Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty-three non-Hodgkin lymphomas classified according to the Kiel classification have been studied with regard to surface immunoglobulin (sIg) on cells in suspension and cytoplasmic immunoglobulin (cIg) by the peroxidase anti-peroxidase method (PAP) on formaline-fixed tissue sections. Fifty-six out of 66 examined (i.e. 85%) revealed a monoclonal staining pattern for sIg, whereas 37/70 (53%) gave a monoclonal staining pattern for cIg by PAP. The methods combined gave a monoclonal staining pattern in 73/83, i.e. in 88%, of the biopsies tested. The discrepancies between the two methods were largest in centroblastic/centrocytic and lymphocytic lymphomas. With regard to the light chain staining patterns, complete agreement between the two methods was obtained in the 20 cases that allowed such analysis to be made. This suggests that the specificity of PAP, as carried out in this study with reagents purified by immunoabsorbent techniques, is satisfactory. On a basis of heavy chain isotypes centroblastic/centrocytic, lymphoplasmacytoid, and immunoblastic lymphomas could be divided into distinct immunological subgroups. In four biopsies the sIg heavy chains were mu + delta, whereas mu + gamma chains were detected by PAP. This finding may be relevant to the mu leads to gamma switch known to occur during normal B-cell differentiation. Immunoglobulin inclusions were found in 8 cases--3 belonging to the immunoblastic group, and 5 to the lymphoplasmacytoid group.
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PMID:Cell-associated immunoglobulin in human non-Hodgkin lymphomas. A comparative study of surface immunoglobulin on cells in suspension and cytoplasmic immunoglobulin by immunohistochemistry. 702 87

A monoclonal antibody, F11, was produced against a tumor-associated antigen from the spent medium of the M14 human malignant melanoma cell line which was grown continuously in serum-free medium. Ouchterlony double-diffusion study revealed that the F11 monoclonal antibody is an immunoglobulin G1. The F11 monoclonal antibody reacted positively with seven of eight (88%) melanoma, five of five (100%) carcinoma, zero to five normal, and zero of two lymphoblastoid cell lines by indirect immunofluorescence test. Also, by indirect immunofluorescence test, F11 monoclonal antibody reacted with cryostat sections from four of five (80%) melanomas, six of seven (86%) carcinomas, zero of one benign nevus, and zero of two benign breast diseases. By the indirect avidin:biotin:peroxidase complex immunoperoxidase method, the F11 monoclonal antibody reacted positively with cryostat sections from five of five (100%) melanomas, five of five (100%) breast cancers, two of two (100%) colon cancers, zero of one benign nevus, and zero of one Hodgkin's disease spleen. Thus, the tumor-associated antigen that the F11 monoclonal antibody recognizes appears to be expressed by melanomas and carcinomas, hence the designation melanoma-carcinoma-associated antigen. Microscopic observations disclosed that the melanoma-carcinoma-associated antigen is present in the cytoplasm, on the membrane of melanoma and carcinoma cells, and in the lumen of glandular structures of breast and colon carcinomas. The molecular weight of the melanoma-carcinoma-associated antigen in spent medium from the M14 CEM cell line is 100,000 as determined by sodium dodecyl sulfate:polyacrylamide gel electrophoretic analysis of indirect immunoprecipitates obtained with the F11 monoclonal antibody.
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PMID:Mouse monoclonal antibody to a melanoma-carcinoma-associated antigen synthesized by a human melanoma cell line propagated in serum-free medium. 704 18

Two in vitro cell lines (L428, L439) were established from pleural effusions of two patients with Hodgkin's disease. The histological diagnosis was ascertained in both cases by two independent pathologists. The neoplastic nature of the culture cells is indicated by the demonstration of several structural and numerical chromosome abnormalities associated with a monoclonal pattern of marker chromosomes. Heterotransplantation in nude mice was achieved by intracranial inoculation and by subcutaneous transplantation of cultured cells embedded in a plasma clot. EBV-specific antigens (EBNA, VCA) were not detectable in either cell line. Ia-like antigens, receptors for T cells, acid phosphatase and acid esterase were shown to be present in the cultured cells. The L428 and L439 cell line lacked surface- or cytoplasmic Ig, HTLA, receptors for C3b, C3d, IgG-Fc, mouse E or sheep E, and were devoid of lysozyme, peroxidase and chloracetate esterase. These features do not correspond to those of B cells, T cells, myeloid cells, monocytes or macrophages; the morphology and the marker pattern of the culture cells, however, is identical with that of freshly obtained Hodgkin (H)- and Sternberg-Reed (SR)- cells, except for the lack of Clg in the in vitro cells, which is explained by the culture conditions. These findings suggest that the L428 and L439 cell lines are indeed derived from H- and SR-cells and offer the possibility of gaining new information upon the nature of Hodgkin's disease.
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PMID:Two neoplastic cell lines with unique features derived from Hodgkin's disease. 721 41

