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Preinvasive colorectal lesion transcriptomes correlate with endoscopic morphology (polypoid vs. nonpolypoid).

Cattaneo E, Laczko E, Buffoli F, Zorzi F, Bianco MA, Menigatti M, Bartosova Z, Haider R, Helmchen B, Sabates-Bellver J, Tiwari A, Jiricny J, Marra G - EMBO Mol Med (2011)

Bottom Line: The latter also displayed fewer and less dramatic expression changes than polypoid lesions.This finding, along with TMIGD1 protein expression patterns in tissues and cell lines, suggests that TMIGD1 might be associated with intestinal-cell differentiation.We conclude that molecular dysregulation in slightly elevated, nonpolypoid, precancerous colorectal lesions may be somewhat less severe than that observed in classic adenomatous polyps.

View Article: PubMed Central - PubMed

Affiliation: Institute of Molecular Cancer Research, University of Zurich, Switzerland.

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Related in: MedlinePlus

Principal component and between-group analyses of gene expression data for the 84 colorectal tissue samplesThree-dimensional PCA score plot of log2 expression intensity values for the 42 normal mucosa samples (red spheres); 25 nonpolypoid lesions (blue); and 17 polypoid lesions (green). The first three principal components (PCs) account for 50.3% of total variance. PC axis 1 (PC1), the main direction of spread within all three tissue groups, reflects intragroup, interindividual variability. PC2 reflects intergroup variance based on tissue type, the factor responsible for segregating specimens into three groups. No specific biological variables correlated with the variance explained by PC3 (<5% of total) or the remaining variance in the data set (49.7% of the total). The data quality and model reliability are reflected in the absence of outliers and the high proportion of variance explained by PCs 1 and 2 (46.3% vs. 25% in a randomized PCA model of this set of samples and genes).BGA based on correspondence analysis (CoA) of log2 gene expression intensity values for samples grouped by tissue type. CoA discriminated between normal and lesional samples (axis 1) and between polypoid and nonpolypoid lesions (axis 2). The dispersion of scores along axis 2 reflects high-interindividual variability. Lower panel: Projection of scores on axis 1.
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fig01: Principal component and between-group analyses of gene expression data for the 84 colorectal tissue samplesThree-dimensional PCA score plot of log2 expression intensity values for the 42 normal mucosa samples (red spheres); 25 nonpolypoid lesions (blue); and 17 polypoid lesions (green). The first three principal components (PCs) account for 50.3% of total variance. PC axis 1 (PC1), the main direction of spread within all three tissue groups, reflects intragroup, interindividual variability. PC2 reflects intergroup variance based on tissue type, the factor responsible for segregating specimens into three groups. No specific biological variables correlated with the variance explained by PC3 (<5% of total) or the remaining variance in the data set (49.7% of the total). The data quality and model reliability are reflected in the absence of outliers and the high proportion of variance explained by PCs 1 and 2 (46.3% vs. 25% in a randomized PCA model of this set of samples and genes).BGA based on correspondence analysis (CoA) of log2 gene expression intensity values for samples grouped by tissue type. CoA discriminated between normal and lesional samples (axis 1) and between polypoid and nonpolypoid lesions (axis 2). The dispersion of scores along axis 2 reflects high-interindividual variability. Lower panel: Projection of scores on axis 1.

Mentions: Expression of 23,768 transcript clusters was analysed in all 42 precancerous lesions and their corresponding samples of normal mucosa (see Materials and Methods and Supporting Information). Unsupervised principal component analysis (PCA; Fig 1A) demonstrated that much of the variance among the samples was due to interindividual variability (PC axis 1, PC1), but a considerable portion of the residual variance was accounted for by tissue type (i.e. normal mucosa, polypoid lesions and nonpolypoid lesions; PC2). This variable was therefore used as the prime grouping factor in the supervised between-group analysis (BGA) based on correspondence analysis (CoA; Fig 1B). Normal mucosa samples were clearly segregated from the precancerous lesions, and the polypoid and nonpolypoid subsets within the latter category were also clearly distinct. [These distinctions were still evident after exclusion from the BGA of the three nondysplastic serrated lesions (Supporting Information Fig 1).]


