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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fine needle aspirates from 54 consecutive patients with primary or recurrent blastic (high-grade malignant) non-Hodgkin's lymphomas (NHLs) were analyzed by cytomorphology and immunocytochemistry. The cytologic diagnoses induced follicular center-cell-derived (centroblastic or anaplastic centrocytic) lymphoma (31 cases), immunoblastic lymphoma (11 cases), lymphoblastic lymphoma (9 cases) and histiocytic lymphoma (3 cases). Immunocytochemistry showed a B-cell phenotype of the neoplastic lymphocytes in all lymphoblastic lymphomas, 29 follicle center-cell lymphomas and 4 immunoblastic lymphomas. Four of the immunoblastic lymphomas were of T-cell origin while one case was not evaluable due to necrosis. A histiocytic origin was confirmed in two of the three cases that had a cytologic diagnosis of histiocytic lymphoma; the third case was shown by immunocytochemistry to be a true Ki-1-positive large cell lymphoma. Histologic and immunohistochemical analysis were performed on surgical biopsies from 18 patients. The results were in agreement with those on the fine needle aspiration (FNA) material in 14 cases. Three lymphomas could be phenotyped on aspirated material while marker studies on excised material were inconclusive. One lymph node aspirate contained mostly necrotic cells, which were unsatisfactory for adequate immunocytochemistry. However, sections from a removed tonsil from the same patient could be used for conclusive histology and phenotyping. In conclusion, the high diagnostic accuracy of combined cytomorphologic and immunocytochemical assessment of FNA samples validates the use of the technique in the diagnostic work-up of blastic (high-grade malignant) NHLs. In fact, the diagnostic accuracy seems so high that the technique can safely be used in the final diagnosis of blastic NHLs.
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PMID:Cytomorphology and immunocytochemistry of fine needle aspirates from blastic non-Hodgkin's lymphomas. 272 90

The Ki-1-antibody was raised against a cell-line of Hodgkin-cells, and reacts with most Hodgkin- and Reed-Sternberg-cells. By use of this antibody a new entity of non-Hodgkin's lymphomas has been identified; the anaplastic large cell lymphoma. We report our experience from studying 16 such tumours diagnosed during the period October 1986 to February 1988. In three cases the anaplastic large cell lymphoma appeared in patients who presented Hodgkin's disease as well. Of 15 cases studied using frozen section immunohistochemistry, ten showed T-, one B-, and one monocyte/macrophagephenotype, whereas three cases presented a mixed T-, B- and monocyte/macrophagephenotype. All cases showed a high proliferative activity as evaluated by presence of activation antigens. In paraffin sections six of 16 cases expressed epithelial membrane antigen (EMA). In 13 cases EMA, leucocyte common antigen (LCA) and Ber-H2 (a Ki-1-antibody) reactivity was compared in paraffin and frozen sections. The EMA reactivity was of nearly equal intensity in paraffin and frozen sections, while the reactivity of LCA and Ber-H2 was significantly reduced in paraffin sections, implying only partial preservation of the antigens. Clinically, most cases were in an advanced (III and IV) stage by the time of diagnosis. Of 14 actively treated patients, nine went into complete and two into partial remission, while three patients did not respond. Six patients are dead, five after less than one year. The coexistence of anaplastic large cell lymphoma and Hodgkin's disease and the common Ki-1 (CD30) antigen expression in these tumours suggest a possible histogenetic relationship.
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PMID:[Giant cell anaplastic anemia]. 277 96

Skin biopsy specimens from normal skin and from 115 patients with benign dermatoses, pre- or pseudo-malignant disorders or malignant cutaneous lymphomas have been examined immunohistologically for expression of the Reed-Sternberg cell associated antigen CD30 detected by monoclonal antibodies Ki-1 and Ber-H2. The antibodies stained the atypical cells in lymphomatoid papulosis, a proportion of the neoplastic cells in some cases of mycosis fungoides and most of the neoplastic cells in six large cell anaplastic/pleomorphic non-Hodgkin's lymphomas. The lymphoid cells in all other specimens were Ki-1- and Ber-H2-negative. In all cases, expression of the Ki-1/Ber-H2 antigen was accompanied by expression of activation and proliferation associated markers (i.e., HLA-DR, IL-2 receptor, transferrin receptor and the Ki-67 nuclear antigen). These data indicate the value of antibodies Ki-1 and Ber-H2 in distinguishing between lymphomatoid papulosis and other types of pre- or pseudo-malignant disorders and support the view that lymphomatoid papulosis, Hodgkin's disease and some types of non-Hodgkin's lymphoma constitute a spectrum of related disorders, originated from activated lymphoid cells.
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PMID:Expression of a Hodgkin and Reed-Sternberg cell associated antigen (Ki-1) in cutaneous lymphoid infiltrates. 282 Mar 16