Four in vitro cell lines (L 428, L 439, L 538, and L 540) were established from different materials of three patients with Hodgkin's disease: pleural effusions, peripheral blood, and bone marrow. The histological diagnosis was confirmed in all cases by several independent histologists. All four cell lines have been in culture for over 6 months up to over 3 years. The neoplastic nature of the culture cells is indicated by the demonstration of several structural and numeric chromosome abnormalities associated with a monoclonal pattern of marker chromosomes. EBV-specific antigens (EBNA, VCA) were not detected in either cell line. Ia-like antigens, receptors for human T cells, acid phosphatase, and acid esterase were showen to be present in the cultured cells. All cell lines lacked surface or cytoplasmic Ig, HTLA, receptors for C3b, C3d, IgG-Fc, mouse E or sheep E, and were devoid of lysozyme, peroxidase, and chloracetate esterase. The described features do not represent B cells, T cells, myeloid cells, monocytes, or macrophages. The morphology and the marker pattern of the culture cells, however, is identical with that of freshly obtained Hodgkin's (H)- and Sternberg-Reed (SR)-cells, except for the lack of CIg in the in vitro cells, which is explained by the culture conditions. Heterotransplantation in nude mice was achieved by intracranial inoculation and by s.c. transplantation of cultured cells embedded in a plasma clot. The described findings suggest that these cultured Hodgkin's cell lines are indeed derived from H and SR cells. The cellular origin of these cells is not clear, the loss of cellular differential markers during the process of possible dedifferentiation is discussed.
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PMID:Hodgkin's disease: establishment and characterization of four in vitro cell lies. 727 66

Phagocytosis and lysis of C. pseudotropicalis by peripheral blood monocytes from Hodgkin's and non-Hodgkin's lymphoma were analysed. In Hodgkin's disease, there was a decrease in the phagocytic activity of blood monocytes; moreover, the candidacidal activity was significantly decreased as compared with normal controls. Although monocytes from non-Hodgkin's patients presented normal phagocytic function, the ability to kill C. pseudotropicalis was impaired. In both groups of lymphomas, the data showed that the abnormal findings were not related to treatment. These results indicate that monocytes from Hodgkin's and non-Hodgkin's lymphoma posses a deficiency in killing C. pseudotropicalis, which could be due to an intrinsic macrophage defect in the myeloperoxidase-independent mechanisms and which may be responsible for the predisposition of the se patients to candida infections.
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PMID:Defective function of peripheral blood monocytes in patients with Hodgkin's and non-Hodgkin's lymphomas. 738 72

In vitro culturing of lymph node cells from a human non-Hodgkin lymphoma gave rise to several colonies of eosinophil-like cells. Eosinophil colonies originated from cells that during the first week of culture had a fibroblast appearance and were adherent to plastic. The tissue culture was sacrificed after 14 days. At that time each colony was formed by 20-50 cells with intracytoplasmic peroxidase-positive and eosinophilic granules. Cells comprising the colonies exhibited different degrees of differentiation. Some of the cells (26.6%) were mature eosinophils, the majority (66.8%) resembled eosinophil myelocytes, and some other (4.6%) had a fibroblast appearance. One or two multinucleated giant cells were often present in the center of most of the colonies. These cells contained up to 10 nuclei, which were arranged in a "ring form" or centrally located; giant cells with a single, central, large, multilobed nucleus were also observed. Cells belonging to other myelopoietic lines could not be identified in the tissue culture. Histological examination of the lymph node revealed extensive presence of eosinophils at various degrees of maturation but absence of other myelopoietic lines.
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PMID:In vitro formation of eosinophil-like colonies by lymph node cells from a human lymphoma. 744 97

The immunoreactivity of a CD1a monoclonal antibody (MAb), denoted 010, was investigated by means of the streptavidin-biotin-peroxidase method in formalin-fixed and paraffin-embedded tissues from 47 cases. The samples comprised reactive lymphoid proliferations of skin, tonsil, and lymph node including dermatopathic lymphadenopathy and Langerhans' cell histiocytosis, Hodgkin's and non-Hodgkin's lymphomas, and thymomas. Interdigitating and dermal dendritic cells, veiled cells, Langerhans' cells, and also cortical thymocytes and their neoplastic counterparts displayed immunostaining with MAb 010 in paraffin sections. These results are identical to previous ones reported for other CD1a MAbs in fresh or frozen specimens. The findings suggest that the binding site of 010 is a fixation-resistant epitope of CD1a antigen which has not been previously identified.
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PMID:Immunohistochemical detection of CD1A antigen in formalin-fixed and paraffin-embedded tissue sections with monoclonal antibody 010. 750 72

