Table 1. Frequency of MDM gene or protein alterations in selected human cancers.
| Tumour type | MDM2* | MDMX* | Detection‡ | Refs | ||||
|---|---|---|---|---|---|---|---|---|
| Overall | p53 wild-type | p53 mutant | Overall* | p53 wild-type | p53 mutant | |||
| Glioblastoma§ | 14% | 20% | 0% | 7% | 8% | 0% | Genome | 5 |
| Well-differentiated liposarcoma§ | 70% | 70% | 0% | 0% | 0% | 0% | Genome | 8 |
| Cutaneous melanoma║ | 37% | 46% | 0% | 68% | 85% | 100% | Protein | 10 |
| Breast | 31% | 80% | 14% | 38% | 80% | 24% | Protein | 6 |
| Oesophagus | 18% | 21% | 14% | NA | NA | NA | Genome | 3 |
| Osteosarcoma | 16% | 14% | 14% | 35% | NA | NA | Genome | 7,8 |
| Colorectal | 9% | 65% | 35% | 49% | NA | NA | Genome (MDM2); protein (MDMX) | 4,9 |
NA, not available.
The overall frequency at which alterations were present for both MDM2 and MDMX are listed. All numbers are converted to percentages for clarity. Where possible, the fraction of tumour samples with wild-type or mutant p53 that displayed MDM2 or MDMX amplification is listed.
Detection method was either immunofluorescence or western blot (protein) or gene amplification (genome).
Glioblastoma and well-differentiated liposarcoma show clear mutual exclusivity for MDM deregulation and p53 mutation, whereas this is less clear in other tumour types (for example, colorectal cancer).
Note that the sample size with validated mutant p53 in the cutaneous melanoma study was small (n = 3) and so more studies are required.
Data correlating amplification status with p53 status were not available in these studies.