Relevant bibliographies by topics / Colorectal Cancer/Preclinical Model/Drug screening

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  1. Journal articles
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  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Colorectal Cancer/Preclinical Model/Drug screening'

Author: Grafiati
Published: 9 March 2023

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Journal articles on the topic "Colorectal Cancer/Preclinical Model/Drug screening"

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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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Sensi, Francesca, Edoardo D’Angelo, Martina Piccoli, Piero Pavan, Francesca Mastrotto, Paolo Caliceti, Andrea Biccari, et al. "Recellularized Colorectal Cancer Patient-Derived Scaffolds as In Vitro Pre-Clinical 3D Model for Drug Screening." Cancers 12, no. 3 (March 13, 2020): 681. http://dx.doi.org/10.3390/cancers12030681.

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Colorectal cancer (CRC) shows highly ineffective therapeutic management. An urgent unmet need is the random assignment to adjuvant chemotherapy of high-risk stage II and stage III CRC patients without any predictive factor of efficacy. In the field of drug discovery, a critical step is the preclinical evaluation of drug cytotoxicity, efficacy, and efficiency. We proposed a patient-derived 3D preclinical model for drug evaluation that could mimic in vitro the patient’s disease. Surgically resected CRC tissue and adjacent healthy colon mucosa were decellularized by a detergent-enzymatic treatment. Scaffolds were recellularized with HT29 and HCT116 cells. Qualitative and quantitative characterization of matched recellularized samples were evaluated through histology, immunofluorescences, scanning electron microscopy, and DNA amount quantification. A chemosensitivity test was performed using an increasing concentration of 5-fluorouracil (5FU). In vivo studies were carried out using zebrafish (Danio rerio) animal model. Permeability test and drug absorption were also determined. The decellularization protocol allowed the preservation of the original structure and ultrastructure. Five days after recellularization with HT29 and HCT116 cell lines, the 3D CRC model exhibited reduced sensitivity to 5FU treatments compared with conventional 2D cultures. Calculated the half maximal inhibitory concentration (IC50) for HT29 treated with 5FU resulted in 11.5 µM in 3D and 1.3 µM in 2D, and for HCT116, 9.87 µM in 3D and 1.7 µM in 2D. In xenograft experiments, HT29 extravasation was detected after 4 days post-injection, and we obtained a 5FU IC50 fully comparable to that observed in the 3D CRC model. Using confocal microscopy, we demonstrated that the drug diffused through the repopulated 3D CRC scaffolds and co-localized with the cell nuclei. The bioengineered CRC 3D model could be a reliable preclinical patient-specific platform to bridge the gap between in vitro and in vivo drug testing assays and provide effective cancer treatment.
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Ramzy, George M., Thibaud Koessler, Eloise Ducrey, Thomas McKee, Frédéric Ris, Nicolas Buchs, Laura Rubbia-Brandt, Pierre-Yves Dietrich, and Patrycja Nowak-Sliwinska. "Patient-Derived In Vitro Models for Drug Discovery in Colorectal Carcinoma." Cancers 12, no. 6 (May 31, 2020): 1423. http://dx.doi.org/10.3390/cancers12061423.

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Lack of relevant preclinical models that reliably recapitulate the complexity and heterogeneity of human cancer has slowed down the development and approval of new anti-cancer therapies. Even though two-dimensional in vitro culture models remain widely used, they allow only partial cell-to-cell and cell-to-matrix interactions and therefore do not represent the complex nature of the tumor microenvironment. Therefore, better models reflecting intra-tumor heterogeneity need to be incorporated in the drug screening process to more reliably predict the efficacy of drug candidates. Classic methods of modelling colorectal carcinoma (CRC), while useful for many applications, carry numerous limitations. In this review, we address the recent advances in in vitro CRC model systems, ranging from conventional CRC patient-derived models, such as conditional reprogramming-based cell cultures, to more experimental and state-of-the-art models, such as cancer-on-chip platforms or liquid biopsy.
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Voutsadakis, Ioannis A. "Cell Models for Chromosome 20q11.21 Amplification and Drug Sensitivities in Colorectal Cancer." Medicina 57, no. 9 (August 24, 2021): 860. http://dx.doi.org/10.3390/medicina57090860.

