Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical significance of radioreceptor assay for transferrin receptors of human cancerous tissues was evaluated. Fresh surgical specimens from various carcinoma tissues were solubilized with 1% Triton X-100 and the extracts were mixed with 125I-labelled diferric transferrin. The free transferrin and the receptor-bound transferrin were separated by 15% polyethylene glycol precipitation. The % specific transferrin binding to gastric, colonic, lung and mammary carcinoma tissues ranged between 3.9 and 13.9%, whereas those for normal stomach and colon were less than 2%. The concentrations of transferrin receptors in these cancerous tissues ranged between 3.7 and 28.3 pmole/g tissues. It was concluded that the amounts of transferrin receptors were significantly increased in all of the tumor tissue extracts examined and may thereby provide a useful marker for the diagnosis of malignancies.
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PMID:Transferrin receptors in human cancerous tissues. 343 81

The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) irreversibly dissipates the electrical potential difference (PD) across LLC-PK1 renal epithelial cell sheets in a dose-dependent manner. The promoter is equally effective when presented to either cell surface. TPA is also equally effective at dissipating the apical-negative PD or the heretofore undescribed apical-positive PD, both of which can exist spontaneously across this monolayer. Diffusion potentials arising from imposed NaCl gradients across LLC-PK1 cell sheets are likewise reduced by TPA. The non-tumor-promoting parent compound, phorbol, is ineffective, but the more hydrophilic TPA analogue, phorbol 12,13-dibutyrate (PDBU) is as effective as TPA. Unlike TPA, the effects of PDBU are reversible. By observing the (paracellular) fluxes of D-mannitol and polyethylene glycol, these effects on PD are shown to be due to increased permeability of the tight junctions. This effect is immediately reversible once PDBU is removed. These findings are discussed in light of the ramifications of the breakdown of epithelial compartments in vivo and the role this could play in the regulation of epithelial cell growth.
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PMID:Effects of tumor promoters on LLC-PK1 renal epithelial tight junctions and transepithelial fluxes. 346 17

The Dunning R3327 tumor represents a system for studying prostate cancer in Copenhagen X Fischer rats. Animals bearing variant sublines (H, G, and MAT-LyLu) differing in growth rate, differentiation, hormone responsiveness, and metastatic ability were assayed for three immunological markers. Spleens were passed through a tissue sieve, and mononuclear cells were obtained by Ficoll-Hypaque centrifugation. These were assayed for leukocytic subsets using monoclonal antibodies. An adherent population was isolated and evaluated using thin-layer chromatography for conversion of radiolabeled arachidonic acid to E series prostaglandins. Finally, sera from these animals were assayed for levels of circulating immune complexes using polyethylene glycol precipitation. Data from 52 rats bearing the various tumors were obtained, correlated with subline aggressiveness, and compared to 15 controls. Each tumor group demonstrated significantly lower helper/suppressor T-cell ratios than controls, probably due to general tumor presence. In addition, the most aggressive R3327 MAT-LyLu variant had significantly increased prostaglandin E synthesis by adherent spleen cells compared to the H or G sublines and significantly increased levels of circulating immune complexes relative to the H subline. G subline values for both prostaglandin E and circulating immune complexes levels were intermediate, suggesting that these markers correlate better with tumor aggressiveness than helper/suppressor T-cell ratios.
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PMID:Immunoregulatory markers in rats carrying Dunning R3327 H, G, or MAT-LyLu prostatic adenocarcinoma variants. 349 74

The ability of a purified major histocompatibility antigen to serve as the target cell antigen for alloreactive CTL (H-2d anti-H-2k) was examined. Tumor cells syngeneic with responding CTL were used as targets following modification with purified alloantigen (H-2Kk). A short incubation of tumor cells with H-2Kk liposomes followed by the addition of polyethylene glycol (PEG) yielded modified tumor cells that were recognized and lysed by CTL. The macrophage-like cell line P388D1 was readily recognized following liposome and PEG modification; apparently because these cells can withstand PEG mediated insertion of H-2Kk and lipid into their membrane. The generation of targets by PEG mediated modification was most efficient using liposomes prepared with an H-2Kk:lipid ratio of about 1:500. H-2Kk containing liposomes prepared with negatively charged phospholipids readily attached to P388D1 cells, however these cells were not targets for CTL unless PEG was added. The specificity of CTL recognition and lysis of liposome modified cells was shown by the reactivity of CTL primed against alloantigens other than H-2Kk and by antibody (anti-H-2Kk) blocking of recognition and lysis. These results demonstrate that purified H-2Kk can serve as the alloantigen for CTL lysis and suggest that the H-2 must be oriented in the target cell lipid bilayer to serve as the alloantigen for CTL mediated target cell lysis.
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PMID:Generation of targets for alloreactive CTL using purified H-2Kk in liposomes and polyethylene glycol. 349 26

