Posterior probability density of the transcript concentration (number of transcripts per µg total RNA) for the oncogene in two different cervix tumours

<p><b>Copyright information:</b></p><p>Taken from "Genome-wide estimation of transcript concentrations from spotted cDNA microarray data"</p><p>Nucleic Acids Research 2005;33(17):e143-e143.</p><p>Published online 4 Oct 2005</p><p>PMCID:PMC1243803.</p><p>© The Author 2005. Published by Oxford University Press. All rights reserved</p> The mode of this density is the estimated concentration as listed at . There was a significant difference in the concentration between the tumours ( < 0.001, Kolmogorov–Smirnov test). The qRT-PCR data (relative to TBP) were 0.24 for MM14 and 0.023 for MM18, in agreement with our estimates

Posterior probability densities of transcript concentrations (number of transcripts per µg total RNA) of genes known to be involved in communication (green), growth (orange) and signal transduction (blue) for cancer cell lines () and cervix cancer ()

<p><b>Copyright information:</b></p><p>Taken from "Genome-wide estimation of transcript concentrations from spotted cDNA microarray data"</p><p>Nucleic Acids Research 2005;33(17):e143-e143.</p><p>Published online 4 Oct 2005</p><p>PMCID:PMC1243803.</p><p>© The Author 2005. Published by Oxford University Press. All rights reserved</p> The calculations were based on a pool of 10 cancer cell lines and 12 cervix tumours. The number of genes in each functional group is indicated. Some genes were shared by the groups. The distribution of all 10 157 genes and ESTs is also shown (black). All distributions were skewed to the right and had similar median values

Posterior probability density of transcript concentrations (number of transcripts per µg total RNA) for cancer cell lines (black) and cervix cancer (red)

<p><b>Copyright information:</b></p><p>Taken from "Genome-wide estimation of transcript concentrations from spotted cDNA microarray data"</p><p>Nucleic Acids Research 2005;33(17):e143-e143.</p><p>Published online 4 Oct 2005</p><p>PMCID:PMC1243803.</p><p>© The Author 2005. Published by Oxford University Press. All rights reserved</p> The data of 10 157 genes and ESTs were included, and the calculations were based on a pool of 10 cell lines and 12 cervix tumours. The median value of each distribution is shown as a vertical line and was slightly higher for the cell lines than for cervix cancer. Both distributions were skewed towards higher values, and less abundant transcripts were more frequent than high abundant ones

Transcript concentration (number of transcripts per µg total RNA) for 10 genes in cervix cancer with highest estimated mean concentration

<p><b>Copyright information:</b></p><p>Taken from "Genome-wide estimation of transcript concentrations from spotted cDNA microarray data"</p><p>Nucleic Acids Research 2005;33(17):e143-e143.</p><p>Published online 4 Oct 2005</p><p>PMCID:PMC1243803.</p><p>© The Author 2005. Published by Oxford University Press. All rights reserved</p> Each point represents the estimated value of a single tumour, showing large differences in transcript concentration among the tumours. The within gene range (max–min) varies from 10 (; ) to 100 (; )

Four distinct core modules of putative CRC driver genes were retrieved by Multi-Dendrix analysis.

<p>The nodes comprise both gene breakpoints (red outline) and gene mutations (blue outline). Edges (grey lines) connect genes that are mutually exclusively affected. The thickness of the grey lines and the corresponding number reflect the robustness score. The strongest mutual exclusivity is observed between <i>PIBF1</i> and <i>TP53</i>. Genes marked with a “*” indicate a pool of genes that share probe(s) associated with chromosomal breakpoints: the <i>ZNF337*</i> pool also includes <i>NCOR1P1</i>, <i>FAM182A</i>, <i>FAM182B</i>, <i>FRG1B</i>, <i>MIR663A</i>, <i>MLLT10P1</i>; <i>ZNF519*</i> also includes <i>ANKRD20A5P</i>, <i>ANKRD30B</i>.</p

Gene breakpoint and gene mutation frequencies of the 25 most frequently affected genes in CRC.

<p>Gene breakpoint frequencies (red bars) were based on the analysis of 352 CRC samples and gene mutation frequencies (blue bars) on the analysis of 204 samples. Genes marked with a “*” indicate a pool of genes that share probe(s) associated with chromosomal breakpoints: the <i>PCMTD2*</i> pool also includes <i>LINC00266-1; PARK2*</i> also includes <i>PACRG</i>; <i>ZNF337*</i> also includes <i>NCOR1P1</i>, <i>FAM182A</i>, <i>FAM182B</i>, <i>FRG1B</i>, <i>MIR663A</i>, <i>MLLT10P1</i>; <i>CD99*</i> also includes <i>XG</i>; <i>PARP8*</i> also includes <i>EMB</i>.</p

Clustering of 203 CRC patients by NBS based on gene breakpoints and gene mutations revealed four CRC subtypes.

<p>(A) Co-clustering matrix of CRC samples generated by NBS analysis. The matrix color intensity represents the similarity score. The color bar on top indicates the groups of patients related to the four CRC subtypes (k = 4) as determined by hierarchical clustering after NBS analysis. (B) Kaplan-Meier plot for overall survival (in days) of CRC subtype 1 (n = 80 patients), subtype 2 (n = 45 patients), subtype 3 (n = 27 patients) and subtype 4 (n = 51 patients). There are significant differences in OS among the four CRC subtypes (log-rank <i>P</i> = 0.001), with poorest OS for subtype 3 CRC patients. (C) Kaplan-Meier plot for OS of CRC subtype 3 patients <i>versus</i> patients in other CRC subtypes, showing a hazard ratio (HR) of 2.17 and a median OS of 392 days <i>versus</i> 610 days, respectively (log-rank <i>P</i> = 0.0002).</p

Clinical characteristics of the 199 investigated adenomas.

<p>All adenomas were classified endoscopically using the Paris classification; SSL; sessile serrated lesion, TSA; traditional serrated adenoma, LGD, low grade dysplasia; HGD, high grade dysplasia; proximal colon includes caecum, ascending and transverse colon; distal colon includes sigmoid, descending and splenic flexure.</p

The mutation percentage for the flat and polypoid adenomas.

<p>Only genes that show a mutation in one of the adenoma types are included. White bars represent flat adenomas and grey bars polypoid adenomas. Percentages are calculated using random imputation, horizontal bars represent the 95% confidence interval.</p

Total coverage of the 14 genes investigated, based on the COSMIC database.

<p>On the x-axis the analyzed gene. On the y-axis the mutation percentage is shown, based on large intestine carcinomas in the COSMIC database. In grey, the mutation percentages according to the COSMIC database, in black the mutation percentage covered by this study, on top of the bars the total number of analyzed samples found in the COSMIC database.</p