Furthermore, the phenomenon of amplification in 3q appears to be quite different from that in 5p. For instance, the level of gain or amplification was lower than in 5p and it did not include the entire 3q arm in all the cell lines; instead, only certain sparse regions were found altered recurrently. In fact, the average log2 ratio of MRRs at 5p was almost 2 fold times higher than those located at 3q. The full arm or several regions of 3q were found to be amplified, similarly to the findings in previous reports. This could explain the lower proportion of deregulated genes found in 3q compared with that in 5p. However, even in those cell lines where most of 3q was gained, the proportion of deregulated genes did not rise or increased modestly. In addition, in 3q, the proportion of LY2835219 moa downregulated genes was higher than the proportion of upregulated genes, particularly in 3q26, where 8 of 11 deregulated genes were downregulated, even some of them were recurrently gained. Furthermore, similarly to 5p, deregulated genes seemed to be grouped in GDC-0199 clusters in 3q26�C29. These findings indicate that an increase in the copy number does not necessarily mean that genes located in those regions will be upregulated. It suggests that, in those entirely amplified regions, epigenetic mechanisms could be involved in gene repression. On the other hand, the increased frequency of downregulated genes with the number of amplified SNPs in the subset of genes located in MRRs, which seems to be not entirely amplified, supports that partial gene amplification may be a mechanism of gene silencing. This idea has been proposed theoretically. The 3q26 region has been previously identified as gained or amplified in biopsies or cell lines derived from CC by using CGH or FISH. Recognized tumor genes, such as EVI1 and MDS1, and genes associated previously with CC are located in this region. However, it has not been demonstrated that these genes were upregulated, particularly in the same samples where the CN alterations were found. In this study, EVI1, TERC, PIK3CA, and LAMP3 were neither found CN altered recurrently nor upregulated in all the cell lines studied. TERC was found gained in CaLo, CaSki, and HeLa but upregulated only in HeLa. However, conclusions with these negative results from the microarrays may be too risky without the validation with different methodologies, like qPCR and qRT-PCR. Interestingly, the gene encoding for tumor necrosis factor superfamily member 10, a protein that induces apoptosis in transformed and tumor cells, was found to be downregulated in the 4 cell lines, even though the gene was recurrently gained. This gene is located in the same region as 2 other downregulated and 2 upregulated genes, which have not been previously associated with CC. However, the protein encoded by ECT2 is a transforming protein that is a nuclear guanine nucleotide exchange factor and regulates RhoB-mediated cell death after DNA damage in cervical cell lines.