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Nucleic Acids Research Pages 3453-3459  

The MDM2 gene amplification database
Introduction
Frequency of MDM2 Amplification
Comparison of p53 Genetic Alterations and MDM2 Amplification Frequencies
High Incidence of MDM2 Amplification in Soft Tissue Tumors
Other Mechanisms of MDM2 Overexpression in Human Tumors
p53-independent Functions of MDM2
Other Cellular Mechanisms of Down-regulating p53
The Internet Database
The Future
Acknowledgements
References

The MDM2 gene amplification database

The MDM2 gene amplification database

Jamil Momand*, David Jung1, Sharon Wilczynski2, Joyce Niland1

Department of Cell and Tumor Biology, Beckman Research Institute and Departments of 1Biomedical Informatics and 2Pathology, City of Hope National Medical Center, 1450 East Duarte Road, Duarte, CA 91010-3000, USA

Received March 20, 1998; Revised and Accepted May 27, 1998

ABSTRACT

The p53 tumor suppressor gene is inactivated in human tumors by several distinct mechanisms. The best characterized inactivation mechanisms are: (i) gene mutation; (ii) p53 protein association with viral proteins; (iii) p53 protein association with the MDM2 cellular oncoprotein. The MDM2 gene has been shown to be abnormally up-regulated in human tumors and tumor cell lines by gene amplification, increased transcript levels and enhanced translation. This communication presents a brief review of the spectrum of MDM2 abnormalities in human tumors and compares the tissue distribution of MDM2 amplification and p53 mutation frequencies. In this study, 3889 samples from tumors or xenografts from 28 tumor types were examined for MDM2 amplification from previously published sources. The overall frequency of MDM2 amplification in these human tumors was 7%. Gene amplification was observed in 19 tumor types, with the highest frequency observed in soft tissue tumors (20%), osteosarcomas (16%) and esophageal carcinomas (13%). Tumors which showed a higher incidence of MDM2 amplification than p53 mutation were soft tissue tumors, testicular germ cell cancers and neuro-blastomas. Data from studies where both MDM2 amplification and p53 mutations were analyzed within the same samples showed that mutations in these two genes do not generally occur within the same tumor. In these studies, 29 out of a total of 33 MDM2 amplification-positive tumors had wild-type p53. We hypothesize that heretofore uncharacterized carcinogens favor MDM2 amplification over p53 mutations in certain tumor types. A database listing the MDM2 gene amplifications is available on the World Wide Web at http://www.infosci.coh.org/mdm2 . Charts of MDM2 amplification frequencies and comparisons with p53 genetic alterations are also available at this Web site.

INTRODUCTION

The p53 tumor suppressor gene is the most frequently inactivated gene in human malignancies analyzed to date. In ~40% of the tumor samples p53 is inactivated by mutations within the coding region of the open reading frame (1). In most tumors, a point mutation usually occurs in one allele and the second allele is deleted. In some instances, however, the p53 gene is wild-type but its protein product is inactivated by viral and cellular oncogene products. The prevalence of these alternative mechanisms of p53 inactivation is not yet completely known. One of these alternative mechanisms is through overexpression of the cellular oncogene MDM2 (2,3).

MDM2 was originally cloned from amplified DNA obtained from a spontaneously transformed murine cell line (4,5). Analysis of the putative MDM2 protein sequence showed that it codes for a 483 amino acid residue protein with a zinc-binding RING finger motif (6). The MDM2 protein is phosphorylated on serine residues and its human homolog is located on chromosome 12q13-14 (3). Several recent reviews on general MDM2 function have been published (7-10) and electronic information, including links to its gene structure, can be found on the World Wide Web site maintained by the National Center for Biotechnology Information (http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?164785 ).

Due to the rapid pace of MDM2 research and its clear function in down-regulating p53 activity, we have decided to determine, from original peer-reviewed sources, the frequency of MDM2 gene amplification events in different types of tumors. Such data could help in several ways, such as selecting tissue types to conduct MDM2 research, choosing tumors to test new pharmaceuticals that exploit the MDM2-p53 interaction and seeking a greater understanding of carcinogens that initiate gene amplification.

