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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are different frequencies in the immunological phenotypes of malignant lymphomas in Tohoku and Kyushu districts of Japan. In the Tohoku district, the northern area of Honshu, B-cell lymphomas are more preponderant than T-cell lymphomas. This is just the reverse on the islands of Kyushu and Shikoku. Histologically diffuse lymphoma of large cell type, formerly termed reticulum cell sarcoma or histiocytic lymphoma, was the most frequent (48%) among B-cell lymphomas. It is characteristic of B-cell lymphoma that immunoglobulin is produced in either or both the cellular surface and cytoplasm. Cytoplasmic IgM in lymphoma cells was mainly detected by an electron microscopic enzyme-labeled method. Cytoplasmic-Ig was present both in the nuclear membrane and endoplasmic reticulum. This technique is particularly useful in medium-sized lymphoma cells because of the scanty cytoplasmic rim making light microscopic evaluation difficult. Histological transition from follicular to diffuse pattern is characterized by a change of cellular arrangement from labyrinth-like cellular connections in follicular lymphoma to more simple connections in diffuse lymphoma. The transition is also supported by the fact that a higher deoxyribonucleic acid content is observed in large cells than medium-sized cells in follicular lymphoma. The data also supports the hypothesis that a diffuse lymphoma evolved from follicular lymphoma mainly occurs in cases of large cell lymphomas.
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PMID:Nodal B-cell lymphomas in Japan--particularly in Tohoku district. 660 58

Twenty-two cases of primary gastric non-Hodgkin's lymphoma, which occurred over a 20-year period, were reviewed. Eighteen tumors were studied using an immunoperoxidase method, and the presence of intracytoplasmic monoclonal immunoglobulin (Ig) in nine (50%) suggested a B-cell origin. Four tumors (22%) contained intracytoplasmic muramidase (lysozyme), suggesting a true histiocytic origin. Five tumors (28%) did not contain immunoglobulin or muramidase. The muramidase-positive "true histiocytic lymphoma" could not be differentiated from histiocytic lymphoma of lymphocytic origin using light microscopic examination alone. The patients with B-cell lymphoma survived significantly longer than patients in the other two groups. The differentiation between true histiocytic lymphoma and other conditions is discussed.
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PMID:A combined morphologic and immunologic approach to the diagnosis of gastrointestinal lymphomas: I. Malignant lymphoma of the stomach (a clinicopathologic study of 22 cases). 703 47

Primary lymphoma of bone is a B-cell lymphoma of bone previously called reticulum cell sarcoma. In our patient MRI of this tumor was remarkable with a low signal on both T1 and T2 weighted sequences. This MRI appearance is different from the appearance of other small round cell tumors and may be characteristic of primary lymphoma of bone.
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PMID:[Parker's and Jackson's sarcoma. Contribution of MRI]. 770 34

The spontaneously arising B-cell lymphoma (la+ reticulum cell sarcoma, RCS) in SJL/J mice has been shown to depend on host CD4 T cells for proliferation and growth. Treatment of mice with CD4 monoclonal antibody (mAb) prior to or after inoculation of a lethal dose of RCS tumor cells inhibits cell growth and the mice survive. The mechanism of tumor growth inhibition was studied by adoptively transferring cells from CD4 mAb treated tumor bearers into naive syngeneic mice. The recipient mice developed tumors and died. Tumor growth was dependent on the concentration of the adoptively transferred tumor cells. These results suggested that a state of tumor dormancy was established in the treated mice. Tumor dormancy was long lasting, as cells transferred as late as 11 weeks after the initial RCS inoculation still developed tumors in the recipient. The maintenance of dormancy was not due to failure of the recipient mice to mount an anti-tumor response or to the induction of suppressor cells. These results suggest that in the absence of CD4 cells, the RCS tumor remains dormant and this state of dormancy persists for long periods after total recovery of the CD4 cell subpopulation. Thus, it appears that RCS proliferation and growth is dependent on host CD4 cells but maintenance is under the influence of other cells or factors. Further characterization of this tumor dormant system and its regulation by the host may reveal novel mechanisms of tumor dormancy.
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PMID:Regulation of B-cell lymphoma growth in syngeneic SJL/J mice. establishment of tumor dormancy following administration of anti-CD4 monoclonal antibody into tumor-bearing mice. 823 Dec 49

