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XLS file, 27K, Deregulated genes known to promote carcinogenesis, tumor progression, or metastatic dissemination.

PDF file, 8K.

PDF file, 251K, Supplemental Figure S1 (a) Gene expression profiling of 131 clinical specimens for which we have staging information shows that overexpression of PTTG1 correlates with high tumor stage. (b) Association of increased PTTG1 expression with decreased probability of survival for 5-years. Dashed lines indicate 95% confidence intervals (c) Similarly, ECT2 overexpression is most prominent in high stage ccRCC tumors. (d) PTTG1 and ECT2 are coordinately overexpressed in primarily high stage tumors. (e) Cells completely deficient of ECT2 acquire a highly-branched and spindle-shaped morphology.

PDF file, 646K, Supplemental Figure S2. (a) SiRNA targeting PTTG1 achieved complete suppression of PTTG1 expression for at least 72 hours. (b) Immunofluorescent staining revealed abundant nuclear and cytoplasmic localization of PTTG1 in 786-O cells and suppression of PTTG1 expression upon treatment with targeted siRNA. (c) A 2-dimensional colony formation assay demonstrated that PTTG1 knockdown had little effect on anchorage-dependent growth rate. Crystal violet staining and microscopic imaging of these colonies further revealed that 786-O cells exhibit no major morphological differences following PTTG1 knockdown.

PDF file, 278K, Supplemental Figure S3. Direct targeting of ECT2 by siRNA results in a dose-dependent inhibition of ccRCC cell growth. (a) MTS proliferation assays showed a dose-dependent reduction in 786-O cell growth upon treatment with siRNA's targeting ECT2. (b) Depletion of ECT2 results in an accumulation of cells in G2/M phase. (c) Cells unable to complete cell division acquired a multinucleate phenotype, indicative of cytokinesis defects upon ECT2 knockdown.

PDF file, 27K, FISH Samples: Clinical Features and Maximum PTTG1 Copy Number. Interphase FISH analysis of ccRCC tumor touch preparations. FISH probe locations are shown in Figure 1a.

XLS file, 27K, Known Chromosome 5q Oncogenes.