B16F10 In Vitro Comparative Genomic Hybridization (CGH) Assay

CAT#: ITS-1022-YF82
Target Cell Organism: Mouse
Target Cell Alternative Name: B16-F10
Target Cell Name: B16F10
Assay Type: Genome Alteration Assays
Assay Overview
This assay is to provide B16F10-based In Vitro Comparative Genomic Hybridization (CGH) Assay to accelerate our client's oncology projects. The assay will be customized according to the specific requirements. Please contact our scientists to discuss more details.
Target Cell Name
B16F10
Target Cell Organism
Mouse
Target Cell Background
B16F10 cell line (from Mus musculus C57BL/6J strain) is a convenient and widely used experimental model of highly metastatic melanoma to study cytotoxicity, migration, metastatic spread and tissue invasion. B16-F10 is a cell line exhibiting a morphology of spindle-shaped and epithelial-like cells that was isolated from skin tissue of a mouse with melanoma. Use these cells in your skin cancer research.
Target Cell Alternative Name
B16-F10
Related Diseases
Melanoma
Research Area
Oncology
Assay Name
In Vitro Comparative Genomic Hybridization (CGH) Assay
Short Description
B16F10-cell based In Vitro Comparative Genomic Hybridization (CGH) Assay
Assay Description
CGH is another popular cytogenetic technique, which is used to analyze copy number variations in genomes. In this technique, DNA in the reference sample (tumors) is first labeled with fluorochromes and allowed to hybridize with normal DNA. Human Cot-1 DNA is used to inhibit non-specific hybridization in this technique. Analyzing the ratio between fluorescence signal intensities of labeled DNA in samples and references can be plotted for each chromosome, permitting identification of possible copy number changes. CGH does not give much information about gene dosages and it is reported to be insensitive to structural abnormalities where copy number is not altered.
Assay Type
Genome Alteration Assays
Assay Type Details
Aberrant or somatic mutations are more commonly found in the DNA of cancer cells compared to normal cells. There is an equilibrium that exists between DNA damage and repair in normal cells. However, in cancer cells these events are disturbed, resulting in mutations and genomic instability. Genomic instability in cancer cells causes chromosomal aberrations, microsatellite instability, aneuploidy and uncontrolled gene amplifications and genetic instability in cancer cells are mainly due to point mutations or chromosomal aberrations such as insertions, deletions and translocation, resulting in mutated proteins.
For Research Use Only | Not For Clinical Use
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