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PubMed2000

[Non-Hodgkin lymphoma mimicking renal carcinoma: apropos of 1 case of follicular lymphoma].

Primary renal non-Hodgkin's lymphoma (NHL) is unusual, in contrast to the frequent renal involvement in disseminated NHL. We report a case of follicular lymphoma presenting initially as a renal mass. In the literature, twenty-seven similar cases have been described since 1980. The median age at diagnosis is 64 years with a male predominance. Clinical and radiological findings generally evoke renal carcinoma. Histologically, tumors are usually large B-cell lymphomas. The existence of renal non-Hodgkin lymphoma mimicking renal carcinoma must be recognized. Such lymphomas can either be primitive or be nodal with a renal presentation. Nephrectomy followed by chemotherapy permits long disease free survival.

Aged↗

PubMed2002

Injection of human primary effusion lymphoma cells or associated macrophages into severe combined immunodeficient mice causes murine lymphomas.

The pathogenesis of immunodeficiency-associated lymphoma is poorly understood. During the past several years, numerous lines of evidence implicating a multistep process of malignant transformation, also known as sequential pathogenesis, have emerged. Tumor-associated macrophage production of specific lymphostimulatory products has been demonstrated and hypothesized to be central to this process. While attempting to establish primary effusion lymphoma in severe combined immunodeficient (SCID) mice, we discovered a potential model of murine lymphomagenesis consistent with the sequential pathogenesis model. This pathogenesis-based model of lymphoma could significantly impact the current thinking about posttransplantation and other immunodeficiency-related lymphoproliferative disorders. Human primary effusion lymphoma-derived CD14+ cell-injected SCID mice developed aggressive murine large cell lymphomas. Tumor cell preparations containing CD14 cells or isolated CD14 cells induced lymphoma/lymphoproliferative diseases in 74% (20 of 27) of injected SCID mice. No tumors were induced by tumor-associated CD3 cells (0 of 4), normal human macrophages (0 of 13), or a murine macrophage cell line (0 of 10). Human macrophages were detected in tumor-bearing animals up to 6 months postinjection in association with the murine T-cell tumors but were not detected in controls or unaffected animals. These observations are consistent with the macrophage-initiated sequential pathogenesis model of disease (M. S. McGrath et al., Acquir. Immune Defic. Syndr., 8: 379-385, 1995; M. S. McGrath et al., Infectious Causes of Cancer: Targets for Intervention, pp. 231-242, Totowa, NJ: Humana Press, 2000).

Animals↗

PubMed2004

[Intraocular lymphoma--a clinical study of 14 patients with non-Hodgkin's lymphoma].

AIM: To evaluate the course of clinical picture of intraocular lymphoma, possibilities of examination of this disease and the association with general symptoms of the non-Hodgkin lymphoma (NHL) in patients with manifestations of uveitis. PATIENTS AND METHODS: A retrospective study in 14 patients followed in the period of 1996-2001 in the Center for Diagnostics and Therapy of Uveitis, Ocular Clinic of General Faculty Hospital and 1st Medical Faculty, Charles University in Prague. RESULTS: The group included 7 women and 7 men at the average age of 57.3 years (18-82) with clinical picture of uveitis. The time period from the first symptoms to the diagnosis of NHL was 5-38 months (mean, 14.6 month). In two patients the diagnosis of systemic NHL preceded ocular symptoms, in four other patients the diagnosis of systemic or central nervous system NHL (CNS NHL) was established during ocular manifestations of uveitis. Intraocular lymphoma was the only first manifestation of CNS NHL in six patients for the period of 9-34 months (mean, 15.2). Two patients have been so far affected by primary intraocular lymphoma (PIL) for 8 and 14 months respectively, and presently do not display any signs of systemic or CNS NHL. Clinical signs of intraocular inflammation of both eyes were encountered in 71.4% of patients. Vitritis (85.7%) and tumor infiltration of retina (65.3%) were the most frequent manifestations of NHL. Intraocular NHL was diagnosed on the basis of cytological examination of samples of intraocular fluids in 8 patients (57.1%). In four patients radiotherapy was applied onto 5 eyes and in 5 patients radiotherapy of CNS was used. Nine patients were treated with chemotherapy. 50% of patients died until the end of 2001, the survival from the establishment of diagnosis was 20.6 months on the average. CONCLUSIONS: Intraocular lymphoma should be considered as the eye and life-threatening disease. Cytological examination of intraocular fluids in patients with uveitis who do not respond to the therapy with steroids in the usual way may give more precision and shorten the establishment of diagnosis in this masquerade syndrome. Early diagnosis and therapy may improve the prognosis of NHL.

