Background. Spontaneous regression of non‐Hodgkin's lymphoma, occasionally reported in low grade groups, is a rare phenomenon in high grade groups. Clonal proliferation has not been confirmed in the majority of reported cases. In this woman, age 58 years, who had been diagnosed as having high grade immunoblastic lymphoma after excision of a single cervical lymph node, the remaining bilateral cervical, inguinal, and axillary adenopathy regressed completely without any cytotoxic treatments 22 days after biopsy. At the time of this writing, the patient has been free of disease for 24 months. Methods. Clonality of the lymphoproliferation in the case was examined by immunohistochemistry and poly‐merase chain reaction (PCR) amplification using paraffin embedded biopsy material. Possible implications of Epstein‐Barr virus in the pathogenesis of this process was examined also by PCR amplification and in situ hybridization. Results. The proliferating lymphoid cells showed restricted expression of immunoglobulin (Ig) light chain and amplification of clonally rearranged V‐D‐J regions of Ig heavy chain gene. Epstein‐Barr virus did not appear to be involved in the process. Conclusion. The present study shows that spontaneous complete regression of clonal lymphoproliferation that is morphologically a high grade lymphoma can occur.

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Analysis of macromolecular fraction of platelet release products (PRPr) was undertaken after we observed that pretreatment of human neutrophils with macromolecules (greater than 10(5) daltons) involved in PRPr enhanced phagocytosis of IgG-sensitized sheep red blood cells (IgG-SRBC). Sephadex G-200 gel filtration of PRPr revealed two macromolecular activators and two suppressors of neutrophilic phagocytosis of IgG-SRBC: MAPP(s), macromolecular activator(s) of phagocytosis from platelets; MSPP(s) macromolecular suppressor(s) of phagocytosis from platelets. The estimated molecular weights of the respective MAPPs were 100 kdaltons to 140 kdaltons (kd) (s-MAPP) and 200 kd to 290 kd (I-MAPP) and those of the respective MSPPs were 60 kd to 100 kd (s-MSPP) and 400 kd to 500 kd (I-MSPP). It is suggested that an I-MAPP molecule has at least an s-MAPP molecule as a functional unit and that MAPPs and larger MSPP (I-MSPP) might be glycoproteins, while smaller MSPP (s-MSPP) seems to contain neither carbohydrates nor lipids. As far as the effects of serum and plasma on phagocytosis of IgG-SRBC by neutrophils are concerned, the serum gave twice as much phagocytic activity as the plasma. Substantial MAPP-like activities were observed in the serum and MSPP-like activities were observed in both the serum and plasma.

Substantial amounts of macromolecular activators of phagocytosis from platelets (MAPPs) were released in response to exposure of platelets to the specific agonists thrombin and collagen and to calcium ionophore A23187. Centrifugation of the platelets in culture medium also resulted in a release of MAPPs, but not when the platelets were frozen and thawed prior to centrifugation. In an experiment using outdated platelet concentrates, larger and smaller MAPPs (1-MAPP and s-MAPP, respectively) were purified from the thrombin stimulated supernatant (PRPr-plasma) by sequential steps of ammonium sulfate precipitation, delipidation with ethylacetate, ConA-Sepharose affinity chromatography, MONO Q anion exchange chromatography, and Superose 12 gel filtration. This procedure yielded 59,500-fold and 63,600-fold purified 1-MAPP (0.95 mg) and s-MAPP (0.41 mg), respectively, from 1,320 ml PRPr-plasma containing 84,500 mg protein. By gradient polyacrylamide gel electrophoresis the respective molecular weights (MW) of 1-MAPP and s-MAPP were 290-320 kd and 140-160 kd; isoelectric points were 5.6 and 4.6. Both MAPPs activated neutrophil phagocytosis of IgG-SRBC at concentrations in the range of 1 pM-100 nM. Indirect enzyme-linked immunosorbent assay (ELISA) and comparisons of the concentrations required for phagocytosis activation suggested that the MAPPs were not derived from fibronectin.

This report presents a rare case of a patient with gastric cancer whose clinical course with the development of tumor from early cancer type IIc to advanced cancer of linitis plastica was observed for 9.5 years. The cancer remained in early stage for 3 years and 8 months after the patient’s first endoscopy. At 5 years and 10 months after initial endoscopy, the lesion progressed to advanced cancer, and after 6 years and 7 months sclerotic changes in the gastric wall were detected at the lesion site. After 9 years, advanced gastric cancer of linitis plastica was present throughout the stomach. The initial stage of linitis plastica is considered to be early gastric cancer type IIc with histologically undifferentiated cancer cells. It is widely accepted that a period of 6–8 years is required for this type of cancer to develop from carcinogenesis to completion of lesions. The present case is valuable in that development from early gastric cancer type IIc to linitis plastica during approximately 10 years of follow up was clinically observed, and will contribute to knowledge of the natural history of gastric cancer.