True histiocytic lymphoma (THL) and malignant histiocytosis (MH) have been defined by clinical and histologic findings and enzyme histochemistry. We reviewed cases previously diagnosed as cutaneous histiocytic lymphoma (HL) and MH with cutaneous lesions. These cases had been classified as "histiocytic" on the basis of previous enzyme histochemistry profiles of frozen tissue. Cutaneous tumor cells were reevaluated using a panel of immunohistochemical stains in formalin-fixed, paraffin-embedded tissue in correlation with histopathologic examination. The antibodies used in this study were directed against CD45 (leukocyte common antigen [LCA]), CD20 (L26) for B cells, CD3 and CD45RO (UCHL-1) for T cells, CD68 (KP-1) and lysozyme for histiocytes, as well as CD30 (BerH2) for Ki-1 positive cells. On re-evaluation, the seven cases originally classified as HL were reclassified as one case of THL with neoplastic cells positive for CD68 (KP-1) and lysozyme, two cases with immunohistochemical features of Ki-l lymphoma (including one of T-cell lineage), three cases of T-cell lymphoma, and one case of B-cell lymphoma, all associated with variable degrees of reactive histiocytosis. The four cases originally classified as MH were reclassified as two cases of MH and two cases of uncertain lineage. Although rare, histiocytic malignancies do exist. However, the diagnosis of histiocytic malignancy should be made only after careful correlation of atypical tumor cells in histopathologic sections and sections stained immunohistochemically. Erroneous classification of reactive histiocytes as neoplastic histiocytes using only enzyme histochemistry in frozen sections is a pitfall to be avoided.
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PMID:Cutaneous histiocytic malignancy. Immunohistochemical re-examination of cases previously diagnosed as cutaneous "histiocytic lymphoma" and "malignant histiocytosis". 832 Mar 54

The MHC class II I-A(s) positive B cell lymphomas reticulum cell sarcoma (RCS) that arise in > 90% of SJL mice by the age of 12 months have superantigen-like stimulating properties. In the present study, therefore, RCS cell lines were examined for abnormal expression of endogenous mouse mammary tumor virus (MMTV) proviruses. Extraordinarily high expression of a 1.8 kb mRNA hybridizing with the long terminal repeat (LTR) of MMTV was found in both primary lymphomas and in vitro RCS lines, but not in an SJL B cell lymphoma, NJ101, that does not stimulate syngeneic T cells, or in LPS activated SJL B cells. A cDNA was cloned from cRCS-2 and sequenced. A 31mer oligonucleotide probe, prepared based on the unique C-terminal sequence of this RCS-Mtv LTR, detected the 1.8 kb mRNA in all RCS lymphomas, while a similar probe for the C-terminal sequence of Mtv-8 LTR hybridized with the larger mRNA present in normal B cells and in NJ101. Preincubation with 19mer antisense S-oligonucleotides, prepared based on the sequences of the first two potential translation initiation sites common to both Mtv-8 and the RCS-Mtv LTR, significantly reduced the ability of RCS cells to stimulate syngeneic T cells. Moreover, transfection of NJ101 cells with the cloned RCS-MMTV cDNA conferred V beta 16 T cell stimulating properties on to these cells. It is concluded that expression of the product of this MMTV-LTR mRNA provides RCS with the strong T cell stimulating properties that it needs for its growth. These results thus identify a novel oncogenic property of MMTV-LTR.
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PMID:Linkage of superantigen-like stimulation of syngeneic T cells in a mouse model of follicular center B cell lymphoma to transcription of endogenous mammary tumor virus. 838 94

Introduction and expression of the proto-oncogene bcl-2 (B-cell lymphoma/leukemia 2) has been shown to extend the survival of certain hematopoietic cell lines after growth factor deprivation, by blocking apoptosis or programmed cell death. We investigated the effect of bcl-2 expression on cellular sensitivity to lysis by tumor necrosis factor (TNF), a cytokine capable of inducing apoptosis in several tumor cell lines. Introduction of the human bcl-2 gene in the highly TNF-sensitive L929 mouse fibrosarcoma cell line did not result in altered TNF sensitivity. Likewise, NIH3T3 and REF cells, which are resistant to TNF cytotoxicity but become TNF sensitive upon cotreatment with actinomycin D or upon expression of the adenovirus E1A gene, did not show altered TNF sensitivity upon bcl-2 transfection. Despite constitutive expression of the endogenous bcl-2 gene, human MCF7 breast carcinoma cells, as well as HL60 promyelocytic leukemia and U937 histiocytic lymphoma cell lines were found to be TNF sensitive. bcl-2-overexpressing derivatives of these cell lines did not acquire reduced TNF sensitivity and still exhibited the characteristic pattern of internucleosomal DNA fragmentation of TNF-induced apoptosis. Moreover, bcl-2 expression in the interleukin 3 (IL-3)-dependent myeloid cell line 32D protected these cells from apoptosis resulting from growth factor deprivation, but not from apoptosis induced by TNF. These data clearly establish the absence of a correlation between bcl-2 gene expression and cellular sensitivity to TNF-induced cell lysis. These findings are discussed in the context of the hypothesis of different pathways for induction of apoptosis, only some of which are affected by bcl-2 expression.
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PMID:Effect of bcl-2 proto-oncogene expression on cellular sensitivity to tumor necrosis factor-mediated cytotoxicity. 845 35

