We made use of hematoxylin and eosin (H&E) stain, Verhoeff van-Gieson stain for elastic tissue (EVG), and factor VIII-related antigen (FVIII-RA) to stain tissues excised from 94 patients with colorectal carcinoma. Of these 94, 49 died of disease within two years (Group I), and 45 survived for five years or longer (Group II) after surgery. In the tissues from both groups, the use of EVG stain revealed a higher incidence of vascular invasion than was seen with H&E stain. In Group I, the rates were 28.6 percent and 61.2 percent with H&E and EVG, respectively, and those in Group II were 4.4 percent and 31.1 percent, respectively. Conversely, the FVIII-RA stain showed a decrease in the incidence of vascular invasion in both groups. In Group I, when vascular invasion was examined in EVG-stained tissues, the incidence was 81.3 percent in cases of hematogenous metastases and 23.5 percent in those without hematogenous metastases (P less than 0.01). These differences were not evident with H&E. When observing the site of vascular invasion in tissues of the colorectal wall stained with EVG, intramural and extramural types of vascular invasion were seen in 20 percent and 80 percent of cases in Group I and in 93 percent and 7 percent of those in Group II, respectively. Thus, not only the frequency, but also the site, of vascular invasion into the colorectal wall evidenced with EVG stain provides a more precise prediction of the recurrence of hematogenous metastases.

A clinicopathologic study of 42 mucinous gastric carcinomas (MGC) and 73 nonmucinous gastric carcinomas (NGC) was done. The tumor was defined as MGC when more than one half of tumor area had mucin pools. The 5‐year survival rate for curatively treated patients was almost the same in MGC (58%) and NGC (56%), and clinicopathologic features, except for lymphatic permeation, showed no significant difference between MGC and NGC. Findings in MGC patients who died of a recurrence within 3 years included total gastrectomy, upper location, large size, infiltrative growth, extraserosal invasion, positive lymph node metastasis, more advanced stage, and a noncurative operation. There was no significant correlation between the degree of mucin content and other data, including the prognosis. Histologically, MGC were divided into well‐differentiated and poorly differentiated types, according to the degree of glandular formation of the tumor cells. In patients with well‐differentiated MGC, the age of onset was older, tumor growth was localized, and there were metastases to the liver. In patients with poorly differentiated MGC, the age of onset was younger, tumor growth was infiltrative, and there was peritoneal dissemination. These results show that the biologic behavior of MGC is similar to that of NGC and that the lesion basically is determined by the histologic subtype, not by the mucin content. Cancer 1992; 69:866–871.

Pulmonary resection of metastatic lesions from colorectal adenocarcinoma was performed in 35 patients. The cumulative 5-year survival was 38%. The primary site of cancer was the colon in about half of the patients. Patients with a solitary metastasis or tumors smaller than 3 cm in diameter survived longer than did patients with multiple metastases or tumors larger than 3 cm but the differences were not significant. Other factors, including age, sex, histologic grade of tumor, location and stage of primary carcinoma, location of pulmonary metastases, disease-free interval, and type of pulmonary resection, had no apparent influence on survival time. The lung was the major site of recurrence following pulmonary resection. Seven patients underwent two or more pulmonary resections for metastasis from a colorectal carcinoma. At the time of last follow-up, four patients were alive and free of recurrent disease at 5, 34, 39, and 58 months after the second pulmonary resection. These data suggest that some patients will survive for a long time following pulmonary resection of colorectal metastases, and for highly selected patients, repeated pulmonary resection may further extend survival.

Ten of 150 patients with primary squamous cell carcinoma of the esophagus and surgically treated, survived for more than 10 years. All 10 underwent a complete resection of the primary tumor and extensive lymph node dissection plus perioperative irradiation. The clinicopathologic findings in these 10 patients were reviewed. Five were female. Seven of the tumors exceeded 6 cm in length; seven were early stage, and the remaining three were advanced stage tumors. Lymph node metastases were evident in three, lymph vessel permeation was recognized in four, and no vascular vessel permeation was seen in any tumor. Two tumors had a characteristic appearance of carcinoma with lymphoid stroma, suggesting a good prognosis. In six for which cytophotometric DNA analysis could be done, four were type II, two were type III, and none was type IV. Thus, a complete resection of the primary tumor and extensive lymph node dissection can lead to a long survival time even for those with an advanced primary esophageal carcinoma.

Mucosa adjacent to colorectal disease was studied mucin-histochemically. Selected specimens were also studied immunohistochemically for carcinoembryonic antigen (CEA). Transitional mucosa, which showed elongation of crypts and marked sialomucin secretion, accompanied by a marked reduction in the normal sulfomucin content, was evident in 96 of 100 carcinomas (96 percent), 18 of 36 adenomas (50 percent), and 10 of 30 metaplastic polyps (33 percent). When considering the appearance of transitional mucosa, not only in the neoplastic lesions such as carcinoma or adenoma but also in the begin polyp, the transitional change adjacent to the carcinoma cannot be classified as a precancerous phenomenon; rather, it is a secondary one. The mucin-histochemical study disclosed transitional mucosa in all the 21 carcinomas less than 1 cm in diameter and immunohistochemical staining for CEA showed no remarkable change in the adjacent mucosa. Thus, it seems apparent that a change in mucous secretion precedes that of CEA expression in the mucosa adjacent to the carcinoma.