TC-71 In Vitro Representational Difference Analysis (RDA) Assay
CAT#: ITS-1122-YF2079
Target Cell Organism: Human
Target Cell Name: TC-71
Assay Type: Genome Alteration Assays
Assay Overview
This assay is to provide TC-71-based In Vitro Representational Difference Analysis (RDA) 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
TC-71
Target Cell Organism
Human
Target Cell Background
Established from the tumor of a 22-year-old man with metastatic Ewings sarcoma that arose in the humerus; cell line was derived in 1981 from a biopsy of recurrent tumor at the primary site.
Related Diseases
Ewing Sarcoma
Research Area
Oncology
Assay Name
In Vitro Representational Difference Analysis (RDA) Assay
Short Description
TC-71-cell based In Vitro Representational Difference Analysis (RDA) Assay
Assay Description
This technique can detect sequence differences of two different DNA segments. In representational difference analysis, genomes to be compared are digested by specific restriction enzymes and ligated to specific oligonucleotide linkers, providing two different representations of the two genomes to be generated by PCR with primers specific for oligonucleotide linkers. Following the generation of amplicons, oligonucleotide linkers are removed and a new linker is attached only to test amplicons. These amplicons (tester) are then mixed with driver amplicons, which lack linkers. Amplification only occurs with DNA fragments specific to the tester (with primers specific for linkers).
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.