Mouse Double Minute 2 (MDM2) Test Cost & Procedure

Brief Description

This test identifies amplification of the MDM2 gene to classify specific adipocytes. Well-differentiated lipomas, including atypical lipomas (WDL/ALT), and well-differentiated lipomas often show MDM2 amplification. (LLS). It can be difficult to differentiate these tumors morphologically from other high-grade benign sarcomas and tumors. Other soft tissue sarcomas rarely show amplification and benign lipomas do not. To kill p53, MDM2 acts as an E3 ubiquitin ligase. MDM2 binds to ARF, another tumor suppressor. This interaction locks MDM2 from p53 in the nucleus, activating p53. There are many other proteins that interact with MDM2. There are also known uses of MDM2 that are independent of p53.

Important Factor

MDM2 amplification from multiple tumors on additional chromosomes or markers leads to p53 suppression.

Commonly used to identify well-differentiated lipomas from well-differentiated lipomas and to characterize atypical lipomas from simulations.

Separation of benign fibrous and fibrous lesions from low-grade osteosarcoma and osteosarcoma (positive). (negative)

FISH is commonly used for testing, along with IHC and bicolor in situ hybridization (DISH/CISH); FISH is often considered the gold standard.

P53 is a common target.

The tumor suppressor p53 is a major target of Mdm2. Mdm2, a p53-interacting protein that inhibits the transcriptional activity of p53, was detected. Mdm2 inhibits the N-terminal transactivation domain of p53 by binding to and inhibiting it. Mdm2 is a p53-sensitive gene, which means that p53 can activate its transcription. Thus, Mdm2 transcription is also enhanced when p53 is stabilized, resulting in higher Mdm2 protein levels. Non-P53-associated role of Mdm2

Inhibition of DNA double-strand break repair by overexpressing Mdm2 was found to be p53-independent and mediated by a novel direct interaction between Mdm2 and Nbs1. Regardless of p53 status, the amount of Mdm2 is elevated, but Mdm2 does not lack its Nbs1-binding domain, resulting in chromosomal abnormalities, chromosomal delays, and genomic instability. These results suggest that Mdm2-induced genomic instability may be mediated by Mdm2:

Nbs1 interaction without p53 involvement.

Clinical features

• MDM2 immunostaining corresponds to gene amplification as detected by comparative genomic hybridization, qualitative PCR, FISH or DISH. (Vichhows Arch 2010;456:
• 167, Application of Mol Morphol Immunohistochemistry 2019;27:758, Med Cold Spring Port Outlook 2016;6:a026336)
• Resistance to radiation, chemotherapy, tyrosine kinase inhibitors, and immune checkpoint inhibitors has been implicated in the amplification and overexpression of MDM2 in tumours. (Int 2019;19 Cancer Cells:216)
• Especially in tumors involving the ER signaling pathway, the MDM2 SNP309 (rs2279744) GG (small allele) genotype is associated with increased expression levels of MDM2 and possibly a higher risk of cancer. a little bit. (Cold Spring Harbor Perspect Med 2016; 6:
• a026336) Breast tumors with mutant TP53 were more likely to have the TT or TG genotype of MDM2 SNP309 than the GG genotype. (Int J Mol Science 2019;20509)
• In Asians but not Caucasians, MDM2 SNP309 may be a risk factor for leukemia (Leuk Lymphoma 2012; 53:2245)
• MDM2 SNP285 (rs117049649) SNP309 G is found in only a small percentage of Caucasians and genotype C is associated with it. Its effects may be altered or counteracted by genotype C. (Cold Spring Harb Perspect Med 2016; 6:a026336)
• Cancer Genome Map data analysis revealed the global impact of MDM2 single nucleotide polymorphisms on MDM2 expression levels.