FREQUENCY OF MDM2 AMPLIFICATION

To date, 3889 tumor tissue samples have been examined for MDM2 amplifications (Table 1). (For the purposes of this review, the term tumor will be used to signify both benign and malignant growths.) A compilation of these data shows that the overall frequency of MDM2 amplification is 7%. The highest frequency is observed in soft tissue tumors (20%), which includes Ewing's sarcoma, leiomyosarcomas, lipomas, liposarcomas, malignant fibrous histiocytomas, malignant Schwannomas and other sarcomas such as rhabdomyosarcomas. Osteosarcomas have the second highest frequency of MDM2 gene amplification (16%). At the other end of the spectrum, several tumors show no MDM2 amplification, including Wilms' tumors, leukemias, lymphomas, hepatoblastomas and pancreatic carcinomas. Amplification ranges between 2- and 10-fold. The most common technique for detecting MDM2 amplifications was Southern blotting, although quantitative PCR amplification was employed in a few studies (11,12).

Table 1. Summary of MDM2 gene amplification frequencies from 28 human tumors
Tumor type MDM2 amplification
(na) (%)		 References
Brain tumors 6.7 (239) 57-60
   Astrocytomas 8.1 (37) 57,60
   Glioblastomas 6.8 (191) 57,58,60
   Medulloblastomas 0 (8) 59
   Other 0 (3) 60
Breast carcinomas 5.9 (1774) 61-65
Cervical carcinomas 1.1 (88) 19,66
Esophageal carcinomas 13 (96) 14,67
Leukemias/lymphomas 0 (304) 68-70
Hepatoblastomas 0 (38) 71
Lung 5.7 (88) 72-74
   Lung cancers (NSCLC) 6.0 (83) 72,74
   Lung (not specified) 0 (5) 73
Nasopharyngeal carcinomas 2.1 (46) 75
Neuroblastoma 2.0 (51) 76-78
Osteosarcomas 16 (207) 3,79-82
Ovarian carcinomas 3.1 (190) 64,83
Pancreatic carcinomas 0 (25) 84
Soft tissue tumors 20 (479) 3,36,76,79,80,85-90
   Ewing's sarcomas 10 (30) 85
   Leiomyosarcomas 0 (46) 79,86,88
   Lipomas (benign) 30 (43) 80,86
   Liposarcomas 29 (87) 3,79,80,87,89
   Malignant fibrous
   histiocytomas		 21 (163) 3,79,80,86,90
   Malignant Schwannomas 19 (16) 79
   Sarcomas (non-specific)b 13 (85) 36,76
   Variousc 33 (9) 76,79,86
Testicular tumors 4.6 (64) 91,92
Thyroid carcinomas 0 (22) 93
Urothelial carcinomas 2.2 (137) 94,95
Wilms' tumors 0 (40) 76
Total number of tumor samples analyzed was 3889 and the average MDM2 gene amplification frequency was 7.2%.
aNumber of samples analyzed.
bSarcomas of soft tissue origin that were not specified.
cSoft tissue tumors that did not fall into the listed classes. The number of samples was less than five in any individual class.

COMPARISON OF p53 GENETIC ALTERATIONS AND MDM2 AMPLIFICATION FREQUENCIES

Since p53 and MDM2 are directly antagonistic, we hypothesized that p53 mutations and MDM2 amplification would tend not to occur in the same tumor samples. To test this we compared the frequency of p53 genetic alterations and MDM2 amplification for each tumor type (Fig. 1). The p53 mutation data is the sum of the missense mutations, mutations in introns affecting splicing, and small frameshift mutations (1,13). Most p53 mutation data were obtained from reviews (1) and the Web site, http://perso.curie.fr/Thierry.Soussi , maintained by Thierry Soussi (13). However, for soft tissue tumors and osteosarcomas, original publications were used as the source of p53 mutation frequency data.

Analyses of primary tumor samples show that p53 mutation and MDM2 amplification do not generally occur within the same tumor sample (Table 2). Since a p53 mutation and a MDM2 gene amplification both prevent p53 function, one would expect a negative association between these two outcomes. If one considers only tumor types where either p53 mutations or MDM2 amplification have been observed, then, out of a total of 93 such tumors, 60 had p53 mutations, 33 had MDM2 amplification and four had both p53 and MDM2 genetic alterations.