Anti-Tac is a monoclonal antibody that appears to recognize the interleukin-2 receptor. With the use of a frozen-section immunoperoxidase technic, a large series of non-Hodgkin's lymphomas were investigated for the presence of Tac-antigen on neoplastic cells. Approximately one-fourth of cases expressed the Tac antigen, including 27% of B-lineage lymphomas, 6% of the T-lineage lymphomas, and three of four cases of Ki-1-expressing lymphoma. The B-lineage lymphomas with the highest incidence of Tac antigen expression were the large cell lymphomas, both diffuse and follicular, where about one-half of cases expressed the Tac antigen. All major categories of lymphoma expressed Tac except plasma-cytoma/myeloma, small noncleaved cell (Burkitt's and non-Burkitt's), and lymphoblastic malignancies.
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PMID:Expression of Tac antigen by non-Hodgkin's lymphomas. 282 94

Two cases of Ki-1 lymphomas in childhood were analyzed immunohistochemically and immunoelectron microscopically. They expressed Hodgkin's disease associated antigen, Ki-1, interleukin-2 receptor (IL2R), OKT9, and HLA-DR. Histologically, the tumour cells were large in size with abundant cytoplasm and atypical nuclei. Lymph node involvement was characterized by parafollicular and marginal sinus infiltration. These features were identical to those reported in Ki-1 lymphomas. Electron microscopically tumour cells had abundant cytoplasmic organelles with pleomorphic nuclei but had no specific granules. Some tumour cells had marked interdigitation of cell membrane. Immunoelectron microscopically Ki-1 was positive on cell membrane. Tumour cells had no T-cell or B-cell antigens except for Leu-3 (T4). Unexpectedly they expressed epithelial membrane antigen (EMA) strongly. EMA was positive on cell membrane and in the cytoplasm. EMA was detected effectively in paraffin-embedded sections. Among the malignant lymphomas in childhood tested, two cases were EMA-positive. The pattern of EMA-reactivity and the histology were very similar to Ki-1 lymphomas. These results strongly suggest that Ki-1 lymphomas in childhood may arise from non-lymphoid haematopoietic cells and that EMA can be used as a new marker to distinguish certain type of Ki-1 lymphomas in childhood.
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PMID:Ki-1 lymphomas in childhood: immunohistochemical analysis and the significance of epithelial membrane antigen (EMA) as a new marker. 283 Jul 12

The aim of this study was to elucidate the origin of Hodgkin's and Reed-Sternberg cells. Lymph node cytospins and frozen sections from 20 cases of Hodgkin's disease of different histological subtypes were immunostained by the immuno-alkaline phosphatase technique using a panel of monoclonal antibodies. As expected, the Hodgkin's and Reed-Sternberg cells of all cases were positive for the CD30 (Ki-1), CD15 (hapten X) and CD25 (Tac) antigens. In eight cases, a variable percentage of typical Hodgkin's and Reed-Sternberg cells showed a clear-cut cytoplasmic and/or surface positivity for the T-cell-associated antigens CD3, CD5, CD6 and CD4 (seven cases) or CD8 (one case), but consistently lacked B-cell and macrophage-associated markers. The best visualization of T-cell antigens was obtained in cytocentrifuge preparations and in areas of lymph node frozen sections that had been infiltrated by clusters of Hodgkin's and Reed-Sternberg cells. In two cases of Hodgkin's disease (nodular sclerosis, mixed cellularity) the neoplastic cells weakly expressed the B-cell antigens CD19 and CD22, but not T-cell or macrophage-associated markers. In 10 cases, Hodgkin's and Reed-Sternberg cells were negative for all the lymphoid- and macrophage-associated antigens. These results suggest a lymphoid (either T or B) rather than histiocytic origin for the Hodgkin's and Reed-Sternberg cells in a number of Hodgkin's disease cases.
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PMID:Expression of lymphoid-associated antigens on Hodgkin's and Reed-Sternberg cells of Hodgkin's disease. An immunocytochemical study on lymph node cytospins using monoclonal antibodies. 283 Nov 31

