Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02003 (NBT)
 1,323 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently, adoptive immunotherapy for cancer with lymphokine activated killer (LAK) cells has been widely used experimentally. The therapy has several problems, including difficulty in handling, sterilization, and time consumption. To solve these problems, new materials able to induce antitumor immune cells were investigated. Pokeweed mitogen (PWM) and PWM-conjugated materials (CMC-1) could induce strong killer cells by short-term stimulation of human peripheral blood lymphocytes (PBL). The induced killer cells showed a wide killing spectrum in vitro against human tumor cell lines (MKK-1, PRMI4788, NBT-2, ZR-7530, H-1, Hela, KB, HMV-1, PC-10, C-1). Human PBL stimulated for a short time by CMC-1 also showed a tumoricidal effect on tumor bearing (MKN-1, MKN-45) nude mice. These results suggest that CMC-1 may solve the problems with currently used LAK therapy and may provide easily applicable extracorporeal immunotherapy for cancer.
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PMID:Basic studies on a new material for inducing antitumor immune cells. 225 59

During metastatic spread, locomotion mediated by extracellular matrix components of basement membranes and connective tissues has been invoked as a prerequisite to invasion. We studied the interactions of the rat bladder carcinoma cell line NBT-II with fibronectin, laminin, and collagens (types I, III, IV, and V). They all promoted cell attachment and spreading. To analyze their scatter potential, we studied epithelial outgrowth and/or peripheral cell dispersion from tumor aggregates. All matrix components allowed partial collapse of the aggregate and the appearance of a cellular monolayer forming a halo around the aggregate. No peripheral cell dispersion occurred on fibronectin and laminin. Collagens (especially types I and III) promoted the dispersion of peripheral NBT-II cells with various speeds of locomotion, as revealed by time-lapse videomicroscopy. With the exception of cells at the periphery on collagens, cells inside the halo did not exchange neighbors, migrated transiently as an epithelial sheet during halo formation, and finally remained stationary. These effects were reproduced with NBT-II tumor fragments obtained from nude mice. Tumor cells were linked together with desmosomes (as revealed by immunoreactivity against desmoglein). Migration on collagens correlated with the mechanical disruption of intercellular contacts and consequently with the progressive disappearance of desmoglein immunoreactivity. Immunofluorescence studies also revealed a reduced expression of the epithelium-specific cell adhesion molecule liver cell adhesion molecule after contact with collagens. These results suggest that direct interactions with collagens may favor single cell infiltration by bladder carcinoma.
Cancer Res 1990 Jan 01
PMID:Collagen-mediated dispersion of NBT-II rat bladder carcinoma cells. 229 46

A new cell line DEL, established in vitro, was isolated from a pleural effusion of a boy who died of malignant histiocytosis. Its principal characteristics are: strong positivity with monoclonal antibodies (MAbs) to CD25, CD30, CD45R, KiM7, EMA, HLA Cl I and II; constant presence of acid phosphatase, ANAE, alpha-anti-trypsin, alpha-anti-chymotrypsin and NBT reductase activity; rearrangement of the immunoglobulin heavy-chain gene (JH) and a germ-line configuration of the T-chain gene; and finally a translocation between chromosomes 5-6 with a breakpoint in 5q35. The DEL cell line is appropriate for studying the role of the 5q localized c-fms oncogene and of the genes of the mononuclear phagocyte growth factor (CSFI) and of their receptors in the dynamics and etiology of malignant hemopathies associated with a 5q35 breakpoint.
Int J Cancer 1990 Mar 15
PMID:DEL cell line: a "malignant histiocytosis" CD30+ t(5;6)(q35;p21) cell line. 230 42

The reduction of nitrotetrazolium blue with stimulated and unstimulated granulocytes was performed in 40 patients with breast cancer. Blood was collected from peripheral vein before surgical intervention, during surgery from vein draining of tumor, two weeks after surgery and three months after surgery when radiotherapy was finished. In parallel experiments the NBT test was made in the peripheral blood of 20 healthy individuals. We have observed decreased reduction of nitrotetrazolium blue in stimulated granulocytes, which may indicate that granulocytes from these patients are unable for efficient stimulation. No evident effect concerning the advancement of disease and applied therapy could be found. The importance of determining the NBT test in cancer patients is briefly discussed.
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PMID:Nitroblue tetrazolium test in patients with breast cancer undergoing mastectomy and radiotherapy. 241 Mar 39