The Mantel-Haenszel [chi]2 test was used to examine the association between p53 mutations and MDM2 amplification, stratifying by tumor type. Significance was set at an [alpha] level of 0.05 and the test was performed two-sided. The Breslow-Day test for homogeneity was used to compare odds ratios across strata. Because there was no significant difference in odds ratios across tumor types (P = 0.40), a combined odds ratio over all strata and the 95% confidence interval were calculated using the Mantel-Haenszel logit method. There was a statistically significant negative association between the occurrence of p53 mutations and MDM2 amplification (P = 0.038). The odds of a p53 mutation occurring if MDM2 amplification was present was less than a third of that for patients with no amplification present (odds ratio 0.30, 95% confidence interval [0.09, 0.93]).

It is possible that the four esophageal carcinomas reported as having both genetic alterations was the result of a random distribution of mutations (14). Another possibility is that these tumors were heterogeneous in their genetic makeup (i.e. some cells with wild-type p53/MDM2 amplification, other cells with mutant p53/normal MDM2). Finally, it is possible that MDM2 may play a p53-independent role in tumor formation. Overall, however, the data suggest that p53 mutation and MDM2 amplification tend to be mutually exclusive events and that inactivation of wild-type p53 is the chief responsibility of MDM2 amplification.

Since p53 and MDM2 lie in the same signaling pathway, one would expect that in tumor types in which the p53 mutation frequency is low, a higher frequency of MDM2 amplification would be observed. Figure 1 shows that the MDM2 amplification frequency is higher than the p53 mutation frequency in only three tumor types: soft tissue tumors, testicular cancers and neuro-blastomas. In these tumors, MDM2 amplification frequencies were 20, 4 and 2% respectively, whereas p53 genetic abnormalities occurred in 14, 0 and 1% of these tumors. Overall, p53 does not appear to be inactivated by either p53 mutation or MDM2 amplification in testicular cancers or neuroblastomas. The reason for preferred p53 inactivation through MDM2 amplification in soft tissue tumors is unclear. One may speculate that the types of mutagens that these tissues are exposed to may predispose them to gene amplification events, rather than deletions and point mutations.

Table 2. Simultaneous analysis of MDM2 amplification and p53 genetic alterations suggests that mutations at each locus tend to be mutually exclusive
Tumor type na p53 mutation p53 wild-type MDM2 amplification MDM2 amplification +
P53 mutationb		 Reference
Osteosarcomas, soft tissue tumors 94 10 84 10 0 79
Esophageal tumors 72 29 43 13 4 14
Urothelial tumors 50 17 33 2 0 94
Liposarcomas 13 4 9c 8 0 89
Total 229 60 169 33 4  
aTotal number of tumors in study.
bStatistically significant negative association between p53 mutation and MDM2 amplification (P = 0.038, Mantel-Haenszel [chi]2 test).
cIncludes one silent mutation.

A corollary to the above scenario is that in tumors with extremely high p53 mutation frequencies, MDM2 amplification may be suppressed. Two cancers with high p53 mutation frequencies are lung and urothelial cancers, where the percentage of p53 genetic alterations is 70 and 61% respectively (Fig. 1), while the frequency of MDM2 amplifications is only 6 and 2.2% respectively. These gene amplification frequencies are not drastically lower than the average MDM2 amplification frequency (7%), but the relative genetic alteration frequencies do indicate that the p53 pathway is preferentially inactivated by mutations within p53 in these tumor types. Indeed, known tobacco carcinogens, such as benzo[a]pyrene, have been shown to form diol epoxide adducts at lung cancer mutation hotspots within the p53 gene (15).

