By co‐culturing regional lymph node B‐cells and HAT‐sensitive mutant cells obtained from RPMI‐1788 cells, no less than 20,000 Epstein‐Barr (EB)‐transformed colonies were obtained from 32 patients with gastric cancer. From B‐cell cultures generating antibodies reactive with gastric cancer tissues as well as cultured gastric cancer cells, two EB‐transformed cell clones termed C418–59 and C1218–39 were isolated. Both of them produced human IgM‐class antibodies, termed Mab418–59 and Mab 1218–39, respectively. Both antibodies reacted with an antigen with a molecular weight of 45 kd existing in gastric cancer MKN‐45, MKN‐1, and Kato‐III cells, and also with all of 4 adenocarcinomas of the stomach in paraffin sections. The antigen recognized by both antibodies was identified as a kind of cytoskeletal protein, cytokeratin 18, In this study, it was confirmed that B‐cell clones generating autoantibodies against cytokeratin 18 were present in some patients with gastric cancer.

SLex-CMPul was found to have the potential to target drugs to the inflammatory lesion.

Sialyl Lewis X (SLex), an E-selectin ligand, was conjugated with carboxymethylpullulan (CMPul) and the disposition characteristics of this conjugate after intravenous administration were investigated using mice with ear edema. The concentration of 3H-labeled SLex-CMPul in the spleen was significantly high. When CMPul was modified with a saccharide unable to bind to E-selectin, this splenic accumulation was not observed. The uptake of radiolabeled SLex-CMPul by the spleen was completely inhibited by a 100-fold molar of cold SLex-CMPul but not by a sialyl N-acetyllactosamine-CMPul conjugate (SLN-CMPul). Microautoradiography analyses revealed that SLex-CMPul accumulated in the marginal zone of the spleen.