Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1261473 (sarcoma)
 25,952 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

21 patients (6 females and 15 males) with Dermatitis herpetiformis have been studied with special considerations of the small intestinal biopsy-findings. During this investigation the patient's mean age was 45 years (20-68) and the mean age at onset was 38 years (17-64). In 5 patients (23.8%) total villous atrophy (group I) and in 4 patients (19.0%) a severe partial or subtotal villous trophy (group II) was found on small intestinal biopsy. The sprue-like changes were patchy lesions. Histocompatibility-antigens of type HLA-AL were found in 38.1% and of type HLA-B8 in 47.6%. After 20 years of the disease one patient died of a malignant lymphoma of the intestine (immunoblastic sarcoma). In all patients the number of interepithelial lymphocytes in the small bowel mucose was significantly increased, as it was in those patients with a normal villous pattern (group III). In a quantitative analysis of specifically labeled (peroxidase-anti-perosidase complex) IgG-, IgA- and IgM-cells in the intestinal mucosa it was found that the number of all three plasma cell classes are increased significantly (P less than 0.01).
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PMID:["Malabsorptive" dermatitis herpetiformis. A study with particular regard to biopsy findings of the small intestine (author's transl)]. 15 22

Peripheral blood lymphocytes and skin fibroblasts from 12 cancer patients were infected with Epstein-Barr virus (EBV) or SV40 virus. The EBV-transformed lymphoblasts and SV40-transformed fibroblasts were grown as continuous cell lines and expressed the same histocompatibility antigens as tumor cell lines established from the same cancer patients. Sera from 350 melanoma and 195 sarcoma patients were tested for antibody reactive with membrane antigens on three of these tumor cell lines (two melanomas and one sarcoma) by immune adherence (IA) and indirect immunofluorescence (IMI) assays. Antibodies to HLA and other non-tumor-related antigens were completely removed from the most reactive sera by quantitative absorption with 4 x 10(7) lymphoblasts or 10(7) transformed fibroblasts autologous to the tumor target cells. These paired cell lines were used to monitor humoral immune responses in melanoma and sarcoma patients receiving allogeneic tumor cell vaccines.
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PMID:Establishment of paired tumor cells and autologous virus-transformed cell lines to define humoral immune responses in melanoma and sarcoma patients. 20 83

With the objective of developing human T-T cell hybrids producing B-cell growth factor, we fused concanavalin A-activated T lymphocytes with cells of the Jurkat T cell line. The hybrids were selected on the basis of their ability to form colonies in soft agar, whereas the parent Jurkat T cell line did not. T-T cell hybrids were HLA-typed, screened by functional tests, and recloned by limiting dilution. In addition to obtaining B-cell growth factor-producing hybrids, we also obtained certain other T-T cell hybrids (as determined by HLA-typing) producing suppressor factors inhibiting proliferative responses and antibody production by human lymphocytes. Subsequently, a suppressor factor with similar inhibitory properties was identified in supernatants of the Jurkat T cell line. However, the Jurkat factor exhibited different biochemical and functional properties than the hybridoma-derived suppressor factors. Using two-parameter cell cycle analysis and the metachromatic fluorochrome acridine orange, we found that the hybridoma-derived 160 and 169 suppressor factors arrested phytohemagglutinin-induced proliferative of peripheral blood mononuclear cells in the G0/G1 phase of the cell cycle, whereas the Jurkat suppressor factor arrested proliferation in the S phase. Incubation of peripheral blood mononuclear cells with the 160, 169, or Jurkat suppressor factors for 24 hr at 37 degrees C, followed by washing, did not alter their cell cycle progression (or RNA content) in response to stimulation with phytohemagglutinin. The hybridoma-derived 160 and 169 suppressor factors and the Jurkat factor inhibited the growth but not the viability of cells from the following human tumor cell lines: A673 sarcoma cell line, SK-LC-6 and SK-LC-14 lung cell lines, SB, Raji, and Daudi lymphoblastoid cell lines, and FARR malignant melanoma cell line. In contrast, it did not affect the growth of murine L1210 cells and FS-4 normal human diploid fibroblasts. The hybridoma-derived 160 suppressor factor was selected to investigate its effect on cell-mediated cytotoxicity. The 160 suppressor factor did not inhibit natural killer cytotoxicity or its augmentation by interferon alpha or interleukin 2 or the generation of lymphokine-activated killer cells. However, this factor partially inhibited the generation of specific T cell-mediated cytotoxicity.
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PMID:Hybridoma-derived human suppressor factors: inhibition of growth of tumor cell lines and effect on cytotoxic cells. 187 5