The fact that several tumors have a significant number of samples where both p53 and MDM2 are not mutated (i.e. neuroblastomas, hematological malignancies, testicular cancer) leads to the obvious possibility that p53 may be inactivated by other, as yet undetermined, mechanisms. This possibility is clearly borne out in cervical cancers. In uterine cervical carcinomas 90% of patients are infected with oncogenic subtypes of the human papilloma virus (HPV) (16). The E6 oncogene of this virus expresses a product that binds p53 and leads to its degradation (17). Strong data previously showed that in oncogenic HPV-positive cancers, p53 mutations are observed in <4% of the samples tested (1,18). In this cancer type one would expect the frequency of p53 genetic alterations and MDM2 amplification to also be low. This may be the case. In cervical cancer, the frequency of p53 genetic abnormalities is only 7% and the frequency of MDM2 amplification is 1%. However, in one of the two MDM2 amplification studies conducted on cervical cancers, only HPV-negative samples were tested, indicating that the overall frequency of MDM2 amplification (in HPV+ and HPV- samples) is <1% for this cancer (19). Notwithstanding this caveat, the data suggests that p53 can be inactivated by a variety of separate mechanisms.


Figure 1. Comparison of MDM2 gene amplification and p53 mutation frequencies in human tumors. Red columns, MDM2 amplification frequency for each tissue (data from Table 1); green columns, p53 mutation frequency for each tissue. The number of samples for each tumor in which p53 mutation frequencies were calculated were as follows: brain, n = 456 (1); breast, n > 2400 (13); cervix, n = 350 (1); esophageal, n > 680 (13); leukemia/lymphoma, n > 3000 (13); lung, n > 1100 (13); nasopharyngeal, n = 117 (96-99); neuroblastoma, n = 212 (1); osteosarcoma, n = 76 (100); ovarian, n = 386 (1); pancreas, n = 170 (1); soft tissue tumors, n = 167 (11,100-104); testicular, n = 65 (91,92); thyroid, n = 125 (105,106); urothelial, n > 300 (13); Wilms', n = 40 (1). Note that the stippled column indicates that the p53 mutation frequency ranges from 10 (for leukemias) to 30% (for lymphomas).

HIGH INCIDENCE OF MDM2 AMPLIFICATION IN SOFT TISSUE TUMORS

Apparent predisposition of soft tissue tumors to MDM2 amplification warrants a closer look at these tumors. Soft tissue tumors are derived from smooth and striated muscle, fat, fibrous tissue, blood vessels and the peripheral nervous system (20). Soft tissue sarcomas are prevalent in a rare familial cancer syndrome called Li-Fraumeni syndrome, or LFS (21). Approximately 50% of LFS patients inherit one mutant allele of p53 (22-24). The second p53 allele is sometimes deleted in tumors of these patients, in accordance with the classical two-hit hypothesis first put forward by Knudson (25). However, only in ~50% of tumors of LFS patients is the second p53 allele lost (26). In patients where mutant p53 is inherited it would be of interest to determine whether MDM2 amplification or its overexpression can substitute for loss of the second p53 allele. In the LFS patients where germline p53 mutations are not detected, it might be prudent to investigate MDM2 gene amplification as well. However, in one such LFS family it has been shown, by linkage analysis, that the inherited defect does not map to the chromosomal location where MDM2 resides (27). Soft tissue sarcomas also arise as secondary tumors in survivors of familial retinoblastomas (20) and breast cancer radiotherapy. It is unclear if MDM2 plays a role in these secondary tumors.

OTHER MECHANISMS OF MDM2 OVEREXPRESSION IN HUMAN TUMORS

MDM2 may be up-regulated by mechanisms other than MDM2 amplification, including enhanced translation and gene trans-location, although whether these events occur in human tumors is unknown (28,29). MDM2 transcript levels have been shown to be relatively high in several tumors, for example, leukemias and lymphomas, with no gene amplification (30,31). If MDM2 is overexpressed through another abnormal mechanism, it would suggest that gene amplification analysis leads to an artificially low frequency of MDM2 involvement in human tumors. A simple model is that an MDM2 promoter-specific transcription factor can be up-regulated. Such a factor would lead to direct inactivation of p53.

