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Over-expression of cellular protooncogenes has been proposed to function in the initiation and maintenance of malignancies. In order to distinguish malignant lymphoma from reactive proliferative diseases, we surveyed the expression levels of three protooncogenes(c-myc, c-fos and c-myb) in malignant lymphoma and reactive proliferative diseases. An increased level of c-myc or c-fos mRNA was observed in one case, respectively, out of three malignant lymphomata. The other cases exhibited no enhancement in protooncogenes. These oncogenes are critically regulated during differentiation, but the half-life of c-myc mRNA was very short, and the level of the mRNA decreased to the initial level very quickly. Thus, the high level of the expression of these oncogenes may not always be maintained in all malignant cells. We then examined the level of mRNA for poly(ADP-ribose) synthetase in those cases. An enhanced expression for the synthetase gene was observed in all five malignant lymphomata tested, but no increase in the level of the mRNA was observed in any reactive proliferative cases or normal lymph nodes. These results suggest that enhanced expression of poly(ADP-ribose) synthetase gene seems to be a common characteristic of protopathic malignant lymphoma. By using the characteristics of malignant lymphoma, the level of mRNA for the synthetase may be applicable for differential diagnosis of malignant lymphoma from several pathologically indistinguishable diseases.

A scanning acoustic microscope (SAM) calculates the speed of sound (SOS) through tissues and plots the data on the screen to form images. Hard tissues result in greater SOS; based on these differences in tissue properties regarding SOS, SAM can provide data on tissue elasticity. The present study evaluated whether tissue modifications, such as formalin fixation, periodic acid-Schiff (PAS) reactions and protein degradation, changed the acoustic properties of the tissues and whether SAM could be a useful tool for following chemical changes in sections. The fixation process was observable by the increased SOS. During the PAS reaction, the glycosylation of tissues was characterized by an increased SOS. Mucous or glycogen distribution was visualized and was found to be statistically comparable among lesions and states. Protease digestion by pepsin led to a decreased SOS. Tissue sensitivity to proteases varied due to the stage, cause and duration of inflammation or ageing. Changes in acoustic properties were more sensitive than those in optical histology. SAM facilitates the visualisation of the time course or distribution of chemical modifications in tissue sections, thus aiding their comparison among tissues. SAM may be an effective tool for studying changes such as protein cross-linkage, tissue repair and ageing.

± standard error; 545.2 ± ± ± ± 18.6 U/mL) rather than with lymphoma type ATL (327.62 ± ± ± ± 94.85 U/mL). In four patients whose sera were stored and examined longitudinally, the levels decreased following the response to chemotherapy but not in patients with chemotherapy resistance. Thus, our results imply that sCD30 levels may be another useful marker for the activity and aggressiveness of ATL. A dult T-cell leukemia/lymphoma (ATL) is a highly aggressive leukemia/ lymphoma which was first proposed as a new disease entity in 1977.(1,2) Subsequently, Shimoyama and the Lymphoma Study Group classified four clinical subtypes: acute type, lymphoma-type, chronic type, and smoldering type.(3) The long clinical latency and low incidence of ATL indicate that some genetic changes are involved in the malignant transformation and monoclonal expansion of human T-cell leukemia virus type 1 (HTLV-1)-infected cells. Monoclonal proliferation of HTLV-1-infected cells is observed in some virus carriers, who are considered to be the high risk group for development of ATL.(4) Constitutive activation of STAT proteins as well as the functional impairment and stabilization of p53 protein found in the peripheral blood mononuclear cells (PBMC) of ATL patients are supposed to be one base for ATL development.(5,6) However, it remains to be studied what the additional factors are that allow the monoclonal proliferation of ATL cells.CD30, a 120 kDa type I cell surface glycoprotein, is a member of the tumor necrosis factor receptor (TNFR) superfamily. The soluble form (sCD30) is produced by metalloprotease cleavage of the juxta-membrane region releasing as an extracellular region of 85 kDa protein. (7,8) CD30 is normally expressed by activated, but not by resting, B or T cells and also expressed on Hodgkin and Reed-Sternberg (H-RS) cells, anaplastic large cell lymphoma (ALCL) and ATL cells. (9) CD30 regulates their proliferation, differentiation and apoptotic cell death, depending on the cell type and developmental stage.(10) CD30 + cells release sCD30 in vitro and in vivo and it cannot be detected in the sera of healthy donors. (8,11) CD30 ligand (CD30L, CD153) is a type II transmembrane protein and a member of the TNF ligand superfamily.(12) It is expressed on resting B and activated T cells in addition to monocytes, granulocytes and natural killer cells.(7) Its pleiotropic biologic activities were reported, including its proliferative effect and CD30L-induced cell death. In ALCL and Hodgkin's disease (HD), elevated levels of sCD30 in the sera of patients are correlated with a poor prognosis, perhaps because a high level of sCD30 reflects a high tumor burden or because sCD30 blocks the biologic effects of CD30L.(15-17) Moreover, sCD30 is detectable in the sera of ATL patients. (11) In this study, we investigated the clinical significance of the membrane type of CD30 (mCD30) expression and serum sCD30 levels in ATL. Our results revealed the relationship between sCD30 levels and other serum markers of ATL.

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