Ki-1 (CD30) antigen expression has been considered to be restricted to hematopoietic tissues including the recently described anaplastic large cell lymphoma and Reed-Sternberg (RS) cells in Hodgkin's disease. Its presence on some activated lymphocytes in non-neoplastic lymphoid tissues has been used as evidence that such cells might represent the physiologic counterpart of RS cells. In this study expression of CD30 antigen in 117 nonhematopoietic tumors was investigated using monoclonal antibody Ber-H2. The antigen was regularly expressed in frozen section (strongly) and paraffin section (less strongly) by embryonal carcinomas (8 of 10 studied) and the embryonal elements of mixed germ cell tumors (4 of 4), but not in other types of germ cell tumors (0 of 11) or nonhematopoietic tumors (0 of 92). Normal adult, neonatal, and fetal testes were negative for CD30 antigen, as were other fetal tissues and placenta. Ki-1 antibody gives similar results in frozen section. These findings have implications for theories suggesting an origin of RS cells from activated lymphocytes. They are also important for determining the diagnostic significance of CD30 positivity in a tumor of unknown origin, and suggest possible new uses for CD30 antibodies in routine diagnostic immunohistology.
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PMID:Ki-1 (CD30) antigen is regularly expressed by tumor cells of embryonal carcinoma. 284

The abnormal cell population in lymphomatoid papulosis was studied by immunohistochemistry, light and electron microscopy in five cases. It resulted in a comprehensive description of all the main variants within the abnormal cell population. In one of the cases an irreversible intracytoplasmic process in the abnormal lymphocytes made it possible to demonstrate the derivation of lymphomatoid cells with cerebriform nuclei resembling the mycosis cells in mycosis fungoides from large histiocyte-like cells resembling the Reed-Sternberg cells in Hodgkin's disease. Variable numbers of the abnormal cells expressed Ki-1 reactivity in all four cases tested and T-cell associated antigens in two cases.
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PMID:Abnormal T-lymphocytes in lymphomatoid papulosis. A cytomorphological study with a reconstruction of a major part of the cell differentiation cycle. 288 64

Thirty patients, 13 female and 17 male, have been followed from 3 months to 22 years (mean, 81 months; median, 63 months) and special studies have been performed on a proportion of these in order to try to predict malignant evolution. Age at onset was from 20 to 70 years (mean, 43 years; median, 42 years). Duration of disease was from 1 to 30 years (mean, 119 months; median 161 months). Seven patients also had parapsoriasis en plaque or plaque-stage mycosis fungoides at the time of diagnosis and one patient had erythroderma. None of the 22 uncomplicated lymphomatoid papulosis patients developed malignant cutaneous lymphoma during the period of observation, while the remaining 8 patients who had concurrent parapsoriasis en plaque, mycosis fungoides, or erythroderma did not deteriorate further. Single-cell deoxyribonucleic acid (DNA) measurements on the dermal infiltrate were done in 13 patients and were abnormal in 7 patients. Two of these had greatly abnormal DNA histograms and at the same time an abnormal clinical presentation with multiple nodules and tumors. The remaining five patients had DNA histograms that indicated a potential for malignancy. Monoclonal antibody studies were performed on skin biopsy specimens of 10 patients. The dermal infiltrate was dominated by T-helper lymphocytes and some Hodgkin and Reed-Sternberg cells could be detected by the antibodies Ki-1, Ki-24, and Ki-27. Human T-lymphotropic virus type I (HTLV-I) antibodies were found in 3 of 18 patients examined. Treatment with psoralens plus ultraviolet A (PUVA) was effective (partial or complete remission) in six patients but they relapsed at cessation of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lymphomatoid papulosis. A follow-up study of 30 patients. 288 56

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.
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PMID: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. 289 11


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