Hbl-2 In Vitro Comparative Genomic Hybridization (CGH) Assay
CAT#: ITS-0123-YF3652
Target Cell Organism: Human
Target Cell Name: Hbl-2
Assay Type: Genome Alteration Assays
Assay Overview
This assay is to provide Hbl-2-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
Hbl-2
Target Cell Organism
Human
Target Cell Background
The HBL-2 cell line is derived from an AIDS-SNCCL (AIDS-associated small non-cleaved cell lymphoma) patient. After immunophenotypic and molecular genetic analysis, the HBL-2 was established from the original tumor clones. The HBL-2 cell line presents surface immunoglobulin and B-cell restricted markers as well as a phenotype consistent with SNCCL; the cell line also displays clonal immunoglobulin gene rearrangement. The HBL-2 cell line is considered useful as a biological model to study AIDS-associated non-Hodgkin lymphomagenesis (AIDS-NHL) and the impacts of biological, immunological, and viral factors involved.
Related Diseases
Mantle Cell Lymphoma; MCL
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.