Non-neoplastic mesenchymal cells, along with 33 benign and 87 malignant soft-tissue tumors (STT) were examined for expression of HLA-A,B,C, beta 2-microglobulin (beta 2m), HLA-DR, -DP, and -DQ molecules and the HLA-D associated invariant chain (Ii). Serial frozen sections were immunostained using monoclonal antibodies (MAbs) to monomorphic framework determinants of HLA sublocus products, beta 2m and Ii, and to CD53, a recently defined broadly distributed pan-leucocyte molecule. Compared with the normal state, an induction/neo-expression of HLA-A,B,C/beta 2m was found in a considerable number of tumors of muscle, peripheral nerve, cartilage-forming, adipose, and vascular tissues. Conversely, some tumors of fibrous origin and of autonomic ganglia showed an abnormal abrogation/loss of HLA-A,B,C/beta 2m with respect to their cells of origin. Small, round tumor cells present in various types of STT exhibited a heterogenous pattern of expression of these molecules with a preponderance of HLA-A, B,C/beta 2m-negativity. HLA-D/Ii determinants were rarely detectable in STT. Besides their expression in some fibrohistiocytic tumors, they were only occasionally found in tumors of smooth-muscle, peripheral-nerve and vascular origin as well as in one clear-cell sarcoma. In all tumors but one, there was no microtopographic association between HLA-D/Ii-positive tumor cells and inflammatory cells. CD53 allowed discrimination between dendritic interstitial cells (DIC) and neoplastic cells and additionally revealed that, in contrast to other solid tumors, STT are generally characterized by an extreme scarcity of lymphohistiocytic infiltrates. Our data indicate that, aside from very rare exceptions, aberrant induction or abrogation of MHC molecules in STT occurs in the absence of lymphohistiocytic stromal infiltrates, suggesting that these alterations might not be a consequence of local cytokine effects.
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PMID:Expression of HLA-A,B,C, beta 2-microglobulin (beta 2m), HLA-DR, -DP, -DQ and of HLA-D-associated invariant chain (Ii) in soft-tissue tumors. 222 10

We present, to our knowledge, the first extensively studied case of lymphoid L2 blast crisis of chronic myelogenous leukemia with a hand mirror cell (HMC) variant. Special stains revealed the leukemic cells to be terminal deoxynucleotidyl transferase positive by immunofluorescence and cytochemically positive for alpha-naphthyl acetate esterase and acid phosphatase (diffuse granular). Immunophenotyping identified the major leukemic cell population as B-cells that expressed CD10+, CD19+, and HLA-DR+. It was not possible to separate the HMC and the non-HMC leukemic population by gating various cell populations, dual staining, cytochemistry, or by terminal deoxynucleotidyl transferase. Gene rearrangements were observed in both Ig heavy-chain alleles and one T-cell antigen receptor gamma-subunit allele. The rearrangements occupied all of the cells, indicating that the HMC and non-HMC were of a common clonal origin. The patient had a mosaic karyotype, with 90% of the cells having t(9;22), t(8;14), and t(9;15) translocations, an additional chromosome 8, and deleted chromosomes 9 and 15. Antibodies to simian sarcoma-associated virus and baboon endogenous virus were isolated in the patient's peripheral blood plasma.
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PMID:Lymphoblastic crisis of chronic myelogenous leukemia. Hand mirror variant. 236 26