Adolescent↗

PubMed1991

Interleukin-9 expression in human malignant lymphomas: unique association with Hodgkin's disease and large cell anaplastic lymphoma.

To test the possibility that interleukin-9 (IL-9), the human homologue of the mouse T-cell growth factor P40, may be involved in the pathogenesis of human lymphomas, we examined IL-9 expression in a variety of tumors both by Northern blot analysis and by in situ hybridization. Of 18 B-cell non-Hodgkin's lymphomas and 11 peripheral T-cell lymphomas, none expressed IL-9 message. By contrast, IL-9 message was found in two of six cases of large cell anaplastic lymphoma (LCAL) and in 6 of 13 cases of Hodgkin's disease (HD). In HD the strongest signals were observed in Hodgkin (H) and Sternberg-Reed (SR) cells, but IL-9 mRNA was also detected in small lymphocytic cells. A search for IL-9 message in a panel of 20 cell lines derived both from hematopoietic and nonhematopoietic tumors confirmed the unique association of IL-9 expression with HD and LCAL in as much as the only two cell lines with IL-9 message were derived from cases of HD and LCAL. These results suggest that IL-9 is not involved as an autocrine growth factor in the pathogenesis of most B- and T-cell lymphomas, but that it may play a role in HD and LCAL.

Blotting, Northern↗

PubMed1986

Diffuse aggressive lymphomas: a curable subset of non-Hodgkin's lymphomas.

The diffuse aggressive lymphomas are a major group of non-Hodgkin's lymphomas characterized by diffuse disease, in most cases, and a rapidly progressive clinical course. Until recently, the disease was fatal. Over the last 10 years, use of intermittent high-dose combination chemotherapy with non-cross-resistant drugs has significantly increased the survival time for patients with both local and advanced disease. For those with advanced disease, the most recent studies show complete response rates of 85%, complete-response relapse rates of 10%, and a 73% rate of survival for more than 3 to 5 years. The role of radiation therapy is also important, particularly in the early stages of disease. Salvage treatment with single-agent chemotherapy has achieved often impressive, but brief, responses usually of less than 1 year. Not all patients can tolerate these intensive regimens, however, and new avenues of therapy are being investigated. Various types of biologic response modifiers have been tried in patients who have been heavily pretreated. Monoclonal antibodies initially produced responses in patients with low or intermediate grade tumors, but overall results are still disappointing. Recent trials with interferons show promise especially in patients with low-grade, indolent B cell lymphomas and cutaneous T cell lymphoma. Because antitumor effects are generally of short duration, however, there is probably only a minimal role for biologic therapy in patients with aggressive lymphomas.

Antibodies, Monoclonal↗

PubMed1989

[Malignant lymphomas (non-Hodgkin's lymphomas and Hodgkin's disease) associated with infection by the human immunodeficiency virus. Study of 9 cases].

Six cases of non-Hodgkin's lymphoma and three of Hodgkin's disease in patients carrying antibodies against human immunodeficiency virus are reported. Mean age was 30.6 years (SD: 6). From the patients with non-Hodgkin's lymphoma, three were homosexual and three were parenteral drug users. The three patients with Hodgkin's disease were parenteral drug users. The primary features of the patients with non-Hodgkin's lymphoma were: degree of malignity intermediate (three patients) or high (three patients), initial extralymphatic involvement (five patients) and advanced stages (IIIA one patient, and IVB four patients). In turn, the patients with Hodgkin's disease presented the following histopathologic varieties: mixed cellularity (two cases) and lymphocytic depletion (one case); advanced stage (III two cases and IV one case) and B symptoms. We wish to emphasize the necessity of determining the existence of antibodies against human immunodeficiency virus in all patients with Hodgkin's disease or non-Hodgkin's lymphomas with high degree of malignity and extralymphatic involvement. In patients with antibodies against the human immunodeficiency virus who present a marked impairment of general condition and/or changes in the clinical features of their adenopathies, the development of a lymphoma must be ruled out.

