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Figure 1.

Endoscopic phenotype of four representative sessile serrated polyps/adenomas (SSA/Ps) located in the ascending colon of patients with the serrated polyposis syndrome.

Panel A. Large 15 mm diameter SSA/P with a mucus cap. Panel B. 20 mm diameter SSA/P. Panel C. 10 mm diameter SSA/P. Panel D. Small 4 mm diameter SSA/P. The size of polyps was estimated using biopsy forceps as a reference. Histopathology analyses were consistent with SSA/Ps (M. Bronner).

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Figure 1 Expand

Table 1.

Demographics of Serrated Polyposis Syndrome Patients.

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Figure 2.

Differentially expressed genes in sessile serrated adenoma/polyps (SSA/Ps) by RNA sequencing (RNA-seq) and microarray analyses.

Panel A. RNA-seq analysis identified 1294 genes (875 increased, 419 decreased) that were significantly differentially expressed (fold change ≥1.5, FDR<0.05) in SSA/Ps as compared to control colon biopsies. Differentially expressed genes in SSA/Ps that were found by RNA-seq analysis (red) and those found in a microarray study (green; 101 total, 59 increased, 42 decreased) are shown in the Venn diagram (23). Panel B. Hierarchical clustering of the differentially expressed genes in Panel A. Note: only 782 genes could be compared in the hierarchical clustering analysis because fewer genes were interrogated in the microarray analysis. Panel C. Hierarchical clustering of differentially expressed genes in SSA/Ps identified by RNA-seq analysis and in adenomatous polyps (APs) identified by microarray analysis (24). 136 genes (75 increased, 61 decreased) with a fold change ≥10 and FDR of <0.05 from both datasets were compared. Four distinct clusters are shown, cluster 1 represents genes increased in only SSA/Ps, cluster 2 represents genes increased in both SSA/Ps and APs, cluster 3 represents genes decreased only in APs, and cluster 4 represents genes decreased in both SSA/Ps and APs. Note: the full range of fold change is not reflected in color bar scale, the maximum fold change in RNA-seq analysis was 582-fold (MUC5AC) in SSA/Ps and 208-fold (GCG) in APs by microarray analysis.

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Figure 2 Expand

Table 2.

Top 50 gene transcripts increased by RNA sequencing in sessile serrated polyps (SSA/P) in serrated polyposis patients compared to controls.

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Figure 3.

Expression of mucin 17 (MUC17), V-set and immunoglobulin domain containing 1 (VSIG1), gap junction protein, beta 5 (GJB5) and regenerating islet-derived family member 4 (REG4) in SSA/Ps, adenomatous polyps (APs) and controls as measured by RNA-seq analysis.

Panel A1. MUC17 RNA-seq results. The y-axis represents the number of uniquely mapped sequencing reads per kilobase of transcript length per million total reads (RPKM) mapped to the MUC17 locus. The x-axis represents the chromosome (Chr) 7 coordinates and gene structure of the MUC17 transcript. Analysis showed an 82-fold increase in MUC17 mRNA in SSA/Ps (red, n = 7 polyps) compared to uninvolved colon (patient matched uninvolved, blue, n = 6) and control colon (screening colon without polyps; green, n = 2). The sequencing read length was 50 base pairs. Panel A2. MUC17 expression measured by qPCR analysis in SSA/Ps, adenomatous polyps and controls in additional patients. Relative mRNA levels of MUC17 in large (>1 cm) and small (<1 cm) SSA/Ps (n = 21), adenomatous polyps (n = 10), uninvolved colon and normal control colon biopsies (n = 10 each) are shown. In small and large SSA/Ps, MUC17 expression was increased by 38 and 71-fold, respectively, compared to controls. qPCR results were normalized to β-actin. The average MUC17 expression level in uninvolved colon tissue was chosen as the baseline. P-values were calculated using the Mann-Whitney U-test. Panel B1. VSIG1 (Chr X) RNA-seq results. A 106-fold increase in expression of VSIG1 was found in SSA/Ps as compared to controls. Panel B2. VSIG1 qPCR results. In small and large SSA/Ps, VSIG1 expression was increased 969 and 1393-fold, respectively. Panel C1. GJB5 (Chr 1) RNA-seq results. A 27-fold increase in GJB5 mRNA was found in SSA/Ps. Panel C2. GJB5 qPCR results. In small and large SSA/Ps, GJB5 expression was increased 446 and 523-fold, respectively. Panel D1. REG4 (Chr 1) RNA-seq results. An 87-fold increase in REG4 mRNA was found in SSA/Ps. Panel D2. REG4 qPCR results. In small and large SSA/Ps, REG4 mRNA was increased 68 and 116-fold, respectively.

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Figure 4.

Immunostaining for VSIG1, MUC17, CTSE and TFF2 in control colon, SSA/Ps, hyperplastic and adenomatous polyps.

Representative images of immunoperoxidase staining with affinity purified polyclonal antibodies and formalin-fixed, paraffin-embedded biopsies of patient matched and normal control colon (Panel A, n = 15, see Methods), syndromic SSA/Ps (Panel B, n = 10), sporadic SSA/Ps (Panel C, n = 15), hyperplastic polyps (Panel D, n = 10) and adenomatous polyps (Panel E, n = 10) are shown. Representative immunohistochemical stains for REG4 in control and polyp specimens are provided in Figure S2 in File S1.

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Table 3.

Immunohistochemical analysis of different serrated and adenomatous polyp types for proteins encoded by genes found to be highly differentially expressed in SSA/Ps.

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