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)

During investigations of serum from patients with carcinoma, elevated levels of two proteins were observed. The larger (MW approximately 44,000) was identified as (alpha-acid glycoprotein. The smaller MW approximately 20,000) has not yet been identified. Further investigation of alpha-acid-glycoprotein-containing seromucoid showed that many red blood cell and tissue antigens were present, for example, I, i, P1, Tja (P+P+Pk), H, A, B, Lea, Leb1, M and N. Differences in antigen content between normal serum and serum from carcinoma patients could be demonstrated quantitatively and qualitatively. Seromucoid preparations from patients with Hodgkin's lymphoma inhibited phytohaemagglutinin-induced lymphocyte transformation more often than seromucoid preparations from normal subjects.
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PMID:Serological studies of seromucoids from normal subjects and patients with malignant and non-malignant diseases. 69 45

S-HCL 2 is the prototype antibody of the recently defined CD72 cluster (human Lyb-2). Under nonreducing conditions, S-HCL 2 monoclonal antibody (mAb) precipitates a glycoprotein of 80-86 kDa. Under reducing conditions, a dimer of 43 and 39 kDa, with core proteins of 40 and 36 kDa, is precipitated. CD72 expression in normal and malignant tissues is different from expression of all other previously described human B-cell antigens. In peripheral blood and bone marrow, the antigen appears to be present on all B lymphocytes, with the exception of plasma cells. In tissue, immunohistochemical staining revealed positivity for all known B-cell compartments; however, pulpa macrophages of the spleen and von Kupffer cells exhibited distinct positivity for CD72 also. Among 83 malignant non-Hodgkin's lymphomas examined by immunohistochemistry (alkaline phosphatase anti-alkaline phosphatase technique), all 54 B-cell lymphomas, including precursor B-cell lymphomas, Burkitt's lymphomas, germinal center lymphomas, chronic lymphocytic leukemias, and hairy cell leukemias, were CD72 positive, but no T-cell lymphomas were. Flow cytometry study of more than 80 mainly acute leukemias (52 B-cell leukemias) showed reactivity with S-HCL 2 mAb over the full range of B-cell differentiation. In particular, very early B cells in cytoplasmic Ig (cIg)-negative, CD19-positive pre-pre-B-cell leukemias and hybrid leukemias (mixed myeloid and B-cell type) were consistently positive for CD72 on the cell surface. Therefore, CD72 may become an important marker for progenitor B-cell leukemias.
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PMID:Human Lyb-2 homolog CD72 is a marker for progenitor B-cell leukemias. 138 16

The origin of the malignant mononuclear Hodgkin's cell and the classic Reed-Sternberg cell in Hodgkin's disease (HD) remains controversial despite extensive immunohistological and lymphoid gene analysis. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) in combination with protein staining and radioactive labelling has not been fully exploited in analysing the HD-derived cell lines available. The NP40 solubilised cellular proteins from the three HD cell lines, L428, KM-H2 and HDLM-2 were analysed using these techniques and compared with other haemopoietic cell lines and leucocytes of myeloid and lymphoid origin. The electrophoretic patterns of the three HD cell lines, although clearly different from one another, had many features in common. No major differences between the cell types were detected by Coomassie brilliant blue staining. The HD cell lines were more readily distinguished from the myeloid and to a lesser extent the lymphoid cell lines by silver staining, but HD cell line specific proteins (13, 19, 36, 60, 150 kD) were detected only on one line, L428. Iodination of cell membrane molecules, SDS-PAGE and subsequent autoradiography revealed three molecules (118, 22, 12 kD) which were restricted to the HD cell lines and the B-cell line Mann, and one molecule (144 kD) restricted to the HD cell lines and U937. Molecules unique to HDLM-2 (211 kD) and L428 (46 kD) were also detected by this method. Cell surface labelling with NaB3H4 identified a glycoprotein of 102 kD limited to HDLM-2 and L428, as well as a glycoprotein of 97 kD present on KM-H2 alone and one of 63 kD on L428 alone. Overall the HD cell line protein profiles displayed little similarity to the patterns of the other cell types studied and provide further evidence to support functional and phenotypic studies which identify Hodgkin's cells as a unique cell type. The molecules identified as HD cell line restricted may have potential as markers for this cell type.
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PMID:Cellular protein profiles of the Hodgkin's disease cell lines L428, KM-H2 and HDLM-2: a comparative study. 156 Jun 74

