It has recently been shown that mdm2 overexpression with stabilization of p53 represents a characteristic of retroperitoneal well-differentiated-dedifferentiated, here renamed evolved (WD-E), liposarcomas at the immunocytochemical, molecular, and cytogenetic level. This make-up appears to be confined to half the cases in non-retroperitoneal well-differentiated liposarcomas, Since in different tumours MDM2 amplification involves amplicons encompassing flanking genes, such as CDK4, the possibility was investigated that in these rumours, CDK4 could act as an alternative or additional gene involved in the transformation mechanism, Forty-one retroperitoneal (R)/non-retroperitoneal (NR) well-differentiated-dedifferentiated (WD-DD) and 33 myxoid/round cell liposarcomas were reanalysed by immunocytochemical, molecular (nine cases) and fluorescence in situ hybridization (FISH) (one case) techniques. The results showed that all but one R WD-E cases carried the mdm2+, p53+, cdk4+ immunophenotype, In NR-WD liposarcomas, this immunophenotype was shared in five cases and the remainder showed mdm2+, p53-, cdk4+ in four and mdm2-, p53-, cdk4+ in one case, showing ring chromosomes by FISH analysis, TP53 mutations are confirmed to be closely correlated with NR-DD liposarcomas and no CDK4 involvement was found in the myxoid/round cell liposarcoma group. As well as confirming the synergistic effect of MDM2 and CDK4, these results are consistent with the concept that amplicon(s) excluding MDM2 may contribute to transformation and support a role of CDK4 in opposing p53 function, particularly in NR WD liposarcoma, (C) 1998 John Wiley & Sons, Ltd

Pilotti, S., Della Torre, G., Lavarino, C., Sozzi, G., Minoletti, F., Vergani, B., et al. (1998). Molecular abnormalities in liposarcoma: Role of MDM2 and CDK4-containing amplicons at 12q13-22. JOURNAL OF PATHOLOGY, 185(2), 188-190 [10.1002/(SICI)1096-9896(199806)185:2<188::AID-PATH53>3.0.CO;2-2].

Molecular abnormalities in liposarcoma: Role of MDM2 and CDK4-containing amplicons at 12q13-22

Vergani, B;
1998

Abstract

It has recently been shown that mdm2 overexpression with stabilization of p53 represents a characteristic of retroperitoneal well-differentiated-dedifferentiated, here renamed evolved (WD-E), liposarcomas at the immunocytochemical, molecular, and cytogenetic level. This make-up appears to be confined to half the cases in non-retroperitoneal well-differentiated liposarcomas, Since in different tumours MDM2 amplification involves amplicons encompassing flanking genes, such as CDK4, the possibility was investigated that in these rumours, CDK4 could act as an alternative or additional gene involved in the transformation mechanism, Forty-one retroperitoneal (R)/non-retroperitoneal (NR) well-differentiated-dedifferentiated (WD-DD) and 33 myxoid/round cell liposarcomas were reanalysed by immunocytochemical, molecular (nine cases) and fluorescence in situ hybridization (FISH) (one case) techniques. The results showed that all but one R WD-E cases carried the mdm2+, p53+, cdk4+ immunophenotype, In NR-WD liposarcomas, this immunophenotype was shared in five cases and the remainder showed mdm2+, p53-, cdk4+ in four and mdm2-, p53-, cdk4+ in one case, showing ring chromosomes by FISH analysis, TP53 mutations are confirmed to be closely correlated with NR-DD liposarcomas and no CDK4 involvement was found in the myxoid/round cell liposarcoma group. As well as confirming the synergistic effect of MDM2 and CDK4, these results are consistent with the concept that amplicon(s) excluding MDM2 may contribute to transformation and support a role of CDK4 in opposing p53 function, particularly in NR WD liposarcoma, (C) 1998 John Wiley & Sons, Ltd
Articolo in rivista - Articolo scientifico
mdm2/cdk4 immunophenotype; 12q13-22 amplicons; molecular-cytogenetic analysis; liposarcoma
English
1998
185
2
188
190
none
Pilotti, S., Della Torre, G., Lavarino, C., Sozzi, G., Minoletti, F., Vergani, B., et al. (1998). Molecular abnormalities in liposarcoma: Role of MDM2 and CDK4-containing amplicons at 12q13-22. JOURNAL OF PATHOLOGY, 185(2), 188-190 [10.1002/(SICI)1096-9896(199806)185:2<188::AID-PATH53>3.0.CO;2-2].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/191130
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