PMC5306990_01
H&E stained sections of grade 2 (moderately differentiated) adenocarcinoma extending through the muscularis propria (pT3). (a) Full-thickness section of the tumor. Adjacent to the tumor and deep to the tumor are lymphoid aggregates composed of tumor infiltrating lymphocytes (20x), (b) areas of tumor highlighting predominantly moderate differentiation (40x), (c) areas of tumor highlighting poor differentiation comprising less than 5% of the overall tumor (40x), (d) tumor originating from surface epithelium (40x), (e) and lymph node metastasis (20x).
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fig1
Histopathology revealed a moderately differentiated colonic adenocarcinoma with invasion through the muscularis propria into the subserosal adipose tissue and areas of CD-like lymphoid aggregates adjacent to and deep to the tumor with mild to moderate intratumoral lymphocytes (Figures 1(a) and 1(b)). While Figure 1(c) highlights a focal area of poorly differentiated adenocarcinoma, the tumor has between 50% and 95% glandular architecture designating it as grade 2 moderately differentiated.  Figure 1(d) shows an in situ component of the adenocarcinoma arising from the luminal surface. Lymphovascular invasion was present, with metastatic disease found in eight out of the 18 lymph nodes sampled.  Figure 1(e) shows an example of one lymph node with metastatic involvement.
Microsatellite Instability Profile demonstrating no loss of protein expression by immunohistochemical staining. Normal internal control of benign colonic mucosa is located at bottom of each picture. (40x) (a) MLH1, (b) PMS2, (c) MSH2, and (d) MSH6.
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fig2
Mismatch repair protein (microsatellite instability [MSI]) immunohistochemical stains were performed at the originating outside regional hospital and revealed no loss of MLH1, MSH2, MSH6, and PMS2 protein expression within the invasive tumor cells (Figures 2(a)-2(d)).
PMC5306990_02
H&E stained sections demonstrating focal chronic-active colitis, consistent with Crohn's disease. (a) Low power view showing dense inflammatory infiltrate composed of lymphoid hyperplasia (center and upper left) combined with transmural neutrophilic inflammation forming deep fissuring ulcer (bottom right) (40x), (b-c) crypt distortion, reactive epithelial atypia with neutrophilic inflammation ((b) 100x, (c) 200x), and (d-f) marked crypt distortion with extensive crypt abscesses in the epithelium ((d) 200x, (e) 100x, and (f) 200x).
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fig3
Upon our pathologic review of the right hemicolectomy case, the background nonneoplastic colonic mucosa located a few centimeters away from the tumor was noted to show focal chronic-active colitis characterized by marked crypt distortion, crypt abscesses, and reactive epithelial atypia (see Figures 3(a)-3(f), which demonstrate focal transmural neutrophilic inflammation forming a deep fissuring ulcer as well as large hyperplastic lymphoid aggregates).