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- W384307517 abstract "4195 Genetic events at chromosome 3p have been implicated in the development of non-small cell lung carcinoma (NSCLC). A number of known and putative tumour-suppressor genes reside within this region, including CACNA2D2 . This is a candidate tumour-suppressor gene which is located at 3p21. Although CACNA2D2 expression has previously been analysed in some lung cancer cell lines, its role in the development of primary NSCLC has yet to be elucidated. In this study, expression of the CACNA2D2 gene was investigated in 55 paired (normal/tumour), surgically excised lung tissue samples from patients with NSCLC. Promoter methylation status and loss of heterozygosity (LOH) at 3p were investigated in 48 of these samples. expression levels of CACNA2D2 were studied using comparative multiplex RT-PCR and subsequent analysis on an Agilent Bioanalyser. We have also developed a pyrosequencing assay on bisulphite treated DNA to examine the methylation status of part of the CACNA2D2 promoter. Analysis was carried out on a PSQ96MA System. LOH was carried out using fluorescent microsatellite markers at three loci (D3S1289, D3S1300, and D3S1263) and analysis on a 377 ABI automated sequencer. CACNA2D2 was underexpressed in 49 (89%) of 55 lung tumours compared to their adjacent normal tissue counterparts. The CACNA2D2 promoter was hypermethylated, in at least one CpG site out of four examined, in 2 (4%) of 48 samples investigated. LOH was detected in 26 (67%) of 39, 26 (60%) of 43 and 23 (70%) of 33 informative cases in markers D3S1289, D3S1263 and D3S1300 respectively. Loss of CACNA2D2 expression was more frequent in tumours with positive than tumours with negative nodes (Fisher’s exact, p=0.05). There was no association between CACNA2D2 expression and histology, T stage, M status and differentiation. These data demonstrate that loss of CACNA2D2 expression is a very frequent event in the development of NSCLC. Promoter hypermethylation of CACNA2D2 is rare and doesn’t appear as a major mechanism accounting for this loss of expression. Other intrinsic or extrinsic factors may contribute to the transcriptional silencing of CACNA2D2 in the molecular pathogenesis of NSCLC. This research was funded by the Roy Castle Foundation UK." @default.
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- W384307517 date "2006-04-15" @default.
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- W384307517 title "Loss of CACNA2D2 expression in non-small cell lung cancer" @default.
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