Background. Protein induced by vitamin K absence or antagonist II (PIVKA‐II) was widely used as a diagnostic marker for hepatocellular carcinoma (HCC), however, its prognostic value is unclear. The authors evaluated PIVKA‐II clinicopathologically as a prognostic marker for HCC. Methods. The relationship between pathologic prognostic factors and plasma PIVKA‐II and alpha‐fetoprotein (AFP) was investigated in 72 patients with resectable HCC measuring less than 6 cm in greatest dimension. Results. PIVKA‐II shows significantly lower sensitivity, but higher specificity than AFP, and the use of these two complementary markers appears to be useful in the diagnosis of HCC. The frequencies of intrahepatic metastasis, portal vein tumor thrombus, hepatic vein tumor thrombus, and capsular infiltration were significantly higher in patients with positive PIVKA‐II than in those with negative‐PIVKA‐II, and the recurrence‐free rate was significantly lower in patients with positive rather than with negative PIVKA‐II. However, there were no significant differences between the patients who were AFP positive and those who were AFP negative in pathologic prognostic factors and the recurrence‐free rate. From univariate and multivariate analyses, the authors find that PIVKA‐II is one of the risk factors for recurrence of HCC after hepatectomy. Conclusions. PIVKA‐II may be a useful marker for the prediction of intrahepatic spread and for the prognosis of HCC. In addition, PIVKA‐II‐positive patients, thus, need aggressive postoperative adjuvant therapy for undetectable residual tumors and careful postoperative monitoring to enable the early recognition of recurrence.

A hypervascular tumor with high CEA and CA 19-9 levels or a hypovascular tumor with a high AFP level may suggest a preoperative diagnosis of MHC in patients with suspected HCC. Extensive surgery is an effective treatment for this disease, except in patients with satellite nodules. Hilar lymphadenectomy may not be necessary in selected patients.

Background. Gastric carcinoma is clinicopathologically divided into differentiated and undifferentiated types. The former is grossly protuberant and often causes hematogenous metastasis to the liver or lung, whereas the latter is mostly depressed or ulcerated from its early stage and rarely causes blood‐borne metastasis. The purpose of this study is to clarify the microvascular architecture of early gastric carcinoma with reference to the histologic subtypes. Methods. A silicone rubber compound (Microfil) injection method with a methyl salicylate clearing technique was used in 32 resected early gastric carcinomas. The microvascular architecture was observed both in the carcinoma and its surrounding noncancerous tissue in each specimen under a stereomicroscope and light microscope. Results. Compared to the surrounding normal mucosa, the differentiated carcinomas (DC) mostly were hypervascular (24%) or normovascular (65%), whereas the undifferentiated carcinomas (UC) often were hypovascular (60%). Irregularity of tumor vessels (67%) and an arcade‐like appearance (33%) was encountered frequently in UC, whereas hypervascularity of the surrounding noncancerous mucosa (29%) often was noticed in DC. Quantitative analysis, including vascular volume, mean vascular diameter, and cut section area, supported these differences between DC and UC. Conclusions. The results suggest that vascular structures of gastric carcinomas are characteristic with regard to their histologic subtypes; DC is normovascular or hypervascular, whereas UC is hypovascular. Cancer 1993; 72:32–6.

Background. The biologic behavior of poorly differentiated medullary carcinoma of the stomach is unclear. Methods. A clinicopathologic study on 74 poorly differentiated medullary carcinomas (PMC) and 73 non‐medullary carcinomas (NMC) of the stomach was done. PMC were defined as gastric carcinomas in which more than 50% of the tumor area contained poorly differentiated adenocarcinoma with no fibrous stroma. Results. They were characterized by a location in the upper 33% of the stomach (49%), grossly expansive growth (69%), frequent vascular permeation (57%), and simultaneous liver metastasis (15%). Although the 5‐year survival rate was similar for PMC and NMC, death of PMC was related more frequently to liver metastasis (47%) and less frequently to peritoneal dissemination (12%). The outcome of patients with PMC was influenced by frequent vascular permeation, extended lymph node metastasis, and simultaneous liver metastasis. Conclusions. These results indicate that PMC are characterized by expansive growth of the tumor and simultaneous or recurrent metastasis to the liver. Therefore, the biologic behavior of poorly differentiated medullary carcinoma is similar to that of well‐differentiated carcinoma of the stomach.

Background. The biologic significance of esophageal dysplasia has not yet been completely elucidated, especially regarding the process of multiple occurrences of squamous cell carcinoma. Methods. The multiplicity of dysplasia in 73 patients with solitary carcinoma of the esophagus (Group I) and 21 with multiple carcinomas (Group II)was compared in surgically resected specimens. Results. Thirty‐nine second carcinomas were identified in 13 patients of Group II, and all were superficial. The incidences of five or more isolated dysplasias in cases without continuity to a carcinomatous lesion, was 6.8% and 66.7% in Groups I and II, respectively (P < 0.01). In a case with three or more carcinomas, the incidence increased to 84.6%. The coexistence of all grades of isolated dysplasias was observed in 10 patients (47.6%) in Group II but in only 6 patients (8.2%) in Group I (P < 0.01). Conclusions. These findings suggest that various degrees of evolving biologically related lesions, such as dysplasia and carcinoma, can occur multicentrically in the same esophagus.