A Standardized Pathology Report for Gastric Cancer: 2nd Edition

Abstract

The first edition of 'A Standardized Pathology Report for Gastric Cancer' was initiated by the Gastrointestinal Pathology Study Group of the Korean Society of Pathologists and published 17 years ago. Since then, significant advances have been made in the pathologic diagnosis, molecular genetics, and management of gastric cancer (GC). To reflect those changes, a committee for publishing a second edition of the report was formed within the Gastrointestinal Pathology Study Group of the Korean Society of Pathologists. This second edition consists of two parts: standard data elements and conditional data elements. The standard data elements contain the basic pathologic findings and items necessary to predict the prognosis of GC patients, and they are adequate for routine surgical pathology service. Other diagnostic and prognostic factors relevant to adjuvant therapy, including molecular biomarkers, are classified as conditional data elements to allow each pathologist to selectively choose items appropriate to the environment in their institution. We trust that the standardized pathology report will be helpful for GC diagnosis and facilitate large-scale multidisciplinary collaborative studies.

Keywords: Endoscopic resection; Gastrectomy; Molecular pathology; Pathology report; Standardization; Stomach neoplasms.

Fig. 1. An example of a tumor deposit. It usually has irregular outlines without identifiable lymph node tissue or identifiable vascular or neural structures.

Fig. 2. Histologic features of lymphovascular invasion in sections of gastric cancer. An example of lymphovascular invasion on hematoxylin and eosin examination (A) and stained for D2-40 (B). Tumors involving vessels with an identifiable smooth muscle layer are considered to have venous invasion (C).

Fig. 3. Sectioning of an endoscopically resected specimen. When the direction of the photograph matches the direction of the closest lateral margin (A). If the direction of the photograph does not match, turn the specimen toward the closest lateral margin for mapping (B).

Fig. 4. Method to measure submucosal invasion depth. Always use the lowest surface of the original, unmodified muscularis mucosae as the reference point (A). When the progressing course of the adjacent muscularis mucosae forms a curve, the virtual line is set as a matching curve (B).

Fig. 5. Method to measure submucosal invasion width. The actual size measured within the slide (A). Number of slices that the invasion spans ×2 mm (thickness of slice) (B).

Fig. 6. Method to measure ulcer size. The actual size measured within the slide (arrow: ulcer size within the slide) (A). Number of slices that the ulcer spans ×2 mm (thickness of slice) (star: ulcer-positive slices, arrow: slices that the ulcer spans) (B).

Fig. 7. Representative pictures of each histologic subtype of gastric carcinoma. Tubular adenocarcinoma (A), papillary adenocarcinoma (B), mucinous adenocarcinoma (C), poorly cohesive carcinoma, not otherwise specified (D), poorly cohesive carcinoma, signet-ring cell type (E), adenocarcinoma with lymphoid stroma (F), hepatoid adenocarcinoma (G), micropapillary adenocarcinoma (H), adenocarcinoma of the fundic-gland type (I, J), undifferentiated carcinoma (K), and crawling-type adenocarcinoma (L).

Fig. 8. Grading of gastric tubular adenocarcinoma. Well-differentiated adenocarcinoma showing glandular structures composed of columnar tumor cells (A). Moderately differentiated adenocarcinoma exhibits more complex tubular structures with cuboidal and/or flat epithelial cells (B). Tubular structure is unclear in most tumor glands in poorly differentiated adenocarcinoma (C).

Fig. 9. Intestinal (A) and diffuse (B) Lauren type gastric adenocarcinomas characterized by well-formed tumor glands and interspersed tumor cells, respectively.

Fig. 10. Tubular adenoma with low-grade dysplasia shows simple tubular architecture composed of elongated tumor cells with preserved polarity (A). More crowding and variation in the size of the tumor glands are noted in high-grade adenoma (B). The diagnosis of adenocarcinoma can be made when tumor cells show single-cell infiltration into the lamina propria (C) and/or marked structural fusion and atypia (D).

Fig. 11. Representative images of HER2-positive gastric cancer. HER2 IHC of this case showed heterogeneous intratumoral expression, composed of some areas featuring a score of 2+ with HER2 gene amplification and others scoring 0 (A). HER2 IHC of this case showed homogenous HER2 positivity (score of 3+) (B).

HER2 = human epidermal growth factor receptor 2; IHC = immunohistochemistry.

Fig. 12. A representative figure of gastric cancer with DNA mismatch repair deficiency. IHC for MLH1 (A) and PMS2 (B) showed loss of nuclear expression in tumor cells and positive nuclear expression in adjacent inflammatory cells. In contrast, IHC for MSH2 (C) and MSH6 (D) showed retained nuclear expression in tumor cells.

IHC = immunohistochemistry; MLH1 = mutL homolog 1; PMS2 = PMS1 homolog 2; MSH2 = mutS homolog 2; MSH6 = mutS homolog 6.

Fig. 13. A representative figure of EBV in situ hybridization. Diffuse positive EBER signals (A). Heterogenous pattern of EBER signals in cancer cells. EBER signals appear within a few intratumoral lymphocytes (B).

EBV = Epstein-Barr virus; EBER = EBV-encoded small RNA.

Fig. 14. A representative example of programmed death ligand 1 staining. (A) CPS <1, (B) CPS >1 and <5, and (C) CPS >5.

CPS = combined positive score.