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Background and objectives: The chromosome locus 20q11.21 is a commonly amplified locus in colorectal cancer, with a prevalence of 8% to 9%. Several candidate cancer-associated genes are transcribed from the locus. The therapeutic implications of the amplification in colorectal cancer remain unclear. Materials and Methods: Preclinical cell line models of colorectal cancer included in the Cancer Cell Line Encyclopedia (CCLE) collection were examined for the presence of amplifications in 20q11.21 genes. Correlations of the presence of 20q11.21 amplifications with gene essentialities and drug sensitivities were surveyed on salient databases for determination of therapeutic leads. Results: A significant subset of colorectal cancer cell lines in the CCLE (12 of 63 cell lines, 19%) bear amplifications of genes located at 20q11.21. Cancer-associated genes of the locus include ASXL1, DNMT3B, BCL2L1, TPX2, KIF3B and POFUT1. These genes are all amplified in the 12 cell lines, but they are variably over-expressed at the mRNA level, compared to non-amplified lines. 20q11.21 amplified cell lines are sensitive to various tyrosine kinase inhibitors and are resistant to chemotherapy drugs targeting the mitotic apparatus and microtubules. CRISPR and RNAi dependencies screening revealed, besides the β-catenin and KRAS genes, a few recurrent gene dependencies in more than one cell line, including YAP1 and JUP. Conclusions: Cell line models of colorectal cancer with 20q11.21 gene amplifications display dependencies on the presence of specific genes and resistance or sensitivity to specific drugs and drug categories. Observations from in vitro models may form the basis for clinical drug development in this subtype of colorectal cancer. Genetic lesions conferring synthetic lethality to certain drugs or categories of drugs could be discovered with this approach.
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Rupp, Tristan, Christophe Legrand, Marion Hunault, Laurie Genest, David Babin, Guillaume Froget, and Vincent Castagné. "A Face-To-Face Comparison of Tumor Chicken Chorioallantoic Membrane (TCAM) In Ovo with Murine Models for Early Evaluation of Cancer Therapy and Early Drug Toxicity." Cancers 14, no. 14 (July 21, 2022): 3548. http://dx.doi.org/10.3390/cancers14143548.

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Ethical considerations, cost, and time constraints have highlighted the need to develop alternatives to rodent in vivo models for evaluating drug candidates for cancer. The tumor chicken chorioallantoic membrane (TCAM) model provides an affordable and fast assay that permits direct visualization of tumor progression. Tumors from multiple species including rodents and human cell lines can be engrafted. In this study, we engrafted several tumor models onto the CAM and demonstrated that the TCAM model is an alternative to mouse models for preliminary cancer drug efficacy testing and toxicity analysis. Tumor cells were deposited onto CAM, and then grown for up to an additional 10 days before chronic treatments were administered. The drug response of anticancer therapies was screened in 12 tumor cell lines including glioblastoma, melanoma, breast, prostate, colorectal, liver, and lung cancer. Tumor-bearing eggs and tumor-bearing mice had a similar chemotherapy response (cisplatin and temozolomide) in four human and mouse tumor models. We also demonstrated that lethality observed in chicken embryos following chemotherapies such as cisplatin and cyclophosphamide were associated with corresponding side-effects in mice with body weight loss. According to our work, TCAM represents a relevant alternative model to mice in early preclinical oncology screening, providing insights for both the efficacy and the toxicity of anticancer drugs.
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Invrea, Federica, Simona Punzi, Consalvo Petti, Rosalba Minelli, Michael D. Peoples, Christopher A. Bristow, Valentina Vurchio, et al. "Synthetic Lethality Screening Highlights Colorectal Cancer Vulnerability to Concomitant Blockade of NEDD8 and EGFR Pathways." Cancers 13, no. 15 (July 28, 2021): 3805. http://dx.doi.org/10.3390/cancers13153805.

