The meeting of the German Society of Human Genetics (gfh) was held in Weimar, Germany this week and of course the attendees had the opportunity to visit the joined booth of MetaSystems and MetaSystems Probes. Main topics of the exhibition have been the latest advancements of the Neon case and imaging platform and RapidHyb, the revolutionary fast hybridization times of MetaSystems Probes' FISH probes.
- Order Number
- Package Size
- 100 µl (10 Tests)
The tumor suppressor gene TP53 is a key regulator in the cell cycle and is involved in apoptosis, genomic stability and angiogenesis. Inactivation of TP53 function prevents the antiproliferative effect and contributes to the development of many types of cancer. Several mechanisms of TP53 loss of function are known as gene mutations, interaction of p53 with viral proteins and association of p53 with the MDM2 oncoprotein. MDM2 is an ubiquitin ligase negatively regulating p53. MDM2 is amplified in about 7% of all human cancers with the highest frequency of about 20% in soft tissue tumors. MDM2 might also have p53 independent transforming capabilities. Well-differentiated liposarcomas/atypical lipomatous tumors (WDL-ALT) and dedifferentiated liposarcomas are among the most common soft tissue tumors in adults. Both entities share the same genetic aberration, an amplification of the chromosomal region including MDM2. WDL-ALT and benign lipomatous tumors can be morphologically similar and a clear assignment based on histological features might be difficult. The analysis of the MDM2 amplification status by FISH is considered as a useful technique for the differential diagnosis of WDL-ALT and benign lipomatous tumors since benign lesions do not harbor MDM2 amplifications. Furthermore, MDM2 overexpression has been reported to be a potential cause of p53 dysfunction in Chronic lymphoblastic leukemia.
- Chronic Lymphocytic Leukemia (CLL)
- Solid Tumors (Solid Tumors)
Two green (2G) and two orange (2O) signals.
Aberrant Cell (typical results):
Two green (2G) and three orange (3O) signals, indicating a duplication of the MDM2 locus.
- Haidar et al (1997) Am J Hematol 54:189-195
- Momand et al (1998) Nucleic Acids Res 26:3453-3459
- Weaver et al (2008) Mod Pathol 21:943-949