sensitivity Screening of Bioprinted Tumor Organoids using High-Speed Live Cell Interferometry." In CLEO: Applications and Technology. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleo_at.2022.atu5i.5.

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We develop a method to apply a high-throughput quantitative phase imaging-based assay to functional biomass accumulation measurements of 3D tumor organoids with single-organoid resolution, and demonstrate its utility for drug screening and therapy selection.
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Semertzidou, Anita, Richard Williams, Nadia Fernandes, Jan Brosens, David MacIntyre, Julian Marchesi, Phillip Bennett, and Phillip Bennett. "2022-RA-726-ESGO Endometrial cancer organoids can reliably be used as replicas of primary tumour in endometrial cancer research." In ESGO 2022 Congress. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/ijgc-2022-esgo.230.

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Puca, Loredana, Rohan Bareja, Reid Shaw, Wouter Karthaus, Dong Gao, Chantal Pauli, Juan Miguel Mosquera, et al. "Abstract 992: Patient-derived tumor organoids of neuroendocrine prostate 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.am2017-992.

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Nizam, Aaron, Charlie Chung, Gary L. Goldberg, and Semir Beyaz. "Abstract LB236: Utilizing endometrial tumor organoids to model cancer immunomodulation." 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-lb236.

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Gillette, Amani, Cheri Pasch, Chris Babiarz, Dustin Deming, and Melissa Skala. "Fluorescence Lifetime Imaging of Treatment Response in Neuroendocrine Tumor Organoids." In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/omp.2017.oms2d.6.

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Martin, Maria Laura, Guoqiang Hua, Zhaoshi Zeng, and Philip B. Paty. "Abstract A06: Exploring mechanisms of colorectal tumor radioresistance in organoids." In Abstracts: AACR Special Conference on Developmental Biology and Cancer; November 30 - December 3, 2015; Boston, Massachusetts. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.devbiolca15-a06.

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Kuo, Calvin J. "Abstract IA08: Organoid modeling of tumor and tissue microenvironments." 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-ia08.

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Madej, Mariusz, Cinthya Del Angel Zuvirie, Jara García Mateos, Leo Price, Lidia Daszkiewicz, Kuan Yan, and Bram Herpers. "Abstract A065: Differential sensitivity of normal and tumor organoids to targeted therapies." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-a065.

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Gillette, Amani A., Christopher P. Babiarz, Cheri A. Pasch, Dustin A. Deming, and Melissa C. Skala. "Abstract 1941: Fluorescence lifetime imaging of treatment response in neuroendocrine tumor organoids." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1941.

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You might also be interested in the extended bibliographies on the topic 'Tumour organoids' for particular source types:
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