SHP-77 In Vitro Comparative Genomic Hybridization (CGH) Assay
CAT#: ITS-0123-YF2497
Target Cell Organism: Human
Target Cell Name: SHP-77
Assay Type: Genome Alteration Assays
Assay Overview
This assay is to provide SHP-77-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
SHP-77
Target Cell Organism
Human
Target Cell Background
SHP-77 epithelial cells are derived from a non-encapsulated primary lung tumor from the apical portion of the upper lobe of the left lung of a 54-year-old, White male in 1977. SHP-77 cells can serve as an in vitro target in 51Cr and 111 in release cytotoxicity assays as well as in vivo nude mice assays for evaluating immune reactivity of cells and serum from lung cancer patients. The cells can be used to evaluate the immune status of patients with SCLC who are treated with radiation or chemotherapy.
Related Diseases
Lung Cancer
Research Area
Oncology
Assay Name
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.