The utility of the lipid-associated sialic acid (LASA or LSA) test as a serum marker for malignancy is reviewed. The name LASA or LSA test is confusing because it suggests that only or mainly lipid-bound sialic acid is measured. In reality, glycoprotein-bound sialic acid is determined predominantly. The assay appears to have a particularly high positivity rate in leukemia, Hodgkin's disease, melanoma, sarcoma, advanced ovarian carcinoma and oropharyngeal tumors, suggesting that LASA may serve as a valuable marker in these malignancies. As a consequence of the rise of sialic acid-rich acute-phase proteins, such as alpha 1-acid glycoprotein, in inflammatory diseases the specificity of LASA and therefore its diagnostic accuracy is low. LASA can be useful for monitoring cancer patients during treatment, especially in combination with other tumor markers.
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PMID:The utility of lipid-associated sialic acid (LASA or LSA) as a serum marker for malignancy. A review of the literature. 162 78

Cryostat sections from lymph nodes of 47 Hodgkin disease patients were examined by immunohistology for the Epstein-Barr virus (EBV)-encoded latent membrane protein (LMP), nuclear antigen 2, and late viral glycoprotein gp350/250. A distinct LMP-specific membrane and cytoplasmic staining was detected exclusively in Hodgkin and Reed-Sternberg cells in 18 patients (38%); EBV nuclear antigen 2 and gp350/250 immunoreactivity was absent in all instances. Thirty-two of 47 (68%) cases contained EBV-specific DNA sequences as detected by PCR, all LMP-positive cases being in this category. Our results confirm previous studies establishing the presence of EBV genomes in Hodgkin and Reed-Sternberg cells by demonstrating expression of an EBV-encoded protein in the tumor-cell population. The finding of LMP expression in the absence of EBV nuclear antigen 2 suggests a pattern of EBV gene expression different from that of B-lymphoblastoid cell lines and Burkitt lymphoma, whereas this finding shows similarities with that seen in undifferentiated nasopharyngeal carcinoma. Because the LMP gene has transforming potential, our findings support the concept of a pathoetiological role of EBV in many cases of Hodgkin disease.
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PMID:Epstein-Barr virus latent membrane protein expression in Hodgkin and Reed-Sternberg cells. 164 16

Monoclonal antibodies (MAbs) were developed against immunodominant HHV-6 (GS isolate) late and early proteins. The major late protein was identified as a probable glycoprotein with a molecular weight of approximately 110 kDa (gp 110). Immunoblotting of the early antigen yielded proteins of 41 and 38 kDa (p41/38). The MAb to the early protein reacted with cells infected with 14 different HHV-6 isolates. In contrast, the MAb against the late protein reacted with only 10 of these isolates, indicating that there was strain variation in this glycoprotein. The percentage of antibody-positive sera reactive with gp110 in the ELISA ranged from 56% to 96% among the different serum donor categories. In contrast, only 10-30% of the sera were positive for antibodies to p41/38 with the exception of sera from patients with African Burkitt's lymphoma (ABL) and Hodgkin's disease (HD). These antibody patterns denote the presence of active HHV-6 replication in patients with ABL and HD.
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PMID:Sero-epidemiological investigations on human herpesvirus 6 (HHV-6) infections using a newly developed early antigen assay. 165 63

Epstein-Barr virus (EBV)-specific DNA sequences were detected by polymerase chain reaction analysis in 15 of 47 (32%) DNA extracts prepared from CD30-positive (Ki-1 antigen-positive) anaplastic large cell (ALC) lymphomas. EBV-encoded RNA (EBER) transcripts could be detected by in situ hybridization in the tumor cells of 9 of 11 EBV DNA-positive cases. Twenty-eight cases were examined by immunohistology on cryostat sections for the presence of the EBV-encoded latent membrane protein (LMP), the nuclear antigen 2 (EBNA2), the BZLF1 transactivator protein, and the late viral glycoprotein gp350/250. A distinct LMP-specific membrane and cytoplasmic staining was detected exclusively in lymphoma cells of five cases (18%); two of these cases additionally expressed EBNA2. BZLF1 protein and gp350/250 immunoreactivity was absent in all instances. All LMP-positive cases contained EBV DNA and EBER sequences. The pattern of EBV latent protein expression in ALC lymphomas showed heterogeneity with respect to EBNA2 expression: LMP-positive/EBNA2-negative cases displayed a pattern previously described for undifferentiated nasopharyngeal carcinomas and Hodgkin's disease, whereas LMP-positive and EBNA2-positive cases showed parallels to lymphoblastoid cell lines. Because the LMP gene has transforming potential, our findings support the concept of a pathoetiologic role for EBV in a proportion of CD30-positive ALC lymphomas.
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PMID:Epstein-Barr virus DNA and latent gene products in Ki-1 (CD30)-positive anaplastic large cell lymphomas. 166 8