Cytotoxic human T cells from different sources were fused with different types of human T-lymphoma cells and mouse B-myeloma cells using variations of the polyethylene glycol (PEG) method and electrofusion. Both techniques yielded proliferating hybridomas. The frequency of wells with proliferating hybridomas depended on the tumor fusion partner used; the best results were obtained with HSB-1, whereas fusions with JURKAT-1 and HPB-1 did not yield any hybridomas. For one tumor cell line (HSB-1), considerably more hybridomas were obtained with electrofusion than with the PEG fusion (with or without heat shock). There was no consistent relationship between the presence or absence of cytotoxic activity of the T lymphocytes against the tumor fusion partner and the yield of hybridomas. In human-human as well as in human-mouse hybridomas most of the lymphocyte derived chromosomes were lost. Four of the more than 600 hybridomas tested showed transient cytotoxic activity, but in none of them this function could be immortalized. Two of the hybridomas obtained with CEM-1 as tumor fusion partner expressed low levels of lymphocyte-derived CD3 antigens. Two hybridomas obtained with HSB-1 were highly invasive in vitro in rat hepatocyte cultures, whereas HSB-1 tumor cells were not.
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PMID:Efforts to produce human cytotoxic T-cell hybridomas by electrofusion and PEG fusion. 349 59

Human lymphocytes obtained from regional draining lymph nodes of patients with cancers of the cervix, kidney, prostate, and vulva were immortalized by polyethylene glycol-mediated somatic cell hybridization with either human UC 729-6 or murine P3-NS-1-Ag4-1. Four reactive human IgM-secreting hybridomas, termed CLNH5, MHG7, VLN1H12, and WLNA67 were isolated and characterized. Hybrids obtained by fusions with UC 729-6 have remained tetraploid for over 18 months, have doubling times from 25-35 hours, and have continuously secreted approximately 0.5-5.0 micrograms IgM/10(6) cells/ml per day. MHG7, a mouse-human hybrid, required subcloning every 4-6 months to maintain human IgM secretion. Binding of these human monoclonal antibodies (MoAbs) against a panel of cell lines was assessed by an enzyme-linked immunoassay (EIA). CLNH5 reacted with carcinomas of the cervix, lung, and vulva. MHG7 reacted with carcinomas of the prostate, stomach, and vulva. VLN1H12 reacted with carcinomas of the cervix, lung, prostate, stomach, and vulva. WLNA6 reacted strongly with a carcinoma of the lung. All four human MoAbs failed to react by EIA with hematopoietic cells or normal fibroblast cell lines. The data suggest that regional draining lymph nodes of cancer patients have been primed to produce antibodies against antigens associated with tumor cells and that UC 729-6 served as a genetically suitable vector for the capture and immortalization of these Ig-secreting B lymphocytes.
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PMID:Genetically stable human hybridomas secreting tumor-reactive human monoclonal IgM. 350 29

Thirty-seven dogs with malignant lymphoma were treated with either polyethylene glycol conjugated (PEG) asparaginase alone (10-30 IU/kg intraperitoneally [IP] weekly--20 dogs) or PEG-asparaginase combined with one cycle of chemotherapy (vincristine, cyclophosphamide, methotrexate, and prednisone), followed by maintenance PEG-asparaginase (30 IU/kg, IP weekly--17 dogs). In the 20 dogs (eight were chemotherapy resistant) treated with PEG-asparaginase alone, seven had a complete response (CR), seven had a partial response (PR), five had no response (NR), and one was not evaluable (NE). The duration of response (CR + PR) ranged from 14 to 102 days (median, 48 days). In the eight chemotherapy-resistant dogs (seven were previously resistant to L-asparaginase) four had responses (one CR and three PR). In the 17 dogs treated with combined PEG-asparaginase and chemotherapy, 13 had a CR, two had a PR, and two had NR. None of the dogs had had prior chemotherapy, and the duration of response (CR + PR) ranged from 7 to 840+ days, with a median of 126+ days. Four dogs are still on maintenance PEG-asparaginase at 16+, 21+, 26+, and 28+ months. Toxicity consisted of death due to massive tumor breakdown (two dogs), disseminated intravascular coagulation (DIC--one dog), hypersensitivity reaction (one dog), vomiting (three dogs) and soft stools (three dogs). Four normal dogs were given very high doses of PEG-asparaginase (200 IU/kg and 1200 IU/kg) once weekly for two treatments without any significant toxicity. These results indicate that PEG-asparaginase has antitumor activity in dog with spontaneously occurring malignant lymphoma.
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PMID:A preliminary study on the evaluation of asparaginase. Polyethylene glycol conjugate against canine malignant lymphoma. 356 63