True histiocytic lymphoma is considered a rare entity, and its diagnosis requires the concordance of morphological, immunophenotypic, and molecular findings. The association of malignant lymphoma with tumors in the monocyte-macrophage system has rarely been described. We present a case of mucosa-associated lymphoid tissue (MALT)-type low-grade B-cell lymphoma of the stomach, contiguous to a large tumoral mass that fulfills the morphological criteria (large cells with abundant pale cytoplasm and lobulated or kidney-shaped nuclei) and immunophenotypical features (human leukocyte antigen-DR locus, CD68, S-100, lysozyme immunoreactivity, and negative B- and T-cell markers) required for the diagnosis of histiocytic lymphoma. The patient remains in complete remission 18 months after surgery. The association of low grade-malignant lymphoma with tumors of monocyte-macrophage system cells is an exceedingly rare phenomenon. Whether these tumors are directly related or occur due to pure chance requires the identification of new cases and further study.
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PMID:True histiocytic lymphoma of the stomach associated with low-grade B-cell mucosa-associated lymphoid tissue (MALT)-type lymphoma. 889 46

Vi bacterial polysaccharide is a homopolymer of alpha 1-4 N-acetyl polygalacturonic acid with variable O-acetylation at position C-3 and forms a capsule around many bacteria. It has been referred to as the virulence factor of Salmonella typhi and is also a candidate vaccine against typhoid fever. The present study reports the interaction of this polysaccharide with murine mononuclear phagocytes and lymphocytes, and with human monocytes. Vi showed a dose-dependent binding to the murine monocyte cell lines WEHI-274.1 and J774. This binding was abrogated if the polysaccharide was deacetylated, suggesting involvement of acetyl groups in this interaction. Vi also bound to the murine B-cell lymphoma line A20, to peritoneal exudate cells and to a lesser degree to spleen cells and thymocytes from BALB/c mice. The polysaccharide also interacted with the human histiocytic lymphoma line U937 but not with the human monocyte cell line THP-1. Stimulation with Vi led to up-regulation of surface major histocompatibility complex (MHC) class II expression on A20 cells. Immunoprecipitation of Vi-bound molecules from cell surface biotinylated A20 and WEHI-274.1 revealed two bands with MW of about 32,000 and 36,000. The study demonstrates that Vi capsular polysaccharide can interact with mononuclear phagocytes and lymphocytes through specific cell surface molecules and modulate MHC class II expression.
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PMID:Identification of specific recognition molecules on murine mononuclear phagocytes and B lymphocytes for Vi capsular polysaccharide: modulation of MHC class II expression on stimulation with the polysaccharide. 937 Sep 37

This is the second report of histiocyte-rich B-cell lymphoma and the first case analyzed by flow cytometry and cytogenetic study. The immunophenotype determined by flow cytometry was that of a B-cell antigen-positive, surface immunoglobulin-negative B-cell lymphoma with 79% CD11c positive histiocytes. The lymphoid cells were composed of 76% neoplastic B-cells and 24% reactive T-cells. Immunohistochemical staining showed large numbers of histiocytes positive for CD68 and lysozyme in the lymph node and the bone marrow. Neoplastic lymphoid cells were positive for CD20, CD45, CD74 and CDw75. The monoclonality of the tumor cells was established by the evidence of rearrangements of the heavy chain and kappa light chain genes and a complex clonal cytogenetic abnormalities including t(8;14)(q11;q32). The tumor cells were large, pleomorphic lymphoid cells and showed no features resembling those of the L/H cells of Hodgkin's disease as previously reported. The rapidly progressive clinical course in the present case is consistent with the clinical features shown in the original study. The histiocytic component in this tumor is presumably recruited by a lymphokine with the nature of a growth factor from the tumor cells that may also be responsible for the rapid proliferation of the tumor cells and the aggressive clinical course. This entity merits special recognition because it leads to a predictable poor prognosis and because of its potential of being misdiagnosed as true histiocytic lymphoma.
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PMID:Histiocyte-rich B-cell lymphoma. 938 44


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