Two distinct mechanisms by which bladder carcinoma cells of the NBT-II cell line dissociate and migrate away from an in vitro reconstituted epithelial sheet were examined as regards intercellular adhesion and cell locomotion. Scattering of NBT-II bladder carcinoma cell line was promoted by 2 distinct culture protocols: (i) deposition of some components of the extracellular matrix onto the culture substratum (glass or plastic) induced cell dispersion of the epithelial sheet of carcinoma cells, and (ii) addition of Ultroser G, a serum substitute, to the culture medium induced scattering and acquisition of motility of NBT-II cells. Under both culture conditions, NBT-II cells dissociated, lost their epithelial morphology, acquired fibroblastic shape and migrated actively. We show that, among different extracellular matrix proteins, only collagens were able to promote the transition towards fibroblastic phenotype (referred as epithelium-to-mesenchyme transition or EMT). Furthermore, the native 3-dimensional helical structure of collagens was required for their function. During induction of EMT of NBT-II cells with Ultroser G, the junctions between epithelial cells were split, polarized epithelial cell organization was lost, and the resulting individual cells became motile and assumed a spindle-like fibroblastoid appearance. Using immunofluorescence microscopy techniques, we demonstrate that this change is accompanied by redistribution of desmosomal plaque proteins (desmoplakins, desmoglein, plakoglobin) and by reorganization of the cytokeratin and the actin-fodrin filament systems. Intermediate-sized filaments of the vimentin type were formed de novo in the fibroblastoid cell form. The observed transition towards fibroblastic phenotype (epithelium-to-mesenchyme transition or EMT) was fully reversed by removing the inducing factors from the culture medium, as shown by the disappearance of vimentin filaments and the reappearance of desmosomes in the newly formed epithelial cells.
Int J Cancer Suppl 1989
PMID:Reversible transition towards a fibroblastic phenotype in a rat carcinoma cell line. 250 87

Cytosine-arabinoside (ARA-C) in low doses induces complete remissions in myelodysplastic syndromes and acute leukemia. Evidence is accumulating that these remissions are not reached by differentiation induction but through cytotoxicity. In HL60 cells differentiation was measured by a comprehensive panel of quantitative and qualitative markers of maturation. After exposure to ARA-C (10(-7) M) for 4 days HL60 cells did not mature morphologically. Cell volume increased. The increase in esterase activity was small and did not reach the amount measured in normal monocytes. There was no significant difference in latex phagocytosis and NBT reduction between cultures with and without ARA-C. HL60 cells were arrested in S-phase and clonogenic capacity persisted. The observed changes after exposure to ARA-C seem to be caused by impeded cell division while synthesis of protein continues. We conclude that ARA-C in low dose exerts its effect by halting proliferation through cytotoxic effects and not by differentiation induction.
Eur J Cancer Clin Oncol 1989 Nov
PMID:Low dose cytosine-arabinoside has only minimal differentiation inducing capacity in HL60 cells. 259 48

One of the major problems with cancer chemotherapy is the development of drug resistance during treatment. Two mechanisms are considered as the cause of drug resistance, natural and acquired. It is now considered that cancers can be composed of multiple clonal subpopulations of cancer cells. In this study, we separated three clones (C1, C3 and C8) from NBT-2 (human bladder cancer cell line) by limiting dilution. We examined the growth rate and the transplantability to nude mice and performed chromosomal analysis of three clones. The doubling time of C1 is 22 hours, and those of C3 and C8 were 25 and 36 hours, respectively. Each clone was transplantable to nude mice, but we could not find out any histological difference among them. The chromosome numbers of C1 was 66, and those of C3 and C8 were 68 and 63, respectively. We could also find out karyotypic difference among them. We could therefore consider that these three clones had different biological features and studied the difference in drug sensitivity among these three clones and the parent cell line. Cells (1 x 10(4)/well) were incubated in microplates with ten different chemotherapeutic agents for 72 hours. Then 3H-thymidine (1 microCi/ml) was added to each. After 24 hours, cells were harvested and the uptake of 3H thymidine was counted with a liquid scintillation counter. According to the reaction pattern, these chemotherapeutic agents were divided into three groups. 1. The radio isotope uptake of three clones and parent cell line was proportionally inhibited by increasing the drug concentration (carboplatin, (glycolato-o, o-) diammine platinum (II), ifosfamide).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The analysis of the difference in anti-cancer drug sensitivity of 3 clones separated from bladder cancer cell line]. 262 19

