The incidences of chromosome abnormalities involving the bands including the loci of the immunoglobulin genes and the T cell receptor genes were studied in 54B lymphomas and 44T lymphomas. Breaks in band 14q32, the site of the immunoglobulin heavy chain genes, were more frequent in B lymphoma (37%) than in T lymphoma (16%) (p<0.05). Breaks in band 14q11, where the T cell receptor alpha chain gene resides, were found in only T lymphoma (p<0.05). All the other bands, i.e. 2p12, 7p15, 7q35, 11q23, and 22q11, where immunoglobulin light chain genes, T cell receptor beta and gamma chain genes, and T3-complex genes reside, however, were involved much less frequently. We conclude that chromosome aberrations may be detectable on light microscopy only in part of the cases which undergo molecular rearrangements of immunoglobulin or T cell receptor genes in malignant lymphoma.

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We analyzed 176 cases of lymphoproliferative disorders by molecular genetical approach in conjunction with phenotypical examinations.
Tγ/LGL proliferative disorder has been revealed to consist of at least two groups; one is CD3(+), TcR gene rearranged group which is considered as T-cell lineage, the other is CD3(-), TcR gene germ line one which is cosidered as “NK cell” origin.
Many AILD cases with some atypic cells (AILD-T) have rearranged TcR genes and are supposed to be related to T-cell lymphoma. Though we examined the gene expression of IL-4, 5 to clarify the clinical features of AILD, we failed to observe distinct participation of IL-4, 5.
We frequently observed dual genotype (simultaneous rearralgements of Ig and TcR genes) cases in CD20(+) c-ALL and stage II T-ALL/LBL. It has been supposed that common recombinase and accessibility for it are activated at such specific stages of lymphocyte maturation.
In addition, we analyzed precise biallelic IgH gene structure by examining 5'D region of IgH, and observed difference of rearrangement patterns which are specific for diseases or maturational stage.

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Five T cell lymphoma cases, which changed histological pictures between successive biopsies, were studied by Southern blot method with TCR β gene probe. Three cases showed disease progression from low grade to high grade peripheral T cell lymphoma. Two cases showed the histological changes between low grade lesions. Four of 5 cases showed clonal rearrangements of TCR β genes and both successive biopsied samples of each case showed the rearrangement bands of the same size. These results suggested that a single clone could make different histological pictures, which might be attributed to the change of lymphokine synthesis and secretion.

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In order to improve postoperative prognosis of gastric cancer patients we have performed preoperative endoscopic intratumoral injection of various biological response modifiers. In the present study we have investigated the distribution of intratumorally injected PSK by immunohistochemical methods using anti PSK antibody and various antibodies. PSK-containing cells were detected in the tumor tissues and marginal zone of the follicles in regional lymph nodes. Intratumorally administrated PSK appeared to be phagocytized by the histiocytes and give them character as antigen presenting cells. It is expected that these cells play a major role in augmenting immune responses of gastric cancer patients.

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By examination of both protein markers (cell-surface immunoglobulin) and DNA markers (immunoglobulin-gene rearrangements), “biclonal B-cell lymphoma” was proposed. However, the further investigation revealed that genotypic and phenotypic biclonal B cell lymphomas were derived from a single progenitor cell. We present here a case of true biclonal B-cell lymphoma, in which change in clones occurred accompanied by the morphologic transformation of follicular lymphoma to diffuse lymphoma.
A 59-year-old Japanese male was found to have right-sided cervical lymphadenopathy and tonsillar swelling. In April, 1986, a cervical lymph node biopsy was performed and was interpreted as showing malignant lymphoma, follicular mixed small cleaved cell and large cell. The lymphoma cells expressed monoclonal surface immunoglobulins and they had a karyotype of 47, XY, +12, t(3;14) (q27;q32). He was diagnosed as having the clinical stage II disease and he received treatment of irradiation. After a remission of 18 months duration, again he noticed lymph node swelling on the both-sided cervical region, and was readmitted to our hospital because of increasing difficulty in breathing. In February, 1988, he underwent an emergency tracheotomy and the second lymph node biopsy, which revealed malignant lymphoma, diffuse large cell. The lymphoma cells did not express any surface immunoglobulin. However, they were shown to be of B cell origin by the positive reaction to monoclonal antibodies of CD19(B4), CD20(B1), and CD21(B2). And the modal karyotype was 48, XY, +21, t(2;7) (q31;q34), +der(7) t(2;7) (q31;q34). The patient was treated with a variety of combination chemotherapies, initially with VEPA followed by intermediate dose of MTX combined with other cytotoxic drugs. But the tumor was refractory to these treatments, and his condition rapidly deteriorated and he died of respiratory insufficiency in September, 1988. Southern blot analysis of immunoglobulin heavy chain gene, using the JH region probe, indicated the differently rearranged configurations before and after the histologic transformation. Therefore, this is the first case of transformed follicular lymphoma in which the tumor clone changed.

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Three independent mouse monoclonal antibodies (mAbs) ID1 (IgG3), ID2 and ID3 (IgM) were raised against whole cells of a surgically resected human interdigitating cell sarcoma (ICS). In immunoperoxidase staining, these mAbs strongly stained the cytoplasm of ICS neoplastic cells as well as interdigitating cells in normal lymphoid tissues. These mAbs also detected monocyte/macrophages and dendritic cells, although their staining was highly variable depending on tissue distribution of the cells. Additional immuno-histological and enzyme histochemical study revealed that the neoplastic cells of ICS had cytoplasmic acid phosphatase and membranous alkaline phosphatase activity, and also possessed S100beta protein, Ki-1 antigen, DAKO-macrophage antigen, and weak vimentin. Neither rearrangement of immunoglobulin heavy chain gene nor of T-cell receptor genes was detected in the DNA of ICS by Southern hybridization. These observations provide further confirmation of our previous finding (Nakamura et al. 1988) that the origin of ICS is interdigitating rather than lymphoid cell, and indicate that our mAbs could be useful as a cellular differentiation marker of interdigitating cells and for diagnosis of ICS.

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An autopsy case of discordant lymphoma comprising large cell B lymphoma and histiocytic sarcoma (true histiocytic lymphoma) was reported. A 70-year-old woman with large cell B lymphoma of 14 months duration developed fever, anemia, and jaundice. She died of gastric bleeding shortly after the initiation of chemotherapy. Autopsy findings revealed multiple nodular masses throughout the liver, lungs, bone marrow and paraaortic lymph nodes. These masses consisted of containing atypical histiocytes associating with common phagocytic figures, with immunohistochemical features of histiocytic sarcoma. The original large cell B lymphoma was still present in the right adrenal gland. Discordant lymphomas are those in which two distinct histological patterns occur in separate anatomic disease sites. This is the first reported case of histiocytic sarcoma arising in association with large B cell lymphoma. Sequential presence of histiocytic sarcoma seemed to be different mutation stages of the neoplastic B lymphocyte in the cell cycle of a single cell type.

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