The MDM2 promoter is also a direct target of p53, which is part of a negative feedback loop that down-regulates p53 (32-35). Thus, it is possible that some tumor cells that exhibit high levels of MDM2 transcript may, in fact, actually have functional p53. Several studies, using immunohistochemical analysis, have shown that MDM2 levels are high in samples where p53 levels are elevated (36,37). Therefore, it is difficult to rule out the possibility that elevated MDM2 levels result from normal p53 signaling in these tumors. If MDM2 expression is due to normal p53 activity then, in such tumors, the p53 pathway is either intact or the pathway is inactivated at a point downstream of its immediate target genes. Alternatively, one may speculate that factors that selectively target p53 to the MDM2 promoter, to the exclusion of other p53-responsive promoters (such as WAF1, GADD45 and BAX), may play a role in knocking out p53 tumor suppressor activity.

p53-INDEPENDENT FUNCTIONS OF MDM2

MDM2 may carry out oncogenic functions independent of p53. In the initial communication describing the cloning of MDM2 from murine cells several sizes of MDM2 cDNAs were obtained. Subsequent sequencing indicated that MDM2 transcripts were alternatively spliced (AS) (5). Two recent studies have shown that five human AS MDM2 transcripts are observed in urothelial, ovarian and brain tumors (38,39). Of these five AS forms (designated a-e), only one (MDM2-e) retains p53 binding capability (Fig. 2). Interestingly, cDNAs coding for all five AS forms could independently transform NIH 3T3 cells, suggesting that these MDM2 transcripts have p53-independent transforming capability. Detectable AS forms of MDM2 transcript positively correlated with late stage forms of ovarian, urothelial and brain tumors. In brain tumors, the most prevalent AS form was MDM2-b, an AS form that retains the RING finger domain. As expected, MDM2-b was distributed randomly between tumors with mutant p53 and tumors with wild-type p53. AS transcripts which express MDM2 products that are negative for p53 binding maintain the extreme N-terminal (residues 1-27) and C-terminal regions (389-491) of the protein. Interestingly, the RING finger domain near the C-terminus has been shown to bind a series of highly related RNAs (40). Whether such binding is important for p53-independent transformation is not clear.


Figure 2. MDM2 point mutations and alternatively spliced MDM2 transcripts observed in human tumors. A full-length schematic diagram of the MDM2 protein is presented. Codon numbers are listed near the top of each transcript and nucleotide numbers are listed near the bottom of each transcript. Nucleotide sequence numbers 1 and 1473 correspond to nucleotide sequence numbers 312 and 1784 in the original publication of the human MDM2 cDNA (3). The conserved domains (I-IV) are listed above the full-length protein and color-coded regions correspond to functional domains. Yellow, p53 and E2F1 binding domain; black, putative nuclear localization sequence; red, acidic domain which binds the L5 ribosomal protein; purple, putative Zn binding motifs, the last two of which comprise the RING finger. The alternatively spliced (AS) forms of the MDM2 transcript are listed, from MDM2-a to MDM2-e (38). The distribution of the AS forms of MDM2 in brain cancers is indicated on the right. Twenty four of 66 brain cancer samples contained MDM2 AS transcripts (39). Above the full-length MDM2 protein is an expanded portion of the first Zn finger, codons 300-324. Eight of 28 short-term cultured human cancer cells contained point mutations within this small coding region (37). In this region seven point mutations were clustered. Two coded for missense protein products, two coded for a single base insertion (one caused a premature stop codon), two were silent and one coded for a premature stop codon. Dashes, identity; i, a single base insertion. The distribution of eight cancers with MDM2 point mutations is presented on the right.

Another unusual mechanism by which MDM2 may contribute to tumor formation is through point mutational activation (41). It was reported that eight of 28 malignant tumor samples, which included follicular lymphomas, leukemias, hepatocellular carcinomas and an osteosarcoma, all sustained point mutations that clustered within the first putative zinc finger domain within residues 302-310 (Fig. 2). All the mutations resided within conserved domain III, a region that is extremely well conserved within MDM2 genes cloned from five different vertebrate species (8). To date, no molecule has been identified which specifically binds this region. The mutations consist of missense, nonsense and frameshift mutations within a 27 nt stretch (nt 1217-1244), but it is unclear whether the putative protein products offer a gain of function. Seven of the eight samples carried double point mutations, indicating that this region of the gene may be hypermutable. The presence of AS forms of MDM2 transcripts and point mutations within the MDM2 gene could indicate that MDM2 plays a more active role in human tumors than previously recognized.