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Colorectal cancer (CRC) is a heterogeneous disease showing significant variability in clinical aggressiveness. Primary and acquired resistance limits the efficacy of available treatments, and identification of effective drug combinations is needed to further improve patients’ outcomes. We previously found that the NEDD8-activating enzyme inhibitor pevonedistat induced tumor stabilization in preclinical models of poorly differentiated, clinically aggressive CRC resistant to available therapies. To identify drugs that can be effectively combined with pevonedistat, we performed a “drop-out” loss-of-function synthetic lethality screening with an shRNA library covering 200 drug-target genes in four different CRC cell lines. Multiple screening hits were found to be involved in the EGFR signaling pathway, suggesting that, rather than inhibition of a specific gene, interference with the EGFR pathway at any level could be effectively leveraged for combination therapies based on pevonedistat. Exploiting both BRAF-mutant and RAS/RAF wild-type CRC models, we validated the therapeutic relevance of our findings by showing that combined blockade of NEDD8 and EGFR pathways led to increased growth arrest and apoptosis both in vitro and in vivo. Pathway modulation analysis showed that compensatory feedback loops induced by single treatments were blunted by the combinations. These results unveil possible therapeutic opportunities in specific CRC clinical settings.
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Cornet, Carles, Sylvia Dyballa, Javier Terriente, and Valeria Di Giacomo. "ZeOncoTest: Refining and Automating the Zebrafish Xenograft Model for Drug Discovery in Cancer." Pharmaceuticals 13, no. 1 (December 24, 2019): 1. http://dx.doi.org/10.3390/ph13010001.

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The xenograft of human cancer cells in model animals is a powerful tool for understanding tumor progression and metastatic potential. Mice represent a validated host, but their use is limited by the elevated experimental costs and low throughput. To overcome these restrictions, zebrafish larvae might represent a valuable alternative. Their small size and transparency allow the tracking of transplanted cells. Therefore, tumor growth and early steps of metastasis, which are difficult to evaluate in mice, can be addressed. In spite of its advantages, the use of this model has been hindered by lack of experimental homogeneity and validation. Considering these facts, the aim of our work was to standardize, automate, and validate a zebrafish larvae xenograft assay with increased translatability and higher drug screening throughput. The ZeOncoTest reliability is based on the optimization of different experimental parameters, such as cell labeling, injection site, automated individual sample image acquisition, and analysis. This workflow implementation finally allows a higher precision and experimental throughput increase, when compared to previous reports. The approach was validated with the breast cancer cell line MDA-MB-231, the colorectal cancer cells HCT116, and the prostate cancer cells PC3; and known drugs, respectively RKI-1447, Docetaxel, and Mitoxantrone. The results recapitulate growth and invasion for all tested tumor cells, along with expected efficacy of the compounds. Finally, the methodology has proven useful for understanding specific drugs mode of action. The insights gained bring a step further for zebrafish larvae xenografts to enter the regulated preclinical drug discovery path.
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Kwon, Junhye, Sungryong Oh, Misun Park, Joon Seog Kong, Sunyi Lee, Hyunsook Lee, Younjoo Kim, Kyu-Tae Kang, Ui Sup Shin, and Joohee Jung. "Advanced Xenograft Model with Cotransplantation of Patient-Derived Organoids and Endothelial Colony-Forming Cells for Precision Medicine." Journal of Oncology 2021 (July 13, 2021): 1–9. http://dx.doi.org/10.1155/2021/9994535.

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Preclinical evaluation models have been developed for precision medicine, with patient-derived xenograft models (PDXs) and patient-derived organoids (PDOs) attracting increasing attention. However, each of these models has application limitations. In this study, an advanced xenograft model was established and used for drug screening. PDO and endothelial colony-forming cells (ECFCs) were cotransplanted in NRGA mice (PDOXwE) to prepare the model, which could also be subcultured in Balb/c nude mice. Our DNA sequencing analysis and immunohistochemistry results indicated that PDOXwE maintained patient genetic information and tumor heterogeneity. Moreover, the model enhanced tumor growth more than the PDO-bearing xenograft model (PDOX). The PDO, PDOXwE, and clinical data were also compared in the liver metastasis of a colorectal cancer patient, demonstrating that the chemosensitivity of PDO and PDOXwE coincided with the clinical data. These results suggest that PDOXwE is an improvement of PDOX and is suitable as an evaluation model for precision medicine.
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Flechner, Marie, Juergen Loskutov, Ulrike Pfohl, Katja Osman, Christian R. Regenbrecht, Katja Uhlig, and Lena Wedeken. "Abstract 6209: TumOC: A tumor organoid-on-chip platform for real-time cell vitality measurements." Cancer Research 82, no. 12_Supplement (June 15, 2022): 6209. http://dx.doi.org/10.1158/1538-7445.am2022-6209.