Acquired Immunodeficiency Syndrome↗

PubMed1988

Production of transforming growth factor-beta activity by Ki-1 positive lymphoma cells and analysis of its role in the regulation of Ki-1 positive lymphoma growth.

The growth of activated human T lymphocytes in response to interleukin-2 (IL-2) is suppressed by transforming growth factor-beta (TGF-beta). This study presents data that show a diminished response of two human lymphoma cell lines to physiologic regulation by TGF-beta. Cell line L-428 was derived from the malignant pleural effusion of a patient with far advanced nodular sclerosing Hodgkin's disease and has been shown to have clonal gene rearrangements characteristic of both B and T lymphocytes. Cell line Mac-1 was derived from the blood of a patient with clinically indolent cutaneous T-cell lymphoma. Both cell lines express the Hodgkin's disease associated antigen, Ki-1. These Ki-1 positive lymphomas are shown to secrete TGF-beta into serum-free culture media. The addition of picogram quantities of exogenous TGF-beta to cell cultures of indolent Ki-1 lymphoma (Mac-1) suppresses IL-2-dependent mitosis; however, the suppression is less than 45%. This suppression correlates with a decrease in the number of IL-2 receptors. No inhibition of Ki-1 positive Hodgkin's cells (L-428) was observed, and proliferation dependent on polyclonal IL-2 was either not affected or was slightly potentiated by TGF-beta. Receptor analysis indicates the absence of IL-2 and TGF-beta receptors on L-428 cells. Thus, these Ki-1 lymphomas derived from activated lymphocytes appear to secrete TGF-beta activity but continue to proliferate because of defective suppression of IL-2 (and related lymphokine)-dependent DNA synthesis.

Cell Division↗

PubMed1988

Molecular genetic analysis in the diagnosis of lymphoma in fine needle aspiration biopsies. II. Lymphomas versus nonlymphoid malignant tumors.

The configurations of immunoglobulin genes and T-cell receptor beta chain genes were analyzed by Southern blotting in DNA derived from nonlymphoid malignant tumors and lymphomas. Gene rearrangements were not detected in any of the 35 cases of nonlymphoid malignant tumors. On the contrary, they were shown in all 14 cases of non-Hodgkin's lymphomas, 2 of 3 cases of Hodgkin's disease and 2 cases diagnosed as non-Hodgkin's lymphoma or angioimmunoblastic lymphadenopathy. The differentiation by light microscopy between lymphoma and nonlymphoid malignant tumors was a diagnostic problem in five cases; the molecular genetic analysis of DNA was contributory in all five diagnostically difficult aspirates. By gene rearrangement studies, the diagnosis of lymphoma was confirmed in two cases and nonlymphoid malignant tumors were accurately indicated in aspirates diagnosed finally as rhabdomyosarcoma (one case) and carcinoma (two cases).

Adolescent↗

PubMed1985

Malignant lymphomas of the skin: their differentiation from lymphoid and nonlymphoid cutaneous infiltrates that simulate lymphoma.

Malignant lymphomas of the skin, excluding mycosis fungoides, are pathologically, immunologically, and clinically heterogeneous. Varying patterns and degrees of cutaneous infiltration are encountered in all histologic subtypes of non-Hodgkin's lymphomas. Immunologic studies have shown relatively equal numbers of cases with B and T cell phenotypes, but true histiocytic lymphomas of the skin also occur. Patients may be of any age, and they may have lymphoma in any clinical stage. A low clinical stage and a low-grade histologic subtype are significant factors for long survival. The differential diagnosis includes a variety of lymphoid infiltrates that are referred to as a group as cutaneous lymphoid hyperplasia; it also includes lymphomatoid papulosis as well as nonlymphoid cutaneous infiltrates such as myeloid leukemias, histiocytosis X, malignant histiocytosis, regressing atypical histiocytosis, and neuroendocrine (Merkel) cell carcinoma. Distinction of cutaneous lymphomas from these entities requires comprehension of multiple variables, including immunologic as well as morphologic and clinical factors.

