Colonic Tumor Induction
Colonic Tumor Induction - Related Videos
07:33
In vitro Organoid Culture of Primary Mouse Colon Tumors
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Cited by 44 •
2013
A simple method to establish primary murine colon tumor organoid is described. This method utilizes the feature that colon tumor cells survive and grow into organoids in media containing limited growth factors, whereas normal colon epithelial do not.
08:14
Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
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Cited by 10 •
2017
Mosaic clone analysis in Drosophila imaginal disc epithelia is a powerful model system to study the genetic and cellular mechanisms of tumorigenesis. Here we describe a protocol to induce tumors in Drosophila wing imaginal discs using the GAL4-UAS system, and introduce a diagnosis method to classify the tumor phenotypes.
02:30
Intestinal Colonization and Diarrhea Induction by Vibrio cholerae in Adult Zebrafish
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2026
Source: Nag, D., et.al. Quantifying Vibrio cholerae Colonization and Diarrhea in the Adult Zebrafish Model. J. Vis. Exp. (2018)This video demonstrates the inoculation of adult zebrafish with a pathogenic Vibrio cholerae strain to study intestinal colonization and disease outcomes. It shows how bacterial toxins disrupt intestinal integrity, leading to fluid leakage, mucus secretion, and watery diarrhea before the fish are prepared for further analysis.
08:55
The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
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Cited by 111 •
2016
Mice bearing the Colon-26 (C26) carcinoma represent a classical model of cancer cachexia. Progressive muscle wasting occurs in association with tumor growth, over-expression of muscle-specific ubiquitin ligases, and reductions in muscle cross-sectional area. Fat loss is also observed. Cachexia is studied in a time-dependent manner with increasing severity of wasting.
09:28
Isolation of Primary Human Colon Tumor Cells from Surgical Tissues and Culturing Them Directly on Soft Elastic Substrates for Traction Cytometry
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Cited by 11 •
2015
A protocol is described to extract primary human cells from surgical colon tumor and normal tissues. The isolated cells are then cultured on soft elastic substrates (polyacrylamide hydrogels) functionalized by an extracellular matrix protein, and embedded with fluorescent microbeads. Traction cytometry is performed to assess cellular contractile stresses.
FAQs
Chemical carcinogens primarily create DNA damage in colonic epithelial cells, whereas genetic manipulation introduces oncogenic changes that alter cellular behavior. Either approach can drive the expansion of abnormal cells into precancerous lesions and tumors. Using one strategy or combining both allows researchers to examine different routes of colorectal cancer development under controlled experimental conditions.
DNA damage can alter the normal behavior of colonic epithelial cells, allowing affected cells to expand rather than remain within normal growth controls. This expansion provides a cellular basis for abnormal crypt growth, precancerous lesion formation, and later tumor development. Studying these changes helps investigators connect initiating carcinogenic events with visible stages of disease progression.
These models can reproduce a sequence that includes abnormal crypt growth, adenoma formation, and malignant progression. The sequence is important because colorectal cancer does not appear only as a final tumor state; it develops through recognizable changes in colonic tissue. Comparing these stages helps researchers investigate when carcinogenic mechanisms, biomarkers, or treatment effects become evident.
A typical experimental design selects chemical carcinogens, genetic manipulation, or a combination of both to initiate changes in colonic epithelial cells. Researchers then control the timing and disease conditions so altered cells can be followed as they expand into lesions or tumors. The resulting progression provides a structured basis for studying cancer formation and treatment.
Researchers use these models to investigate how colorectal tumors form and progress, while also examining approaches to cancer prevention. They can study carcinogenic mechanisms, follow the development of precancerous lesions, and evaluate whether experimental interventions influence disease. The ability to control timing and disease conditions makes the models useful for comparing defined stages of tumor development.
Because the models reproduce abnormal crypt growth, adenoma formation, and malignant progression, investigators can examine biological changes across multiple disease stages. Those stage-related changes may support biomarker development, while the induced tumors provide a context for evaluating targeted therapies. In medicine, this links experimental observations of tumor progression with strategies for detection, prevention, and treatment.