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Abstract Colorectal carcinomas (CRC) are one of the most common malignant tumors. Due to its heterogeneity and high probability to metastasize, the disease is often incurable and novel, improved therapies are needed. Enhanced, physiologically relevant in-vitro tumor models significantly increase the success rate in new drug development, reduce the number of animal experiments and result finally in better therapies for cancer patients. Furthermore, they have the potential to offer new approaches to personalized oncology. In recent years, 3D cell cultures were established as relevant preclinical cancer models, suitable for high-throughput-screening. However, their capacity to model and/or measure physiological processes can still be enhanced. In this project, we developed a tumor organoid-on-chip platform (TumOC) by combining most recent technological advances: We integrated patient-derived 3D cell cultures (organoids) from colorectal carcinomas and microsensor particles measuring oxygen concentration and therefore allowing assessment of cell vitality in real time in a microfluidic system. The resulting TumOC platform allows for defined exposition of cytostatic drugs including dynamic treatments. Measurements of cell vitality in real time enables analysis of not only the final effect of a drug treatment, but also the kinetics of drug response. At the same time, utilizing organoids allows for recapitulating tumor architecture and heterogeneity. Here we report the first proof of principle results generated with this system. We measured the cell vitality in real time over 72 hours during treatment with classic chemotherapeutics or targeted cancer drugs and compared the results to end-point measurements on the same organoids in a static system. In conclusion, our TumOC platform with its ability to recapitulate tumor heterogeneity in combination with dynamic treatments and real-time cell vitality assessment is an in-vitro tumor model closely recapitulating the physiological situation in a patient. TumOC provides an impressive opportunity to test and, consequently, predict the effectiveness of anti-cancer therapies. Therefore, this system is of interest not only for pre-clinical drug development but also for personal oncology. Citation Format: Marie Flechner, Juergen Loskutov, Ulrike Pfohl, Katja Osman, Christian R. Regenbrecht, Katja Uhlig, Lena Wedeken. TumOC: A tumor organoid-on-chip platform for real-time cell vitality measurements [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 6209.
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Mastropaolo, Maria, Helen Kuo, John Nguyen, Florencia Madorsky Rowdo, Jared Capuano, Jenna Moyer, M. Laura Martin, Julianne Hall, and Olivier Elemento. "Abstract B55: Patient-Derived Organoids model time-dependent sensitivities to PARP inhibitors in patients with metastatic colorectal cancer." Cancer Immunology Research 10, no. 12_Supplement (December 1, 2022): B55. http://dx.doi.org/10.1158/2326-6074.tumimm22-b55.

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Abstract Background: Poly (ADP-ribose) polymerase inhibitors (PARPi) have been approved as monotherapy and combination therapy for BRCA-mutated breast, ovarian, and prostate cancer and it is proposed that they may be effective for other BRCA-mutated cancer as well. However, recent clinical trials show inconsistent efficacy of PARPi on BRCA-mutated cancers, partially due to imperfect biomarker definition and unknown resistance mechanism. BRCA status alone may not be a good indicator for PARPi responsiveness as many proteins are involved in the homologous recombination (HR) pathway, which is why this experiment raises the question of whether time plays a role in tumor drug sensitivity. Patient-derived tumor organoids (PDTOs) can be used to study the pharmacogenomics between PARPis and HR deficient cancer. PDTOs are emerging ex vivo cancer models used for precision medicine because they harbor the mutational landscape of primary tumors. The common pipeline for organoid preclinical research includes confirming mutation profile, performing drug screening, and proposing clinically relevant candidates. The goal of this experiment was to model if the responses of patient-derived colorectal cancer organoids with BRCA gene deletion and TP53, SMAD4, and KRAS gene mutations to the PARPi talazoparib and olaparib differ depending on time.Methods: Patient sample: Colorectal: rectal cancer with BRCA1 gene deletion. Mutations in ⦁ KRAS p.Gly12Val ⦁ TP53 p.Arg175His ⦁ SMAD4 p.Arg361Cys + control: Puromycin 2 ug/mL - control: DMSO PARPi: talazoparib and olaparib In a 96 well plate, 1500 cells per well were plated in 10uL of a media/matrigel mixture and 100 uL of additional media were added to each well. The plate was put in the incubator at 37 C for 48 hours. The PARPi talazoparib and olaparib were then added after a serial dilution at max 50 uM concentration. The plates with the drugs (additional 100uL media with 2X drugs) were put in the incubator at 37 C for 120 hours. The plate for timepoint 1 was then read using the viability assay called Cell Titer Glo 3D. The next timepoint was taken after 168 hours using the same method. In addition, cell viability was measured by high content imaging which is being developed at EIPM.Results: Patient-Derived organoids were sensitive to talazoparib at hour 120 and hour 168 (IC50 1.6 and 1.9 respectively). Patient-derived organoids were not sensitive to olaparib at any time point tested and did not yield a meaningful IC50.Conclusion: The sensitivity of patient-derived colorectal cancer organoids with BRCA gene deletion and TP53, SMAD4, and KRAS gene mutations to the PARPi talazoparib and olaparib did not significantly differ depending on time. However, organoids were more sensitive to talazoparib than to olaparib. These results can guide which PARPi should be used in similar ex vivo experiments to yield meaningful results to eventually lead to successful clinical treatments for patients. Citation Format: Maria Mastropaolo, Helen Kuo, John Nguyen, Florencia Madorsky Rowdo, Jared Capuano, Jenna Moyer, M. Laura Martin, Julianne Hall, Olivier Elemento. Patient-Derived Organoids model time-dependent sensitivities to PARP inhibitors in patients with metastatic colorectal cancer [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy; 2022 Oct 21-24; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(12 Suppl):Abstract nr B55.
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Dissertations / Theses on the topic "Colorectal Cancer/Preclinical Model/Drug screening"

