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One is N-terminal DAXX helical bundle (DHB) domain, which has been shown to interact with RASSF1C (Ras-association domain family 1 isoform C), P53 and MDM2 (mouse double minutes 2 homolog) (Escobar-Cabrera et al., 2010).
Amplification of the oncogene MYCN in double minutes (DMs) is a common finding in neuroblastoma (NB).
Alternatively, they may lie on circular extra-chromosomal DNA molecules called double minutes (dmins) [3], [4].
The remaining metaphases showed a high level of chromosomal damage with many fragments, double minutes and a tri-radial rearrangement.
NPM1 haploinsufficiency was significantly associated with monosomies (p<0.001) and gross chromosomal rearrangements, i.e., markers, rings, and double minutes (p<0.001), while NPM1 disomy was associated with structural changes (p = 0.013).
Our studies, along with those of others, have previously reported that the amplified genes on extrachromosomal double minutes (DMs) might be eliminated from the cell via inclusion into cytoplasmic micronuclei [1], [2], [3].
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Murine double minute 2. Positron emission tomography.
Murine double minute 2 (Mdm2) inhibitors enhance apoptosis in tumours harbouring wild-type p53.
It is inactivated by mutation or binding with human double minute 2 (HDM2) protein.
The murine double minute 2 (MDM2) gene encodes a negative regulator of the tumor protein p53.
It has also been shown to interact with the human murine double minute 2 (MDM2) and control its activity [24].
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