Several reports have demonstrated that SEL1L protein expression varies in human tumors relative to matched normal tissues, suggesting an involvement in cancer progression [27] [32].
First, elafin was downregulated in a large proportion of tumor specimens compared to matched normal tissues, suggesting that elafin possesses tumor-suppressive properties.
However, other studies showed that the levels of miR-21, miR-200c and miR-375 were higher in prostate tumours compared with matched normal tissues suggesting their derivation from tumours (Ambs et al, 2008; Ribas et al, 2009; Schaefer et al, 2010).
The allelic ratio in the matched normal samples suggested that both alleles were genomically balanced and expressed equally in each patient.
In this regard, recent studies of SEL1L expression in human colorectal tumors revealed higher p38 levels in adenomas compared to matched normal colonic mucosa, suggesting an association between upregulation of p38 and in vivo colonic tumorigenesis (Ashktorab et al., unpublished results).
Notably, in this pooled analysis (Additional file 2: Figure S10), ENVE exhibited high concordance rates with the SNP array calls for both amplifications (97.72 %) and deletions (92.86 %), as compared to the matched normal analysis, further suggesting that ENVE remains a viable methodology for reliably detecting sCNAs in tumors even in the absence of a matched normal sample.
Most of the tumours showed a higher level of Akt-Ser473 phosphorylation than matching normal tissues, suggesting an association between a high level of Akt phosphorylation and thyroid carcinogenesis.
175 age and sex matched normals were also included.
Down-regulation of a gene in a significant number of tumours compared with matched normal mucosa would usually suggest abrogation of tumour suppressor gene function.
We also examined the miR-205 expression in 9 pairs of matched colon cancer specimens, but found no significant difference in miR-205 expression level between tumors and the matched normal colon tissues (data not shown), suggesting that downregulation of miR-205 may be specific to breast cancer.