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Wan, Xiao. "Development of advanced three-dimensional tumour models for anti-cancer drug testing." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:5342fe46-c676-4fe8-8b6e-96d17a18d17d.

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Animal testing is still the common method to test the efficacy of new drugs, but tissue engineered in vitro models are becoming more acceptable for replacing and reducing animal testing in anti-cancer drug screening by developing in vitro three-dimensional (3D) tumour models for anti-cancer drug testing. In this study, three-dimensional (3D) culture methods were developed to mimic the tumour microenvironment. 3D culturing is to seed, maintain and expand cultured cells in three-dimensional space, in contrast to the traditional two-dimensional (2D) method in which the cells attach to the bottom of culture containers as monolayers. To mimic the intercellular interplay for tumour study, cell co-culture was applied. In this thesis, perfusion culture showed a better homeostasis for 3D tumour model growth over 17 days, with a more controllable working platform and a more reliable response-dose correlation for data interpretation. In the Matrigel sandwich system, the co-culture of breast cancer cells and endothelial cells demonstrated the morphology featuring a vascular network and tumour structures, with the thickness of the three-dimensional structure around 100µm and tubule length 200-400 µm, and maintained for 10 days. The comparisons studies between Matrigel sandwich and other methods suggest that though not fully characterised, Matrigel is still a valuable scaffold choice for developing co-culture 3D tumour model. Finally, the combination of perfusion and co-culture showed the potential of applying this model in angiogenesis assay, with a drug response profile combining cell viability and morphology to mimic in vivo tumour physiology.
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Book chapters on the topic "Colorectal Cancer/Preclinical Model/Drug screening"

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Baxi, Darshee. "Zebrafish: A Versatile Animal Model to Study Tumorigenesis Process and Effective Preclinical Drug Screening for Human Cancer Research." In Handbook of Animal Models and its Uses in Cancer Research, 1–11. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-1282-5_53-1.

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Baxi, Darshee. "Zebrafish: A Versatile Animal Model to Study Tumorigenesis Process and Effective Preclinical Drug Screening for Human Cancer Research." In Handbook of Animal Models and its Uses in Cancer Research, 1039–49. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-3824-5_53.

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Conference papers on the topic "Colorectal Cancer/Preclinical Model/Drug screening"

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Jain, Salvia, Luigi Scotto, Enrica Marchi, Matko Kalac, Jennifer Amengual, Jairo Baquero Buitrago, and Owen A. O'Connor. "Abstract A12: Validation of a novel bioluminescent mouse model of Sezary syndrome for preclinical drug screening." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a12.

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Krona, Cecilia, Cecilia Dyberg, Emma Sandén, Anna Darabi, Malin Wickström, Paul Northcott, John Inge Johnsen, and Peter Siesjö. "Abstract A84: Stereotactic injections of primary medulloblastomas as a representative model of the different subgroups for preclinical drug screening." In Abstracts: AACR Special Conference: Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; November 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.pedcan-a84.

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