Amplification of a gene encoding a p53-associated protein in human sarcomas

@article{Oliner1992AmplificationOA,
  title={Amplification of a gene encoding a p53-associated protein in human sarcomas},
  author={Jonathan Daniel Oliner and Kenneth W. Kinzler and Paul S. Meltzer and Donna L George and Bert Vogelstein},
  journal={Nature},
  year={1992},
  volume={358},
  pages={80-83}
}
DESPITE extensive data linking mutations in the p53 gene to human tumorigenesis1, little is known about the cellular regulators and mediators of p53 function. MDM2 is a strong candidate for one such cellular protein; the MDM2 gene was originally iden-tified by virtue of its amplification in a spontaneously transformed derivative of mouse BALB/c cells2 and the MDM2 protein subsequently shown to bind to p53 in rat cells transfected with pS3 genes3,4. To determine whether MDM2 plays a role in… 

MDM2 Gene Amplification in Metastatic Osteosarcoma1

TLDR
The data suggest that MDM2 gene amplification may be associated with tumor progression and metas tasis in osteosarcoma, and further investigation is warranted on the potential clinicopathological correlates of MDM 2 gene amplification in osteOSar coma.

MDM2 gene amplification in metastatic osteosarcoma.

TLDR
The data suggest that MDM2 gene amplification may be associated with tumor progression and metastasis in osteosarcoma, and further investigation is warranted on the potential clinicopathological correlates.

Amplification and overexpression of the MDM2 gene in a subset of human malignant gliomas without p53 mutations.

TLDR
The results indicate that amplification and overexpression of MDM2 may be an alternative molecular mechanism by which a subset of human malignant gliomas escapes from p53-regulated growth control.

The p53-binding protein MDM2 gene is differentially expressed in human breast carcinoma.

TLDR
Estrogen may play an important role in HBC growth stimulation by modulating the expression of MDM2, which in turn may inactivate the p53 function.

The MDM2 oncoprotein is overexpressed in rhabdomyosarcoma cell lines and stabilizes wild-type p53 protein.

TLDR
It is suggested thatMDM2 overexpression represents an alternative mechanism for p53 inactivation in a subset of childhood RMS without p53 mutations and the results indicate that the elevated MDM2 protein is responsible for wildtype p53 protein accumulation via stabilization.

The mdm2 proto-oncogene.

TLDR
A proposed role for mdm2 in pathways controlling cell cycle response to cellular perturbations is presented and it appears that an auto-regulatory feedback loop exists between these two proteins which keeps the growth suppressive functions of p53 in check during normal cell cycling.

The human MDM-2 oncogene is overexpressed in leukemias.

TLDR
It is suggested that the expression of the MDM-2 gene is altered in a significant fraction of human leukemias and MDm-2 may play a significant role in leukedmogenesis and mechanisms other than gene amplification may play an important role in deregulating the MDD-2 expression.

Low grade amplification of MDM2 gene in a subset of human breast cancers without p53 alterations

TLDR
Findings suggest that a subset of breast cancers without genetic alteration of p53 may also arise by inactivation of the p53 function through interaction with the overexpressed MDM2 protein induced by gene amplification.

Interaction between the retinoblastoma protein and the oncoprotein MDM2

TLDR
Here it is shown that MDM2 interacts physically and functionally with pRB and, as with p53, inhibits pRB growth regulatory function, therefore, both p RB and p53 can be subjected to negative regulation by the product of a single cellular proto-oncogene.

in Human Breast Carcinoma Gene Is Differentially Expressed MDM 2-binding Protein p 53 The Updated

TLDR
Estrogen may play an important role in HBC growth stimulation by modulating the expression of MDM2, which in turn may inactivate the p53 function.
...

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