Serum ferritin levels are often elevated in patients with certain cancers and these elevations are, in part, derived from the tumors. In such patients, the increased levels of serum ferritin are associated with a poor prognosis. This association may be explained in part by biological effects of ferritin on lymphocytes: inhibition of E-rosette formation, masking of cell surfaces and suppression of lymphocytes' response to mitogens in vitro. The authors hypothesized that ferritins from tumor tissues also exert adverse effects on human granulocytes that are involved in tumoricidal activity. Three granulocyte functions were tested: nitroblue tetrazolium test, phagocytosis, and production of hydrogen peroxide. The results supported the authors' hypothesis: NBT reduction and phagocytosis are decreased in granulocytes exposed to ferritins, more so with tumor ferritins, than normal ferritin, and H2O2 production is less in granulocytes previously exposed to ferritins from tumor and nontumor tissues than cells not exposed to ferritins. However, the inhibitory effects of ferritins on H2O2 production can be reversed if granulocytes are further stimulated by phorbol myristate acetate (a membrane stimulant). If the elevated serum ferritin in cancer patients impairs granulocyte functions, in vivo, then it may increase the risk of infection, decrease tumoricidal host responses, and, thereby, contribute to the poor prognosis of these individuals.
Cancer 1989 Jun 15
PMID:Effects of isoferritins on human granulocytes. 272 May 99

The paper discusses the status of polymorphonuclear neutrophils (PMN) in untreated patients with stage III and IV lung and stomach cancer. Pronounced increase in peripheral blood neutrophil count was matched by decrease in the level of leukocyte cationic proteins. In vitro cytotoxic activity of PMN against K-562 cells was significantly higher in cancer patients, as compared to healthy controls, and unaccompanied by reaction of neutrophils to stimuli. NBT-test value variation range appeared wider in cancer patients than in controls.
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PMID:[Neutrophil granulocyte function in patients with malignant neoplasms]. 272 83

Three human T-cell clones with activated killer activity (5B5, 5C1, and 7B5) which could lyse various tumor cell lines were established. The cytotoxic activity of these clones was decreased by incubation with anti-CD3 monoclonal antibody, suggesting that they recognized tumor cells by T-cell antigen receptor. A monoclonal antibody which blocked the cytotoxic activity of clone 5B5 was obtained. This antibody (N1977) blocked the binding and cytotoxic activity of clone 5B5 at the target cell level, suggesting that the antigen defined by N1977 antibody, designated as ATM-1, was a target molecule recognized by 5B5 cells. ATM-1 in the conditioned medium of a cancer cell line (NBT-2) and serum from a patient with lung cancer was characterized by following its immunoreactivity. On gel filtration, both the conditioned medium and the serum gave three peaks of ATM-1 immunoreactivity, corresponding to approximate molecular weights of 1,200,000, 700,000, and 120,000, respectively. They were chromatofocused at pH 4.0, 4.8, and 6.5, respectively. The high molecular weight forms were shown to be molecules with the disulfide-linked elementary glycoprotein with ATM-1 immunoreactivity and approximate molecular weight of 120,000. Most of the molecules with ATM-1 immunoreactivity bound to both concanavalin A and wheat germ agglutinin, and their binding activity to the antibodies was lost by treatment at 60 degrees C for 30 min. An assay of ATM-1 level in sera was performed by a sandwich enzyme immunoassay. The following positive percentages were obtained from preliminary clinical studies: breast cancer, 67% (8 of 12 cases); hepatocellular carcinoma, 83% (10 of 12 cases); gastric cancer, 58% (7 of 12 cases); lung cancer, 41% (5 of 12 cases); hematological malignancies, 0% (0 of 9 cases); systemic lupus erythematosus, 0% (0 of 8 cases); rheumatoid arthritis, 0% (0 of 8 cases).
Cancer Res 1988 Sep 01
PMID:Identification of a tumor-associated target antigen, ATM-1, for a human T-cell clone with activated killer activity and its existence in sera of cancer patients. 304 79


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