Nine human hybridoma cell lines were established from a fusion of axillary lymph node lymphocytes of a patient with breast ductal carcinoma with a human lymphoblastoid cell line. The human hybridoma nature of the fusion products was confirmed by chromosomal analysis and HLA typing. The hybridomas are stable over a year of growth, and can be frozen, thawed and regrown. The carcinoma cells of the patient harbor mouse mammary tumor virus (MuMTV) cross-reacting antigens. The patient's serum and the purified monoclonal antibodies reacted with MuMTV polypeptides. Radioimmunoprecipitation studies using labeled MuMTV confirmed the binding of the patient's serum to the viral proteins. None of the control immunoglobulins reacted with the virus. No binding of the hybridoma immunoglobulins was observed with two other retroviruses (avian myeloblastosis virus and simian sarcoma virus). The ligand binding characteristics of the monoclonal antibodies suggest binding to epitopes on the various structural virus polypeptides. These monoclonal antibodies may serve as a probe to analyze the MuMTV-human breast carcinoma relationship.
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PMID:Human monoclonal antibodies derived from lymph nodes of a patient with breast carcinoma react with MuMTV polypeptides. 302

Human T cell clones cytotoxic for autologous sarcoma cell lines have been developed from patient JM with an osteogenic sarcoma, and from patients EG and RM with malignant fibrohistiocytoma. These clones were derived from the cocultivation of peripheral blood lymphocytes (PBL) with the respective patient's autologous irradiated established tumor cell lines (AIT). After two cycles of stimulation for 5 days in bulk culture, these "educated" lymphocytes were seeded at a density of 1 X 10(6) cells/well in 24-well plates and were cultured in the presence of highly purified natural IL 2 and AIT, the latter serving as a feeder layer. Cell numbers were reduced from the initial seeding density by one log each week until reaching a density of 10(2) cells. These cells were found to be stable in viability and cytotoxic activity, after which limiting dilution was then performed. Within 4 to 6 wk, clones were isolated with unique specificities. These clones were capable of proliferating to a total density of 10(9) cells/ml and maintained their specific cytotoxicity for more than 6 mo. Testing with a panel of target cells of various histotypes, cold-target inhibition assays, and blocking of cytotoxicity with anti-HLA monoclonal antibodies showed that the T cell clones recognize a common sarcoma-associated antigen and that the lysis is HLA restricted. Phenotypically, cytotoxic clones derived from JM were Leu-1+, Leu-2+, and Leu-3-, whereas those derived from EG exhibited either Leu-24 or Leu-3+ markers, the latter phenotype lacking cytotoxicity. RM exhibited mainly Leu-3+ clones with strong cytotoxicity. All were HNK-1- and HLA class II+, with less than 1% of cells of each clone stained by anti-TAC monoclonal antibody. The clones from each patient did not lyse autologous or allogeneic PBL, mitogen-induced T lymphoblasts, normal fibroblasts, cells isolated from benign neoplasms, carcinoma cells, Daudi B lymphoid cells, or K562 cells. With the exception of EG, all clones produced immune interferon in a range from 12 to 50 U/ml. The generation of long-term specific T cell clones can be used to further dissect the cellular immune response to sarcomas. Cytotoxic T cell clones have potential application for tumor immunotherapy.
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PMID:Cellular immune response to human sarcomas: cytotoxic T cell clones reactive with autologous sarcomas. I. Development, phenotype, and specificity. 309 88

