An important disease entity distinct from cutaneous T-cell lymphoma (CTCL) in Japan is adult T-cell leukemia/lymphoma (ATL), which usually shows the same phenotype as CTCL, i.e., a helper/inducer T-cell phenotype (CD4+CD8-), and usually involves the skin. Clinically, both CTCL and ATL are heterogeneous in nature. In this study, we demonstrated differences between CTCL and ATL in terms of clinical and immunopathologic cell surface features. In patients with ATL, the predominant clinical findings were peripheral lymph node involvement, skin lesions, hepatosplenomegaly, leukemic manifestations, and an aggressive course. In patients with CTCL, by contrast, only skin lesions predominated at the onset of the disease and a relatively good prognosis was demonstrated. Phenotypic heterogeneity of ATL in the skin, i.e., CD4-CD8-, CD4+CD8-, and CD4-CD8+, was demonstrated. Expression of Leu8, CD7 (Leu9), and CD45RA (2H4) was high in both the skin-infiltrating ATL cells and peripheral blood and lymph node ATL cells compared with that in the skin-infiltrating CTCL cells. Expression of CD25 (IL-2R), CD71 (OKT9), HLA-DR, and HLA-DQ was higher in the skin-infiltrating ATL cells than in CTCL cells. Expression of CD29 (4B4) was high, and that of CD45RA (2H4) was low in both the skin-infiltrating ATL and CTCL cells compared with the peripheral blood and lymph node ATL cells. Expression of CD45RO (UCHL-1) was not significantly high in the skin-infiltrating CTCL cells compared with that in ATL cells. The most significant phenotypic difference between ATL cells and CTCL cells was the expression of Leu8 (lymph node homing receptor), CD7 and CD25 antigens on the cell surface, and the main phenotypic difference between skin-infiltrating ATL and CTCL cells and peripheral blood and lymph node ATL cells was the expression of CD29 and CD45RA. These findings confirm that the difference in antigen expression on the cell surface might reflect the clinical features of ATL and CTCL, and suggest that the predominant phenotype of peripheral blood and lymph node ATL cells is that of naive, relatively immature or activated T-cells, and that CTCL cells are previously activated (memory) T-cells. In other words, CTCL cells do not share the same origin as ATL cells. These observations support the concept that ATL is a disease distinct from CTCL.

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A case of cutaneous B-cell lymphoma successfully treated by MACOP-B therapy is described. The patient was a 43-year-old man with reddish tumors measuring 3 to 7 cm in diameter on the right cheek and the post-auricles. Histopathologically, massive infiltrations of medium-sized atypical lymphoid cells were found in the reticular dermis and subcutis. A clear zone beneath the epidermis was also detected. The atypical lymphoid cells were positive for CD19, CD20, CD22 and HLA-DR but negative for CD3, CD4, CD5, CD10, CD43, CD45RO and CDw75. The patient was treated successfully with the MACOP-B protocol from March of 1990 to May of 1990. Since April of 1990, he has been free of disease.

A 65‐year‐old man was seen at the Ushioda Hospital in Au‐gust 1989, because of a 1‐month history of a tumor on the scalp. The tumor was excised and the diagnosis was malig‐nant lymphoma. The patient was then referred to our de‐partment in September 1989. Several nut‐sized lymph nodes wvepa‐b and m‐fepa for 2 months. Since then, the patient has been free of disease up to the time of writing, July 1992, a period of 2.5 years. Biopsy samples taken from the tumor on the scalp showed a monomorphous infiltrate of large lymphoid cells throughout the entire dermis and subcutis, with a definite clear zone (Fig.1). A high‐power view showed diffuse large lymphoid cell infiltration. Numerous mitotic figures were also seen. The lymphoid cells had multilobated nuclei and distinct nucleoli (Fig. 2). Monoclonal antibodies such as Leui (CD5), Leu2a (CD8), Leu3a (CD4), Leu4 (CD3), MT‐1 (CD43), Leu14 (CD22), LN1 (CDw75), and Leu26 (CD20), and polyclonal antibodies such as anti‐kappa, anti‐lambda, anti‐IgG, anti‐lgA, anti‐IgM, and anti‐lgD were purchased from commercial sources. Optimal dilutions of the monoclonal antibodies and heteroantisera were assessed beforehand by titration on suitable tissue samples. The antigens recognized by the monoclonal anti‐bodies and heteroantisera were investigated by either the avidin‐biotin peroxidase complex (ABC) method on cryostat sections or the peroxidase‐antiperoxidase complex (PAP) method on paraffin sections, as described elsewhere.1 The immunologic properties of the infiltrating cells were determined using skin biopsied in August 1989, and October 1989. Large lymphoid cells, which formed the major popu‐lation of infiltrating cells, were positive for CD20, CD22, and HLA‐DR and negative for CD3, CD4, CD43, and CD45RO. From these findings the patient was diagnosed as hav‐ing primary cutaneous B‐cell lymphoma, diffuse large non‐cleaved cell type, as classified by the Working Formulation.2

Twenty-one patients with ATL were assessed. The predominant physical findings were lymph node and bone marrow involvement, skin involvement, hepatosplenomegaly and leukemic manifestations. The predominant histopathological findings in both skin and lymph node specimens were the diffuse medium-sized cell type and the diffuse mixed cell type. Some phenotypic discrepancy was found between the neoplastic cells in the peripheral blood, lymph nodes and skin of patients with ATL with respect to CD45RA and CD45RO, and CD7, CD29, CD25 and HLA-DR. That is, the predominant neoplastic cell phenotype was the helper T-cell, which was CD3+, CD4+, CD7+, CD25+, CD45RA+ and HLA-DR+, and CD29- and CD45RO- in peripheral blood and lymph nodes, and CD3+, CD4+, CD7+, CD29+, CD45RO+ and HLA-DR+, and CD45RA- in the skin. In other words, we have described the phenotypic heterogeneity of ATL cells and demonstrated the heterogeneity of CD45R isoform expression on ATL cells in different organs--the skin, peripheral blood and lymph nodes--of the same patient.