Implications of P16/CDKN2A deletion in pleural mesotheliomas.
Homozygous deletion of P16/CDKN2A is found in approximately 75% of mesotheliomas amd may be the most common genetic alteration in this cancer. In terms of diagnostic applications, its high prevalence makes it a useful marker to distinguish malignant mesothelial cells from benign reactive ones in pleural fluid cytologic preparations. In terms of prognosis, P16/CDKN2A loss is associated with more aggressive clinical behavior in mesotheliomas. The homozygous co-deletion of MTAP, encoding the enzyme methylthioadenosine phosphorylase, in approximately 90% of mesotheliomas with P16/CDKN2A loss has potential therapeutic applications because MTAP-deficient tumors may be responsive to inhibitors of de novo AMP synthesis. Finally, global gene expression profiling using Affymetrix U133A chips finds few gene expression correlates of P16/CDKN2A deletion in pleural mesothelioma, consistent with its non-transcriptional mode of direct action through regulation of cell cycle-related kinase signaling.[1]References
- Implications of P16/CDKN2A deletion in pleural mesotheliomas. Ladanyi, M. Lung Cancer (2005) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