A case of recurrent Hodgkin's disease of the "sarcomatoid" or "syncytial variant" type was seen that occurred as an extension from the mediastinum to a previously uninvolved extranodal site (breast) and pericardium after treatment of classical nodular sclerosing Hodgkin's disease based in the lymph nodes. This histologic variant was composed of sheets of large, undifferentiated neoplastic cells with few, if any, diagnostic features of nodular sclerosing Hodgkin's disease. For this reason, the differential diagnosis of this variant was difficult and included non-Hodgkin's lymphoma (peripheral T-cell lymphoma), Ki-1-positive lymphoma, medullary carcinoma, metastatic carcinoma, melanoma, and granulocytic sarcoma. Immunologic analysis by immunoperoxidase technique showed a phenotype consistent with "syncytial variant" Hodgkin's disease: Leu-M1+, Ki-1+, IL-2+, HLA-DR+, T11-, pan B-, K-, lambda-, cytokeratin-, S-100-, muramidase-.
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PMID:Recurrent "syncytial variant" of Hodgkin's disease: an immunohistologic diagnosis. 359 90

A patient undergoing marrow grafting for acute lymphoblastic leukemia from his partially HLA-mismatched sister displayed a widely disseminated immunoblastic sarcoma at autopsy. The tumor was monoclonal by immunoglobulin light-chain staining. Blot hybridization analysis, using a cloned highly polymorphic locus in human DNA as a probe, showed the tumor to be of donor-cell origin. Cytogenetic analysis also demonstrated donor-cell origin. Blot hybridization analysis demonstrated Epstein-Barr virus (EBV) genomes in the tumor. By contrast, reexamination of material from a previously reported case of a donor-type relapse showed no evidence of EBV DNA. In neither case was there evidence of cytomegalovirus DNA. This study documents the association of EBV with a malignant, monoclonal B-cell lymphoma arising in a marrow graft recipient. We conclude that DNA restriction fragment length polymorphisms can be used to prove the origin (donor or host) of neoplastic relapse following allogeneic marrow grafting. Further, cell types different from those of the original leukemia may be involved.
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PMID:A monoclonal immunoblastic sarcoma in donor cells bearing Epstein-Barr virus genomes following allogeneic marrow grafting for acute lymphoblastic leukemia. 628 64

Traditionally, heat shock proteins (HSPs) are believed to be located intracellularly, where they perform a variety of chaperoning functions. Recently, evidence has accumulated that some tumor cells express HSPs on the cell surface. The present study confirms this finding and correlates HSP72 cell surface expression, induced by nonlethal heat shock, with an increased sensitivity to interleukin-2-stimulated CD3-natural killer (NK) cells. After nonlethal heat shock, a monoclonal antibody directed against the major heat-inducible 72-kD HSP (HSP72) stains the cell surface of sarcoma cells (ie, Ewing's sarcoma cells or osteosarcoma cells) but not that of normal cells (ie, peripheral blood lymphocytes, fibroblasts, phytohemagglutin-stimulated blasts, B-lymphoblastoid cell lines) or of mammary carcinoma cell line MX-1 carcinoma cells. In this study, we show for the first time a correlation of HSP72 cell surface expression with an increased susceptibility to lysis by NK effector cells. This finding is supported by the following points: (1) HLA-disparate effector cells show similar, elevated lysis of HSP72+ heat-treated sarcoma cells; (2) CD(3-) NK cells, but not CD3+ cytotoxic T lymphocytes, are responsible for the recognition of heat-shocked sarcoma cells; (3) by antibody-blocking studies, an immunogenic HSP72 determinant, which is expressed selectively on the cell surface of heat-treated sarcoma cells could be correlated with NK recognition; (4) the reported phenomenon is independent of a heat-induced, transient downregulation of major histocompatibility complex (MHC) class-I expression; and (5) blocking of MHC class-I-restricted recognition, using either MHC class-I-specific monoclonal antibody W6/32 on the target cells or alpha/beta T-cell receptor monoclonal antibody WT31 on effector cells, also has no inhibitory effect on the lysis of HSP72+ tumor cells. Finally, our in vitro data might have further clinical implications with respect to HSP72 as a stress-inducible, sarcoma-specific NK recognition structure.
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PMID:CD3- large granular lymphocytes recognize a heat-inducible immunogenic determinant associated with the 72-kD heat shock protein on human sarcoma cells. 763 45


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