Colorectal carcinoma: Pathologic aspects

Abstract

Colorectal carcinoma is one of the most common cancers and one of the leading causes of cancer-related death in the United States. Pathologic examination of biopsy, polypectomy and resection specimens is crucial to appropriate patient managemnt, prognosis assessment and family counseling. Molecular testing plays an increasingly important role in the era of personalized medicine. This review article focuses on the histopathology and molecular pathology of colorectal carcinoma and its precursor lesions, with an emphasis on their clinical relevance.

Keywords: BRAF; Colorectal carcinoma; KRAS; MSI; adenoma; molecular; pathology.

Figure 1

An example of moderately differentiated adenocarcinoma showing complicated glandular structures in a desmoplastic stroma (original magnification ×200)

Figure 2

Desmoplastic reaction characterized by proliferation of spindle cells surrounding an adenocarcinomatous gland (original magnification ×400)

Figure 3

Necrotic debris (“dirty necrosis”) within the lumina of adenocarcinomatous glands (original magnification ×400)

Figure 4

Mucinous adenocarcinoma showing abundant extracellular mucin (original magnification ×200)

Figure 5

Signet ring cell carcinoma (original magnification ×400)

Figure 6

Medullary carcinoma showing a pushing border at the tumor edge (original magnification ×40)

Figure 7

Medullary carcinoma showing poorly differentiated histology and tumor-infiltrating lymphocytes (original magnification ×400)

Figure 8

Tumor cells close to, but not at, the serosal surface, with mesothelial inflammatory and hyperplastic reactions, which may be considered T4a by some investigators (original magnification ×40)

Figure 9

Examples of tubular adenoma (A. original magnification ×200), and tubulovillous adenoma (B. original magnification ×100)

Figure 10

Hyperplastic polyp (original magnification ×100)

Figure 11

Low power (A. original magnification ×40) and high power (B. original magnification ×200) views of sessile serrated polyp. Note the presence of basal serration

Figure 12

An example of traditional serrated adenoma (original magnification ×400). Note the presence of luminal serration, low grade cytologic dysplasia and cytologic eosinophilia

Figure 13

A case of familial adenomatous polyposis. Note the presence of innumerable polyps in the colon

Figure 14

Peutz-Jeghers polyp in the colon. Note the lobular pattern of colonic crypts divided by smooth muscle bundles (original magnification ×100)

Figure 15

Juvenile polyp showing dilated crypts and inflamed stroma (original magnification ×40)

Figure 16

High grade dysplasia showing complex architecture and marked nuclear atypia (original magnification ×400)

Figure 17

A malignant polyp showing adenocarcinomatous glands present within 1 mm of polypectomy margin (original magnification ×100)

Figure 18

Low power (A. original magnification ×40) and high power (B. original magnification ×200) views of pseudoinvasion in a tubular adenoma. Note the presence of hemorrhage and hemosiderin

Figure 19

Molecular pathways in colorectal tumorigenesis. CRC, colorectal cancer; MSS, microsatellite stable; MSI-H, high level microsatellite instability; FAP, familial adenomatous polyposis; AFAP, attenuated FAP; PJS, Peutz-Jeghers syndrome; JPS, juvenile polyposis syndrome; MAP, MUTYH-associated polyposis; CIN, chromosomal instability pathway; MSI, microsatellite instability; CIMP, CpG island methylator phenotype; ?, pathways yet undefined

Figure 20

A MSI tumor showing loss of MLH1 (A) and PMS2 (D) protein expression, and normal expression of MSH2 (B) and MSH6 (C). Note the presence of positive staining in benign colonic crypts and inflammatory cells, which serve as good internal controls for the stains (original magnification ×200)