2004
DOI: 10.1016/j.lungcan.2003.09.010
|View full text |Cite
|
Sign up to set email alerts
|

MDM2 gene amplification: a new independent factor of adverse prognosis in non-small cell lung cancer (NSCLC)

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3

Citation Types

4
43
0

Year Published

2005
2005
2022
2022

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 61 publications
(47 citation statements)
references
References 35 publications
4
43
0
Order By: Relevance
“…The mdm2 gene itself is a downstream target of p53, thus forming a tight autoregulatory feedback loop (9-11). Consistent with this notion, gene amplification and overexpression of MDM2 have also been shown in a variety of tumors, particularly in soft tissue sarcomas, lymphomas, and breast and lung cancers (12)(13)(14)(15)(16). Interfering with the MDM2-p53 feedback loop leads to p53 activation, ultimately preventing neoplasia.…”
mentioning
confidence: 69%
“…The mdm2 gene itself is a downstream target of p53, thus forming a tight autoregulatory feedback loop (9-11). Consistent with this notion, gene amplification and overexpression of MDM2 have also been shown in a variety of tumors, particularly in soft tissue sarcomas, lymphomas, and breast and lung cancers (12)(13)(14)(15)(16). Interfering with the MDM2-p53 feedback loop leads to p53 activation, ultimately preventing neoplasia.…”
mentioning
confidence: 69%
“…Mdm2 overexpression could be linked to gene amplification in several malignancies (eg, malignant melanoma, non-small cell lung cancer and lipomatous tumours (Dworakowska et al, 2004;Nilsson et al, 2004;Muthusamy et al, 2006) but in PCa a specific Mdm2 gene amplification could not be demonstrated by Southern blot analysis so far (Ittmann et al, 1994). Interestingly, frequent gains of chromosome 12q including the regions 12q13-q14 that are in close proximity to the Mdm2 gene locus have been reported in various studies using comparative genomic hybridisation (Sattler et al, 1999;Zitzelsberger et al, 2001) but to date no gene copy number Figure 2 Graphical illustration of the genotype distribution in cases and controls.…”
Section: Discussionmentioning
confidence: 99%
“…It has been shown that even in cancer types that lack TP53 mutations, TP53 function is abolished or attenuated by other mechanisms, such as interaction with virus protein or overexpressed MDM2 protein [Oliner et al, 1992;Bond et al, 2004]. MDM2 is a key negative regulator of the TP53 pathway that targets TP53 for degradation, and overexpression or amplification of MDM2 has been frequently observed in many human cancer types, including lung cancer [Oliner et al, 1992;Higashiyama et al, 1997;Momand et al, 1998;Eymin et al, 2002;Dworakowska et al, 2004]. Second, the association between a high level of constitutive expression of MDM2 and susceptibility to carcinogenesis was previously tested in genetically modified animals.…”
Section: Discussionmentioning
confidence: 99%