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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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Pathologic features of precancerous lesions that correlate with specific gene expression profilesCorrelation circles (left) and BGA plots (right) for variables identified by RDA as the second (A), third (B) and fourth (C) most significant predictors of gene expression patterns (after tissue type; Fig 2).Lesion histology (adenomatous vs. serrated). One-dimensional plot of scores on BGA axis 1 with the top 20 genes responsible for this discrimination (see Fig 2 for details).Lesion diameter (four size groups). For nondichotomous classifiers like this (and dysplasia, shown in panel C), scores on BGA axes 1 and 2 are meaningful, and results are visualized as biplots. Each size group is delimited by a probability ellipse (reflecting the two-dimensional 67% boundaries of a gaussian distribution, i.e. 1 standard deviation unit) with a labelled centroid. Along BGA axis 2, the red and blue ellipses representing smaller lesions (diameter ≤ 30 mm) are clearly separated from those representing larger (≥31 mm) lesions (green and brown). The top 20 genes responsible for segregating these lesions into these two categories are listed on the graph.Degree of dysplasia (high vs. low vs. absent). Lesions with high and low degrees of dysplasia (black and red ellipses, respectively), are completely segregated on axis 2, and the 20 genes that most responsible for this separation are reported. Lesions with and without dysplasia are segregated along axis 1. Results are visualized only for the genes with highest positive (TMIGD1) and negative (CLCA1) scores.
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fig03: Pathologic features of precancerous lesions that correlate with specific gene expression profilesCorrelation circles (left) and BGA plots (right) for variables identified by RDA as the second (A), third (B) and fourth (C) most significant predictors of gene expression patterns (after tissue type; Fig 2).Lesion histology (adenomatous vs. serrated). One-dimensional plot of scores on BGA axis 1 with the top 20 genes responsible for this discrimination (see Fig 2 for details).Lesion diameter (four size groups). For nondichotomous classifiers like this (and dysplasia, shown in panel C), scores on BGA axes 1 and 2 are meaningful, and results are visualized as biplots. Each size group is delimited by a probability ellipse (reflecting the two-dimensional 67% boundaries of a gaussian distribution, i.e. 1 standard deviation unit) with a labelled centroid. Along BGA axis 2, the red and blue ellipses representing smaller lesions (diameter ≤ 30 mm) are clearly separated from those representing larger (≥31 mm) lesions (green and brown). The top 20 genes responsible for segregating these lesions into these two categories are listed on the graph.Degree of dysplasia (high vs. low vs. absent). Lesions with high and low degrees of dysplasia (black and red ellipses, respectively), are completely segregated on axis 2, and the 20 genes that most responsible for this separation are reported. Lesions with and without dysplasia are segregated along axis 1. Results are visualized only for the genes with highest positive (TMIGD1) and negative (CLCA1) scores.

Mentions: Specific gene expression patterns were also associated with lesion histology, size, and degree of dysplasia (Fig 3). Diameter and degree of dysplasia were significantly associated with distinct expression profile clusters, which confirms our previous observations (Sabates-Bellver et al, 2007) in 32 polypoid lesions analysed with a different microarray platform. However, as shown in Fig 3A, the present analysis also revealed that serrated and adenomatous lesions are clearly distinct at the transcriptome level.


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)

Pathologic features of precancerous lesions that correlate with specific gene expression profilesCorrelation circles (left) and BGA plots (right) for variables identified by RDA as the second (A), third (B) and fourth (C) most significant predictors of gene expression patterns (after tissue type; Fig 2).Lesion histology (adenomatous vs. serrated). One-dimensional plot of scores on BGA axis 1 with the top 20 genes responsible for this discrimination (see Fig 2 for details).Lesion diameter (four size groups). For nondichotomous classifiers like this (and dysplasia, shown in panel C), scores on BGA axes 1 and 2 are meaningful, and results are visualized as biplots. Each size group is delimited by a probability ellipse (reflecting the two-dimensional 67% boundaries of a gaussian distribution, i.e. 1 standard deviation unit) with a labelled centroid. Along BGA axis 2, the red and blue ellipses representing smaller lesions (diameter ≤ 30 mm) are clearly separated from those representing larger (≥31 mm) lesions (green and brown). The top 20 genes responsible for segregating these lesions into these two categories are listed on the graph.Degree of dysplasia (high vs. low vs. absent). Lesions with high and low degrees of dysplasia (black and red ellipses, respectively), are completely segregated on axis 2, and the 20 genes that most responsible for this separation are reported. Lesions with and without dysplasia are segregated along axis 1. Results are visualized only for the genes with highest positive (TMIGD1) and negative (CLCA1) scores.
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Related In: Results  -  Collection

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fig03: Pathologic features of precancerous lesions that correlate with specific gene expression profilesCorrelation circles (left) and BGA plots (right) for variables identified by RDA as the second (A), third (B) and fourth (C) most significant predictors of gene expression patterns (after tissue type; Fig 2).Lesion histology (adenomatous vs. serrated). One-dimensional plot of scores on BGA axis 1 with the top 20 genes responsible for this discrimination (see Fig 2 for details).Lesion diameter (four size groups). For nondichotomous classifiers like this (and dysplasia, shown in panel C), scores on BGA axes 1 and 2 are meaningful, and results are visualized as biplots. Each size group is delimited by a probability ellipse (reflecting the two-dimensional 67% boundaries of a gaussian distribution, i.e. 1 standard deviation unit) with a labelled centroid. Along BGA axis 2, the red and blue ellipses representing smaller lesions (diameter ≤ 30 mm) are clearly separated from those representing larger (≥31 mm) lesions (green and brown). The top 20 genes responsible for segregating these lesions into these two categories are listed on the graph.Degree of dysplasia (high vs. low vs. absent). Lesions with high and low degrees of dysplasia (black and red ellipses, respectively), are completely segregated on axis 2, and the 20 genes that most responsible for this separation are reported. Lesions with and without dysplasia are segregated along axis 1. Results are visualized only for the genes with highest positive (TMIGD1) and negative (CLCA1) scores.
Mentions: Specific gene expression patterns were also associated with lesion histology, size, and degree of dysplasia (Fig 3). Diameter and degree of dysplasia were significantly associated with distinct expression profile clusters, which confirms our previous observations (Sabates-Bellver et al, 2007) in 32 polypoid lesions analysed with a different microarray platform. However, as shown in Fig 3A, the present analysis also revealed that serrated and adenomatous lesions are clearly distinct at the transcriptome level.

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