Cell cycle genes co-expression in multiple myeloma and plasma cell leukemia
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
23831116
DOI
10.1016/j.ygeno.2013.06.007
PII: S0888-7543(13)00128-6
Knihovny.cz E-resources
- Keywords
- Cell cycle genes, Multiple myeloma, Overall survival, Plasma cell leukemia, Time-to-progression,
- MeSH
- Survival Analysis MeSH
- Cell Cycle genetics MeSH
- Time Factors MeSH
- Genes, cdc * MeSH
- HeLa Cells MeSH
- Cyclin-Dependent Kinase Inhibitor p16 genetics metabolism MeSH
- Middle Aged MeSH
- Humans MeSH
- Multiple Myeloma diagnosis genetics MeSH
- Tumor Cells, Cultured MeSH
- Leukemia, Plasma Cell diagnosis genetics MeSH
- Prognosis MeSH
- Disease Progression MeSH
- Gene Expression Regulation, Neoplastic MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Cyclin-Dependent Kinase Inhibitor p16 MeSH
The objective of this study was to describe co-expression correlations of cell cycle regulatory genes in multiple myeloma (MM) and plasma cell leukemia (PCL). Our results highlight the presence of dynamic equilibrium between co-expression of activator and inhibitor gene sets. Moreover inhibitor set is more sensitive to the activator changes, not vice versa. We have shown that CDKN2A expression is associated with short-term survival in newly diagnosed MM patients (survival was 30.3 ± 3.9 months for 'low' expressed and 7.5 ± 5.6 months for 'high' expressed group, p<0.0001). Moreover low-expression CDKN2A group showed time-to-progression benefit in newly diagnosed patients (remission was 20.8 ± 3.6 months for 'low' and 8.4 ± 2.7 months for 'high' expressed group, p<0.0001) as well as in whole studied cohort of MM patients (remission was 20.8 ± 2.8 months for 'low' and 9.8 ± 1.1 months for 'high' expressed group, p<0.0001). The overexpression of inhibitors can be explained as a compensatory reaction to growing "oncogenic stress".
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