Table 1.
Tumor location, type, and depth of invasion.
Fig 1.
Variation in the light microscopic appearance of the peritoneal elastic lamina (VVG).
The peritoneal elastic lamina, located between the mesothelium and the soft tissue of the subserosa and mesentery, is composed of a meshwork of elastic fibers and fibrils that typically appears thin and continuous by light microscopy (A, pancreas, 100x). Its appearance, however, can range from wispy, delicate, and discontinuous (B, appendix, 400x), to thick, ropy, and variably compact in long segments (C, stomach, 200x). In serosa that abuts near the muscularis propria, the elastic lamina appears to ramify with the elastic fibers of the subserosa (D, small intestine, 200x). Arrowheads: elastic lamina.
Fig 2.
Histopathologic alteration of peritoneal membranes associated with tumor invasion (H&E and VVG).
Tumor invasion of the peritoneal membrane is associated with localized inflammatory and desmoplastic reaction, resulting in hemorrhage and granulation tissue-like formation, surface fibrinous exudate, fibrosis, edema, and activation and proliferation of myofibroblast-like stromal cells (A, adenocarcinoma, colon, 40x). This is accompanied by retraction of the elastic lamina from the serosal surface toward the tumor (B, adenocarcinoma, colon, 20x) with splaying (C, adenocarcinoma, colon, 200x), attenuation, and fragmentation of its elastic fibers (D, adenocarcinoma, small intestine, 200x). Arrowheads: elastic lamina.
Fig 3.
Tumor invasion of the peritoneal membrane is characterized by neoplastic cells that invade the elastic lamina and the peritoneal connective tissue with activation and proliferation of serosal stromal cells that express cytokeratin (H&E, VVG, and pan-keratin).
Tumor invasion of the peritoneal membrane is associated with retraction, attenuation, and fragmentation of the elastic lamina and proliferation of serosal stromal cells that express cytokeratin, a unique feature not observed in stromal cells of extraperitoneal tissue. The keratin-positive stromal cells involve nearly the entire thickness of the expanded peritoneal membrane, forming a well-circumscribed population that is sharply delimited from the keratin-negative stromal cells of the subserosa by the elastic lamina. Neoplastic cells that invade the peritoneum abut or are surrounded by keratin-expressing stromal cells of the serosal membrane. (A-D, adenocarcinoma, small intestine, 40x, with higher magnification of boxed area in D, 200x; E-H, ductal adenocarcinoma, pancreas, 40x, with higher magnification of boxed area in H, 100x). Arrowheads: elastic lamina.
Fig 4.
Keratin-positive stromal cells are confined within the elastic lamina of the peritoneal membrane (VVG and pan-keratin).
Adenocarcinoma of the colon invades the peritoneal membrane with uneven fraying of the elastic fibers of the elastic lamina. At low magnification, the keratin-positive stromal cells appear to extend past the elastic lamina and into the subserosa (A and B, 20x). Closer inspection at higher magnification, however, reveals that the elastic lamina is unevenly splayed, with inner thin wispy fibers displaced from the bulk of the elastic lamina with deeper retraction toward the tumor (C and D, higher magnification of boxed areas, 100x). The keratin-positive stromal cells extend into the splayed elastic lamina, but are bounded by its innermost elastic fibers of the elastic lamina. Arrowheads: inner retracted elastic fibers of the elastic lamina.
Fig 5.
The degree of peritoneal injury correlates with the degree of stromal proliferation and cytokeratin expression, which is a reflection of the extent of tumor invasion, type of tumor, and magnitude of the tumor-associated fibroinflammatory reaction (H&E, VVG, and pan-keratin).
Serosal membrane in the absence of injury, as in this adenocarcinoma of the stomach confined within lymphovascular channels subjacent to the mesothelium, lacked proliferation of peritoneal stromal cells and expression of cytokeratin (A and B, H&E and pan-keratin, 200x). This adenocarcinoma of the gallbladder focally invades the splayed elastic lamina of the peritoneum with only minimal serosal injury and mild proliferation of weakly keratin-expressing stromal cells (C-E, H&E, VVG, and pan-keratin, 200x). Poorly cohesive/signet ring cell carcinoma of the stomach extends close to the visceral serosal surface, but is associated with little inflammation, desmoplasia, and weak cytokeratin expression in a small population of peritoneal stromal cells (F-H, H&E, VVG, and pan-keratin, 200x). Arrowheads: elastic lamina.
Fig 6.
Tumors confined to the subserosa show neither invasion of the elastic lamina nor the serosal connective tissue that include the keratin-positive stromal cells of injured peritoneal membranes (H&E, VVG, and pan-keratin).
Note the subserosal adipose tissue between the invasive front of the tumor and the peritoneum. (A-C, adenocarcinoma, small intestine, 100x). Arrowheads: elastic lamina.
Table 2.
Depth of tumor invasion and tumor invasion of keratin-positive stromal cells.