B-Lymphocytes↗

PubMed1985

A retrospective histological study of 9,009 cases of malignant lymphoma in China using the NLPCG classification. The Nationwide Lymphoma Pathology Cooperative Group (NLPCG).

A total of 9,009 cases of malignant lymphoma from 13 provinces in China were reviewed in a retrospective study covering the 10-year period from 1972 to 1981. Of these 9,009 cases, 8,572 were of non-Hodgkin's lymphomas (NHL), of which 67% were of B-cell type and 28.5% were of T-cell type. Of the NHL, 5.2% showed a follicular pattern, and 30.1% were extranodal upon presentation, the most frequent site being Waldeyer's ring. Hodgkin's disease accounted for 7.9% of the lymphomas in the regions where the cases of this disease were included in the review. Within China, there was a higher incidence of B-cell types in the middle and western parts of the country as well as in Hainan Island (around 83%), while the T-cell types showed a higher incidence (34-45%) in the eastern part (Nanjing, Suzhou-Wuxi and Hangzhou). A few cases of Burkitt's lymphoma were found in the subtropical island of Hainan. The two cities of southwestern China (Chongqing and Chengdu) had a relatively higher frequency of the small lymphocytic type. The data indicate that the lymphomas in China, unlike those in the U.S.A. and Europe, are fairly similar to those in Japan in distribution of their subtypes, with the exception of the western part of China, where there is a tendency to approximate those in the Western countries.

China↗

PubMed1982

[Treatment of non-Hodgkin's lymphoma with NK-631 (peplomycin)--with special reference to the effect on T and non-T cell lymphomas].

NK-631 (Peplomycin) has an anti-tumor spectrum, equivalent to or higher than its analogue bleomycin and low toxicities to the lungs. Fourteen patients with advanced non-Hodgkin's lymphoma received NK-631 10 to 30 mg once or twice a week. As the results, there were 57.1% response rate of all patients. The response rate according to the immunologic classification were 100%(6/6 cases) for patients with non-T cell lymphoma and 25%(2/8 cases) for patients with T-cell lymphoma. On the other hand, we observed some toxicities such as transient fever in 64.3%, G-I tract symptoms in 21.4%, skin toxicities in 21.4% and pulmonary fibrosis in one case. This agent is considered to be one of the useful agents to non-Hodgkin's lymphoma especially non-T cell lymphoma.

Adult↗

PubMed1983

Atypical adult T-cell leukemia-lymphoma: diverse clinical manifestations of adult T-cell leukemia-lymphoma.

The diverse clinical manifestations of 10 cases of so-called adult T-cell leukemia-lymphoma (ATL)-related T-cell malignancies are described. These cases were anti-ATLA [antibody to ATL virus (ATLV)-associated antigen (ATLA)] positive, and tumor cells had the inducer/helper T-cell phenotype and expressed ATLA when cultured, indicating that these diseases are the same as typical ATL, even though their clinical diagnoses were different from ATL. Accordingly, they are called atypical ATL. Clinically, they could be divided into two subtypes, smoldering type and lymphoma type. In the smoldering type, the disease usually started with skin lesions and rarely with lung lesions. After a prodromal stage of several years, the disease progressed insidiously to the leukemic stage without additional manifestations. The flower cells characteristic of typical ATL were observed in only a small percentage of peripheral lymphoid cells. In two of the five patients the disease progressed to typical ATL after several years from onset. All five patients are alive with a long survival time, more than 6 yr in four, and had high titers of anti-ATLA, suggesting that anti-ATLA might have some role in regulating the proliferation of ATL cells in vivo. In the lymphoma type, morphological diagnosis was not always specific for discriminating ATL-related from ATL-unrelated T-cell lymphomas. Detection of anti-ATLA in the patient's serum and of ATLA in cultured tumor cells, examination of the sera of members of the patient's family for anti-ATLA, and observation of typical flower cells in the peripheral blood though the patients had neither lymphocytosis nor leukemic changes, seem to be useful for the discrimination, especially in an ATL-nonendemic area. Members of the family of a patient with anti-ATLA positive T-lymphoma in an ATL-nonendemic area were also anti-ATLA positive, indicating that healthy ATLV carriers in an ATL-nonendemic area exist as a family colony. This is responsible for sporadic outbreaks of ATL in an ATL-nonendemic area. In summary, the disease entity of ATL is considered, at present, to be a malignancy of inducer/helper T-cells transformed by ATLV or HTLV (human T-cell leukemia virus). In this sense, diverse clinical manifestations of ATL should be recognized as events of viral oncogenesis and host immune response.

