J Pathol Transl Med.  2020 Jan;54(1):1-19. 10.4132/jptm.2019.09.28.

Standardized Pathology Report for Colorectal Cancer, 2nd Edition

• Kim Bh
• Kim JM
• Kang GH
• Chang HJ
• Kang DW
• Kim JH
• Bae JM
• Seo AN
• Park HS
• Kang YK
• Lee KH
• Cho MY
• Do IG
• Lee HS
• Chang HK
• Park DY
• Kang HJ
• Sohn JH
• Chang MS
• Jung ES
• Jin SY
• Yu E
• Han HS
• Kim YW
• The Gastrointestinal Pathology Study Group of the Korean Society of Pathologists

• KMID: 2501591
• DOI: http://doi.org/10.4132/jptm.2019.09.28

Abstract

The first edition of the ‘Standardized Pathology Report for Colorectal Cancer,’ which was developed by the Gastrointestinal Pathology Study Group (GIP) of the Korean Society of Pathologists, was published 13 years ago. Meanwhile, there have been many changes in the pathologic diagnosis of colorectal cancer (CRC), pathologic findings included in the pathology report, and immunohistochemical and molecular pathology required for the diagnosis and treatment of colorectal cancer. In order to reflect these changes, we (GIP) decided to make the second edition of the report. The purpose of this standardized pathology report is to provide a practical protocol for Korean pathologists, which could help diagnose and treat CRC patients. This report consists of “standard data elements” and “conditional data elements.” Basic pathologic findings and parts necessary for prognostication of CRC patients are classified as “standard data elements,” while other prognostic factors and factors related to adjuvant therapy are classified as “conditional data elements” so that each institution could select the contents according to the characteristics of the institution. The Korean version is also provided separately so that Korean pathologists can easily understand and use this report. We hope that this report will be helpful in the daily practice of CRC diagnosis.

Keyword

Colorectal neoplasms; Pathology report; Standardization; Protocol

Figure

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  Fig. 1. Histologic features of intramucosal carcinoma. (A) The intramucosal carcinoma shows irregular invasive glands accompanied by desmoplasia. (B) The glands show excessive budding and luminal serration, which is highly suspicious for disruption of the basement membrane. (C) The elongated nuclei are seen in low-grade dysplasia, regardless of the ratio to the cell length.

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  Fig. 2. Measuring depth of invasion in tumors with submucosal invasion. (A) Haggitt level of invasion is composed of head, neck, stalk, and beyond stalk in pedunculated tumors. (B) The depth of invasion should be measured from the neck of the polyp (Haggitt level 2). (C) In cases with disrupted muscularis mucosae, the depth of submucosa invasion is measured from a continuous line of the residual muscularis mucosae. (D) To highlight indistinct muscularis mucosae, immunohistochemistry for desmin may be performed.

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  Fig. 3. Histologic features of lymphatic invasion and venous invasion. (A) Tumor clusters with retraction artifacts can be misinterpreted as lymphatic invasion (H&E stain and D2-40 immunohistochemical stain). (B) Tumor invasion of small vessels is considered as lymphatic invasion (H&E stain and D2-40 immunohistochemical stain). (C) Tumors involving vessels with identifiable smooth muscle layer or elastic lamina are considered as venous invasion.

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  Fig. 4. Histologic features of premalignant lesions of the colorectum. (A) Tubular adenoma with high-grade dysplasia. Note the architectural complexity including cribriform pattern or back-to-back fusion of dysplastic glands. (B) Tubulovillous adenoma with low-grade dysplasia. Note the retained cellular polarity with pseudostratified, elongated nuclei. (C) Sessile serrated adenoma without dysplasia. Note the dilated base of crypts. (D) Traditional serrated adenoma. Note the deep-invaginated pattern of crypt serration with hypereosinophilic cytoplasm and pencillated nuclei.

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  Fig. 5. Recommended tumor regression grading system. (A) Grade 0, complete response. No residual tumor cells are identified. (B) Grade 1, near complete response. The tumor bed contained abundant fibrosis with only a few or scattered tumor cells. (C) Grade 2, partial response. Residual tumor glands are easily identified in tumor bed. (D) Grade 3, poor or no response. The tumor cells do not demonstrate any response to chemoradiotherapy because abundant residual adenocarcinoma is present.

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  Fig. 6. A representative case of colorectal cancer with MMR deficiency (MLH1 deficiency). (A) MLH1 immunohistochemical staining showed negativity of nuclear expression in tumor cells. Note the retained nuclear expression in adjacent inflammatory cells. (B) MSH2 immunohistochemical staining demonstrated positivity of nuclear expression in tumor cells.

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