OTHER CELLULAR MECHANISMS OF DOWN-REGULATING p53

As the study of p53 nears the end of its second decade we are gaining a clearer picture of the cellular mechanisms that regulate the p53 pathway. The product of a recently characterized tumor suppressor gene, ING1, cooperates with p53 in cell growth control (42). p53 function may be abrogated by a reduction in the level of p33ING1, but it is too early to determine if ING1 is inactivated in human tumors. Another protein that modulates p53 function is the product of the INK4a locus, p19ARF, a protein that binds MDM2 and prevents its ability to inactivate p53 (43,44). It is predicted that cells with reduced p19ARF activity have higher MDM2 activity, leading to p53 inactivation. Interestingly, several human tumors have deletions within the INK4a locus that inactivate p19ARF. However, another product of this locus, p16INK4a is also inactivated by such deletions. p16INK4a is a tumor suppressor that inactivates the cyclin D-CDK4/6 complex, which, in turn, inactivates Rb through phosphorylation (45). Thus, INK4a deletions may inactivate both classical tumor suppressors, p53 and Rb, at a distance. It is quite possible that other genes within the p53 pathway are not functional in tumors (second site mutations), leaving the p53 gene unharmed but its product deactivated.

p53 homologs may substitute for p53 function in some tissues. Three p53 homologs have recently been characterized (46-48). If these homologs parallel the p53 pathway then their inhibition would be subject to selection pressure during neoplastic transformation. The homologs may respond to cell stressors that do not activate p53, although it is difficult to find stressors that do not activate p53.

THE INTERNET DATABASE

As this is the first database that compiles the frequency of MDM2 gene amplifications in human tumors, it was important to make it available to scientists around the globe via the World Wide Web. The database is accessible on the internet at http://www.infosci.coh.org/mdm2 . The database resides on a Microsoft SQL Server and uses Microsoft's Internet Information Server and Active Server Pages to display the data. The Web site includes an option to download the database in Access 97, Excel 97 or comma-delimited ASCII formats. Data in the MDM2 gene amplification database are exclusively from peer-reviewed published sources and include the tumor type and subtype (when applicable), the frequency of DNA amplification and the number of samples tested. There is also an option to view a chart listing the MDM2 amplification frequencies by tumor type and a chart comparing these frequencies with the published frequencies of p53 mutations. This database will be updated semi-annually. Individuals who have published studies on MDM2 gene mutations in human tumors which are not currently included in the database may contribute to the database by sending an Email to jmomand@coh.org with their published paper reference.

THE FUTURE

Two important developments will undoubtedly occur. First, there will be a search for MDM2 homologs that inactivate the p53 homologs. MDMx, a MDM2 homolog, may be a good candidate (49). Second, MDM2 appears to be a likely target for cancer therapy. MDM2 can inhibit p53 activity by increasing the proteolytic susceptibility of p53 (50,51). Any tumor that has wild-type p53, regardless of whether MDM2 is overexpressed, may become susceptible to p53-mediated cell cycle arrest or apoptosis if anti-MDM2 therapy is successful. Several strategies are currently being employed, some of which are predicated on careful mapping of p53-MDM2 interaction domains and structure analysis (52,53). One strategy is to use a MDM2-targeted miniprotein (54). The miniprotein binds a cleft within MDM2 that is normally reserved for p53, thus freeing p53 to elicit proper growth control. Another strategy is to use antisense oligodeoxy-ribonucleotides (or phosphorothioate derivatives thereof) to prevent MDM2 expression (55,56). Cell culture studies demonstrate that p53 activity can be regained, causing cells to undergo apoptosis or cell cycle arrest. The MDM2 amplification database may be used as a guide to target the types of tumors that could be the first candidates for anti-MDM2 therapy in the future.

ACKNOWLEDGEMENTS

The authors appreciate helpful comments on the manuscript by Drs Susan Kane, Sergei Rodin and Roderich Schwarz. This work was supported by a grant from the UC Breast Cancer Research Program (1KB-0102) to J.M.

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