Preinvasive colorectal lesion transcriptomes correlate with endoscopic morphology (polypoid vs. nonpolypoid).

Cattaneo E, Laczko E, Buffoli F, Zorzi F, Bianco MA, Menigatti M, Bartosova Z, Haider R, Helmchen B, Sabates-Bellver J, Tiwari A, Jiricny J, Marra G - EMBO Mol Med (2011)

Principal component and between-group analyses of gene expression data for the 84 colorectal tissue samplesThree-dimensional PCA score plot of log2 expression intensity values for the 42 normal mucosa samples (red spheres); 25 nonpolypoid lesions (blue); and 17 polypoid lesions (green). The first three principal components (PCs) account for 50.3% of total variance. PC axis 1 (PC1), the main direction of spread within all three tissue groups, reflects intragroup, interindividual variability. PC2 reflects intergroup variance based on tissue type, the factor responsible for segregating specimens into three groups. No specific biological variables correlated with the variance explained by PC3 (<5% of total) or the remaining variance in the data set (49.7% of the total). The data quality and model reliability are reflected in the absence of outliers and the high proportion of variance explained by PCs 1 and 2 (46.3% vs. 25% in a randomized PCA model of this set of samples and genes).BGA based on correspondence analysis (CoA) of log2 gene expression intensity values for samples grouped by tissue type. CoA discriminated between normal and lesional samples (axis 1) and between polypoid and nonpolypoid lesions (axis 2). The dispersion of scores along axis 2 reflects high-interindividual variability. Lower panel: Projection of scores on axis 1.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3377079&req=5

fig01: Principal component and between-group analyses of gene expression data for the 84 colorectal tissue samplesThree-dimensional PCA score plot of log2 expression intensity values for the 42 normal mucosa samples (red spheres); 25 nonpolypoid lesions (blue); and 17 polypoid lesions (green). The first three principal components (PCs) account for 50.3% of total variance. PC axis 1 (PC1), the main direction of spread within all three tissue groups, reflects intragroup, interindividual variability. PC2 reflects intergroup variance based on tissue type, the factor responsible for segregating specimens into three groups. No specific biological variables correlated with the variance explained by PC3 (<5% of total) or the remaining variance in the data set (49.7% of the total). The data quality and model reliability are reflected in the absence of outliers and the high proportion of variance explained by PCs 1 and 2 (46.3% vs. 25% in a randomized PCA model of this set of samples and genes).BGA based on correspondence analysis (CoA) of log2 gene expression intensity values for samples grouped by tissue type. CoA discriminated between normal and lesional samples (axis 1) and between polypoid and nonpolypoid lesions (axis 2). The dispersion of scores along axis 2 reflects high-interindividual variability. Lower panel: Projection of scores on axis 1.
Mentions: Expression of 23,768 transcript clusters was analysed in all 42 precancerous lesions and their corresponding samples of normal mucosa (see Materials and Methods and Supporting Information). Unsupervised principal component analysis (PCA; Fig 1A) demonstrated that much of the variance among the samples was due to interindividual variability (PC axis 1, PC1), but a considerable portion of the residual variance was accounted for by tissue type (i.e. normal mucosa, polypoid lesions and nonpolypoid lesions; PC2). This variable was therefore used as the prime grouping factor in the supervised between-group analysis (BGA) based on correspondence analysis (CoA; Fig 1B). Normal mucosa samples were clearly segregated from the precancerous lesions, and the polypoid and nonpolypoid subsets within the latter category were also clearly distinct. [These distinctions were still evident after exclusion from the BGA of the three nondysplastic serrated lesions (Supporting Information Fig 1).]

Bottom Line: The latter also displayed fewer and less dramatic expression changes than polypoid lesions.This finding, along with TMIGD1 protein expression patterns in tissues and cell lines, suggests that TMIGD1 might be associated with intestinal-cell differentiation.We conclude that molecular dysregulation in slightly elevated, nonpolypoid, precancerous colorectal lesions may be somewhat less severe than that observed in classic adenomatous polyps.

View Article: PubMed Central - PubMed

Affiliation: Institute of Molecular Cancer Research, University of Zurich, Switzerland.

Show MeSH
Related in: MedlinePlus