Adult↗

PubMed1980

Genetic resistance to bone marrow transplantation as a leukemia-lymphoma defense mechanism: correlation of "in vivo" lymphoma resistance and "in vitro" NK activity.

(C57 X AKR) F1 hybrid mice, which show genetic resistance to C57 parental bone marrow cells and to AKR lymphoma but not to AKR bone marrow cells in vivo, also show high natural killer cell lysis versus lymphoma cells in vitro. (C3H X AKR) F1 hybrids which show no genetic resistance to parental bone marrow cells or to lymphoma cells in vivo have low levels of NK activity like those of the low responding AKR strain. Thus genetic resistance to bone marrow transplantation and to lymphoma in vivo, correlates with NK lytic activity versus lymphoma cells in vitro, adding to the evidence linking these phenomena.

Animals↗

PubMed1994

Expression of the c-kit receptor in human lymphomas is restricted to Hodgkin's disease and CD30+ anaplastic large cell lymphomas.

The product of the proto-oncogene c-kit is a transmembrane receptor protein that plays an important role in the regulation of normal and neoplastic hematopoiesis via the interaction with its specific ligand termed stem cell factor. To examine whether c-kit product is possibly involved in the pathogenesis of human lymphomas, we analyzed the expression of the c-kit protein in neoplastic cells from a variety of lymphoid tumors by immunostaining of lymph node frozen sections with the 17F11 antibody, detecting an extracellular epitope of the c-kit receptor, and of c-kit RNA by Northern blot hybridization. Of 24 nonHodgkin's lymphomas (NHL) of B- and T-cell phenotype, none expressed immunodetectable c-kit protein that was also not evidenced in lymphoid cells of reactive lymph nodes and normal tonsils. In contrast, c-kit protein was expressed by Reed-Sternberg cells and their mononuclear variants from 11 of 21 Hodgkin's disease (HD) cases, and in tumor cells from 11 of 16 cases of CD30+ anaplastic large cell lymphoma (ALCL). c-kit specific mRNA was also detected in lymph node tissues from HD and ALCL cases but not in neoplastic tissues from NHL other than ALCL. In addition, c-kit/CD30+ tumor cells were evidenced by flow cytometry in a patient displaying massive bone marrow involvement by ALCL. With the exclusion of lymphocyte predominance cases of HD that resulted c-kit expression and the other histologic subtypes of HD or the immunologic phenotype of tumor cells (B, T, nonB-nonT) in both HD and ALCL. The highly restricted expression of the c-kit product among human lymphomas to HD and ALCL provides a further biologic link between these two closely related lymphoma entities.

Hodgkin Disease↗

PubMed1994

A patient with anaplastic large cell lymphoma (Ki-1 lymphoma) showing clonal integration of HTLV-1 proviral DNA.

We encountered a patient with anaplastic large cell lymphoma (Ki-1 lymphoma) that originated in the stomach and showed histiocytic lymphoma-like morphology. CD43 antigen was positive, and rearrangement of TCR-beta gene was observed. The lymphoma was the T-cell type. Though no atypical lymphocytes or histological images specific to adult T-cell leukemia were observed, clonal integration of HTLV-1 proviral DNA was noted. Viruses such as HTLV-1 appear to be involved in the development of some anaplastic large cell lymphomas.

