MB49 In Vitro Comparative Genomic Hybridization (CGH) Assay

This assay is to provide MB49-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.

MB49

Mouse

MB49 cells are derived from C57BL/Icrf-a' mouse bladder epithelial cells that were transformed by a single 24-hour treatment with the chemical carcinogen 7, 12-dimethylbenz[a]anthracene (DMBA) on the second day of a long term primary culture. Transformed cells transplanted into syngeneic mice were shown to generate carcinomas. While of male origin, karyotype analyses indicate the loss of the Y chromosome in 100% of the cells analyzed. This abnormality is a frequent early event in human bladder cancer.

Bladder Cancer

Oncology

In Vitro Comparative Genomic Hybridization (CGH) Assay

MB49-cell based In Vitro Comparative Genomic Hybridization (CGH) Assay

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.

Genome Alteration Assays

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.