Epstein-Barr virus (EBV) has been implicated in the etiology of a large number of malignancies. Most recently several studies have linked EBV to Hodgkin's disease. In this report, formalin-fixed, paraffin-embedded tissues were collected retrospectively from 41 children with Hodgkin's disease treated at our hospital. Lymph node biopsies were examined for the presence of two virus-encoded latent proteins: latent membrane protein (LMP) and Epstein-Barr nuclear antigen-2 (EBNA-2), in Reed-Sternberg (RS) and Hodgkin (H) cells, by peroxidase immunolabeling. Nonisotopic Epstein-Barr encoded RNAs (EBERs) in situ hybridization was also performed and positive labeling in malignant cells was detected. Twenty specimens were EBER+/LMP+, 2 were EBER+/LMP-, and 19 were EBER-/LMP-. However, none of the 41 cases expressed EBNA-2. Twenty-two of 41 (54%) cases were EBV positive including 2 of 6 with lymphocyte predominance, 19 of 25 with mixed cellularity, 0 of 9 with nodular sclerosis, and 1 of 1 with lymphocyte depletion. In the age range of 2 to 6 years, 14 of 17 (82%) samples were EBV-positive, whereas only 8 of 24 (33%) samples from the age range of 7 to 15 years contained EBV. (P = .004), a two-tailed Fisher's test). In 17 samples, polymerase chain reaction amplification was performed using strain specific primers for exon sequences of the EBNA-3C gene of EBV. From 12 positive samples, 8 contained EBV-A and 4 EBV-B. These results support the hypothesis that EBV contributes to the pathogenesis of pediatric Hodgkin's disease, particularly in mixed cellularity Hodgkin's disease and in the younger group.
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PMID:Presence of Epstein-Barr virus and strain type assignment in Argentine childhood Hodgkin's disease. 757 62

The bcl-2 gene product (bcl-2 protein, BCLP) prevents apoptotic cell death. Via a 14;18 chromosomal translocation, BCLP is overexpressed in most follicular lymphomas as well as some other non-Hodgkin's lymphomas, and it has also been documented in other nonlymphomatous malignancies. To address the possible prognostic value of this marker in predefined subsets of non-small cell lung carcinoma (NSCLC), the authors studied 126 T1N0M0 cases seen between the years 1986 to 1991 at our institution. Patients were treated by lobectomy (105 cases) or wedge excision (21 cases) with negative margins; neuroendocrine carcinomas of all grades were specifically excluded. The mean follow-up period was 39 months. Immunostaining for BCLP was done using a monoclonal antibody (clone no. 124; DAKO, Carpinteria, CA), and the avidin-biotin-peroxidase complex (ABC) technique. The study cases included 73 adenocarcinomas (ACs) as well as 40 squamous cell (SCC), five adenosquamous (ASC), and eight large cell/poorly differentiated (LCC) carcinomas. As assessed with the Kaplan-Meier method, overall survival was 64% at 5 years (66% AC vs 59% SC). BCLP was detected in 47 of 126 cases (37%) including 32 AC (44%), 10 SCC 925%), two ASC (40%), and three LCC (38%). No significant difference in 5-year survival was noted in a comparison of all cases with BCLP expression (63%) and those without (59%). There was, however, a significant difference in the survival of grade 1 BCLP(+) cases, when compared with grade 2 or 3 BCLP(+) cases (P = .01). A nonstatistically significant trend toward increased survival was observed in BCLP(+) SCC cases (66% 5-year survival in BCLP[+] vs 45% in BCLP[-] [P = .11]). Proportional hazards analysis failed to disclose significant independent risk factors. These data suggest that bcl-2 protein immunoreactivity has limited prognostic value in the pathological evaluation of NSCLC.
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PMID:Expression of bcl-2 protein in stage T1N0M0 non-small cell lung carcinoma. 759 Jun 97

The oncogenes c-myc and c-ras are known to elicit a cooperative tumorigenicity. In this study we investigated their role in the pathogenesis of Hodgkin's disease. The expression of these oncogenes was determined in Hodgkin's disease patients by avidin-biotin peroxidase complex immunohistochemical staining and was compared to their expression in patients with non-Hodgkin's lymphomas and inflammatory reactive lymph nodes. Of 29 examined patients with different histological types of Hodgkin's disease, 21 (72.4%) showed an elevated expression of c-myc and 28 (96.5%) of c-ras. Although this expression was marked especially in the neoplastic Reed-Sternberg cells, it was also noted in the numerous reactive cells present in the involved lymph nodes. By contrast, a much lower frequency of increased expression of these oncogenes was recorded in 19 patients with different grades of non-Hodgkin's lymphoma and in 29 patients with inflammatory reactive lymph nodes. The elevated expression of c-myc and c-ras in the neoplastic Reed-Sternberg cells may reflect an oncogenic event that directly activates these genes. However, their increased expression in the surrounding non-neoplastic cells probably results from signal transduction induced by certain growth-promoting factors possibly released by the Reed-Sternberg cells and that act paracrinally to stimulate the proliferation of the neighboring cells. Furthermore, the continuous c-ras elevation may impair the normal cell cycle control and thereby promote mutagenesis and overt malignancy.
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PMID:Expression of c-myc and c-ras oncogenes in the neoplastic and non-neoplastic cells of Hodgkin's disease. 767 90


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