Adult↗

PubMed1996

Use of CD23 (BU38) on paraffin sections in the diagnosis of small lymphocytic lymphoma and mantle cell lymphoma.

The CD23 antigen is a low-affinity immunoglubulin E receptor that is expressed during B-cell activation. Recently, it has been shown to be of diagnostic utility in distinguishing between small lymphocytic lymphoma (SLL) and mantle cell lymphoma (MCL), two entities that can have similar morphologic and immunophenotypic features. Such studies, however, generally required viable cells in cell suspension or cryostat sections for detection of CD23. We evaluated staining for the CD23 antigen in paraffin sections, using BU38, an antibody that detects a fixation-resistant epitope of the antigen. We analyzed 44 SLLs, 3 lymphoplasmacytoid lymphomas, and 39 MCLs. Staining was performed on formalin- or B5-fixed paraffin-embedded tissue sections using L26 (CD20), CD3, Leu22 (CD43), and BU38 (CD23) antibodies. All of the cases were of B-cell phenotype (CD20+), and 42/44 SLLs, 3/3 lymphoplasmacytoid lymphomas, and 33/39 MCLs coexpressed the CD43 antigen. CD23 was positive in 41 (93%) of 44 SLLs. The majority of neoplastic cells (75% or more) stained positively, with a membranous pattern of staining. The staining was moderate in intensity and easily interpreted. Only 1/39 MCLs and 1/3 lymphoplasmacytoid lymphomas were CD23 positive. CD23-positive follicular dendritic cells were, however, present in all of the MCLs, either in residual follicles or in large, disordered meshworks. These results demonstrate that the BU38 antibody can detect CD23 on the cells of SLLs in paraffin sections and that this antibody can have diagnostic utility in routine diagnosis.

Biomarkers, Tumor↗

PubMed1997

Production of the immunosuppressive cytokine interleukin-10 by Epstein-Barr-virus-expressing pyothorax-associated lymphoma: possible role in the development of overt lymphoma in immunocompetent hosts.

Malignant lymphomas frequently develop in the pleural cavity of patients with long-standing pyothorax. Thus, the term pyothorax-associated lymphoma (PAL) has been proposed for this type of tumor. Most PALs are diffuse lymphomas of B cell type and contain Epstein-Barr virus (EBV) DNA. We have established two lymphoma cell lines from the biopsy specimens of PAL cases, OPL-1 and OPL-2. Both cell lines contain EBV DNA, but only OPL-1 expresses EBV nuclear antigen 2, which works as a target molecule for the cell-mediated immune response. As systemic immunodeficiency is unlikely to be present in PAL patients, PAL from which OPL-1 derived was not expected to be fully developed. In this study, we examined the expression of immunosuppressive factors in OPLs. Only OPL-1, not OPL-2, expressed interleukin-10 (IL-10) mRNA and secreted IL-10 into culture supernatant. Both OPL-1 and OPL-2 expressed transforming growth factor (TGF)-beta 1 mRNA; however, neither expressed latent TGF-beta-binding protein mRNA at a detectable level by Northern blot analysis. Because TGF-beta expresses its functions in cooperation with latent TGF-beta-binding protein, the biological functions of TGF-beta 1 could be negligible. Neither cell line expressed at a detectable level EBV BCRF-1 mRNA, a viral gene product that is partly homologous to human IL-10 and shares biological activities of IL-10. Although IL-10 is reported to promote the growth of activated or neoplastic B cells, OPL-1 did not respond to human recombinant IL-10 by growing faster. As OPL-1 expresses a target antigen for the host cytotoxic T-cell response, the production of an immuno-suppressive cytokine, IL-10, might contribute to the development of overt lymphoma by inducing locally immunosuppressive circumstances. The present study suggests that an immunosuppressive cytokine plays a role in lymphomagenesis of immunocompetent patients.

Animals↗

PubMed1997

[Pyothorax-associated lymphoma: EBV-positive lymphoma developing in immunocompetent patients].

Empyema, Pleural↗