We evaluated the ability of repeated measurements of circulating immune complexes (CIC) to predict for tumor recurrence in 130 patients with malignant melanoma. Twenty-two patients had level 2, 45 had level 3, and 51 had level 4/5, stage I disease in remission at the start of monitoring, while 12 had stage II disease. The polyethylene glycol precipitation assay was used for serial studies, based on an initial comparative evaluation with the Clq-binding and Raji assays. The study averaged 22 +/- 11 months (6-43 months) and an average of 22 +/- 5.3 assays were performed per patient (range 3-36), with a follow-up of 4 years. CIC were present in sera in recurrent, irregular 'bursts' of activity. Serial measurements doubled the incidence of CIC compared to single determinations. Only 23% of these bursts of activity were clearly related temporarily to documented recurrences, while 34% occurred with treatment events such as surgery or immunotherapy, and 42% occurred without correlation to either recurrence or treatment. CIC activity was greater and more closely related to recurrence in high-risk stage I (level 4,5) and stage II patients. Whether analyzed as positive sera or as bursts of elevated CIC activity, CIC assays predicted for recurrence at the 5% significance level. The assay was highly sensitive (97%), but with poor specificity (21%) with many false positives (79%). The assay was helpful at ruling out recurrences (95%), but poor at ruling them in (29%). The advantage was seen only in high-risk stage I and II patients, and there was no advantage to serial assays over random single determinations. Although generally, CIC in the sera of melanoma patients were found to predict for recurrence, the use of serial CIC measures monitoring of individual patients cannot be recommended.
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PMID:Circulating immune complexes in malignant melanoma: serial studies in 130 patients. 370 59

An ouabain- and 6-thioguanine-resistant mutant (K3T103) of the metastatic MDAY-D2 murine tumor cell line was transplanted s.c. into syngeneic DBA/2 mice in order to isolate K3T103 X host cell hybrids emerging in vivo, and examine their metastatic potential. Of 10 tumor-bearing animals that were analyzed at various time intervals, only 3 developed fusion products in the primary site, present at a frequency ranging between 10(-5) and 10(-4). These hybrids survived in HAT + ouabain medium, had a lymphoblastoid morphology and a hypo-tetraploid karyotype, were non-adherent, and were as rapidly metastatic as K3T103 cells when transplanted s.c. or i.v. into DBA/2 mice. All these characteristics were shared by cloned hybrids generated in vitro following polyethylene glycol (PEG)-mediated fusion of K3T103 cells with normal DBA/2 normal splenocytes. In marked contrast, the products of K3T103 X DBA/2 normal lung fibroblast fusion displayed a fibroblastic appearance, were adherent, progressively ceased to divide and remained dormant for several weeks in culture. These results indicate: that spontaneous fusion of K3T103 cells with host cells in the course of their expansion and subsequent dissemination is a stochastic and rare event, and that since the expression of their tumorigenic and metastatic potential is retained after fusion with splenocytes, host cells of lymphoreticular origin are most likely involved in that process.
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PMID:Sporadic somatic fusion between MDAY-D2 murine tumor cells and DBA/2 host cells: role in metastasis. 371 Jun 19

A double antibody enzyme-linked immunosorbent assay (ELISA) was developed to quantitate circulating immune complexed IgA (IgA IC) in human serum. The serum panel for this study consisted of normal blood donors, benign surgery (BS), head and neck cancer (HN), nasopharyngeal carcinoma (NPC), lung cancer (LC), and colon cancer (CC) patients. Immune complexes (IC) were isolated from these sera by precipitation with 3.5% polyethylene glycol (PEG), washed and then redissolved in 0.1 M phosphate-buffered saline pH 7.2. The amount of IgA IC present were then quantified using the double antibody IgA ELISA. This assay was found to be both sensitive (26.0 ng/ml) and reproducible (intra-assay coefficient of variation 4.0%). The mean IgA IC for each cancer group tested (HN = 11.38 +/- 12.54 micrograms/ml; NPC = 13.36 +/- 17.56 micrograms/ml; LC = 17.39 +/- 13.04 micrograms/ml; CC = 26.50 +/- 4.60 micrograms/ml) were significantly elevated (P = 0.001) over both the normals (5.12 +/- 4.09 micrograms/ml) and the benign surgery controls (5.92 +/- 5.04 micrograms/ml). In addition to providing a new tumor marker the presence of high levels of IgA IC in cancer patients could provide a source of tumor-specific antibody as well as antigen and provide reagents to study immune regulation in cancer patients.
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PMID:Circulating IgA immune complexes in head and neck cancer, nasopharyngeal carcinoma, lung cancer, and colon cancer. 382 45


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