Verapamil was evaluated as a chemosensitizer for reversing multidrug resistance in multiple myeloma both in vitro and in clinical trials. Bone marrows from 59 myeloma patients in relapse were evaluated for several resistance parameters: expression of p-glycoprotein (MDR1), doxorubicin (Adriamycin) and vincristine sensitivity, and the ability of added verapamil to reduce resistance to the cytotoxic agents. We found that verapamil was capable of sensitizing myeloma cells that exhibited resistance to doxorubicin and vincristine in vitro, but did not enhance sensitivity of cells that were drug sensitive (P less than .001). Myeloma cells expressing MDR1 immunohistochemically tended to be more doxorubicin resistant in vitro than MDR1-negative cells. In the clinical trials, 22 patients with myeloma refractory to vincristine-Adriamycin-dexamethasone (VAD) were treated with VAD plus high-dose intravenous verapamil (Ve). Among the 22 patients treated with VAD/Ve, five achieved a partial remission (23%). The median relapse-free survival for the VAD/Ve responders was 5.4 months and their overall survival from the start of VAD/Ve was better than that of the nonresponders. Among the subset of 10 patients whose myeloma cells were MDR1 positive, four responded clinically (40%), whereas none of five patients with MDR1-negative myeloma cells achieved remission with VAD/Ve. We also observed that myeloma cells from three of four VAD/Ve clinical responders exhibited in vitro chemosensitization with verapamil, whereas in vitro verapamil chemosensitization was seen in only one of six clinical nonresponders. Our observations demonstrate that clinical reversal of multidrug resistance can be achieved in some patients with VAD-refractory myeloma with the use of verapamil. In addition to their value in drug development, in vitro tests of MDR1 expression and of chemosensitizers plus cytotoxic drugs on the patients' bone marrow myeloma cells may identify patients who will respond clinically to chemosensitizer-containing regimens. We anticipate that chemosensitizer regimens capable of inhibiting multidrug resistance will play an increasing role in the treatment of hematologic malignancies, including B-cell neoplasms such as multiple myeloma and the non-Hodgkin's lymphomas.
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PMID:Multidrug-resistant myeloma: laboratory and clinical effects of verapamil as a chemosensitizer. 167 18

Anti-BLA.36 is an antibody that recognizes a glycoprotein with an apparent molecular weight of 36 kilodaltons, termed B lymphocyte antigen (BLA.36). By using an immunochemical staining technique, BLA.36 was found to be specifically expressed on Hodgkin's and human B cell lines including early B progenitor cells. Other cell lines representing T cell lymphomas, non-B large cell lymphomas, melanomas and carcinomas were consistently negative. BLA.36 is distinct from the previously identified antigens of hematopoietic cell lineage. The specificity of expression of BLA.36 in tissue sections mirrored that of cell lines. In normal tissues, BLA.36 was detectable predominantly on cells in the germinal center and mantle zone of reactive follicles in lymph nodes and spleens. In hematopoietic malignancy, the antigen was expressed on the surface of Reed-Sternberg cells, mononuclear Hodgkin's cells and also on malignant cells of B cell lineage. BLA.36 was also observed on lymphoid cells of 10 to 24 week fetal liver: a double-antibody-staining method revealed that these BLA.36-positive cells also contained immunoglobulin mu heavy chain consistent with identification as early B cells. Under these conditions, T lymphocytes, histiocytes, granulocytes, macrophages, stromal cells in lymphoid tissue, and both normal and neoplastic epithelial cells were consistently negative for the expression of the antigen, with the single exception of a variable proportion of Kupffer cells in normal liver. The antibody has already established its usefulness for the identification of Reed-Sternberg and Hodgkin's cells, and also normal and malignant B lymphocytes in frozen as well as formalin-fixed tissue sections. Furthermore, binding of F(ab)2 fragments of anti-BLA.36 to antigen-positive cell lines specifically inhibited the proliferation of cells. Such an effect was eliminated by the removal of the antibody from the culture-medium, suggesting a possible growth-related function of the antigen in Hodgkin's and B cells.
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PMID:BLA.36: a glycoprotein specifically expressed on the surface of Hodgkin's and B cells. 169 46

A new monoclonal antibody Ber-MAC3 is reported. It recognises a formol sensitive epitope of a not yet clustered monocyte/macrophage specific 140 kilodalton glycoprotein that is expressed on the cell surface and in the cytoplasm. In 30 cases of acute and chronic leukaemia, Ber-MAC3 staining was restricted to 15 myeloid leukaemias of M4 and M5 types. The tumour cells of two cases of true histiocytic malignancies were Ber-MAC3 positive, whereas those of all 280 malignancies of lymphocytic origin were negative. The latter included 52 cases of Hodgkin's disease and 41 cases of Ki-1 positive anaplastic large cell lymphomas which had previously been classified as true histiocytic lymphomas. Ber-MAC3 therefore seems to be of considerable value for selective identification of monocytes and macrophages at a certain stage of differentiation and seems to be suitable for diagnosing myelomonocytic or monocytic leukaemia and neoplasms of true histiocytic origin.
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PMID:Ber-MAC3: new monoclonal antibody that defines human monocyte/macrophage differentiation antigen. 172 28


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