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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated in vitro lymphocyte-mediated cytotoxicity against the T24 transitional carcinoma cell line and a control melanoma cell line (H894) in a double-blind study involving 25 bladder cancer patients, 19 patients with non-transitional carcinoma and 9 patients with benign conditions using a tritiated proline-labeled tumor cell assay. We found selective reactivity against T24 cells in 16 per cent of bladder cancer patients, 11 per cent of patients with non-transitional cell tumors and 22 per cent of patients with benign conditions. We found no significant differences with respect to the patterns of cytotoxic reactivity among the various patient groups. The use of different methods of lymphocyte purification and different lymphocyte to target cell ratios did not enhance the degree of specificity observed. Prior exposure to alloantigens did not account for the lack of specificity.
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PMID:Lack of specificity of lymphocyte-mediated cytotoxicity against the bladder cancer cell line, T24. 33 Aug 85

Alveoli and ducts isolated from virgin rat mammary glands synthesize basement membrane collagen (typeIV) in primary culture. Using purified antibodies to type IV collagen, prominent intracellular and extracellular fluorescence is observed in the epithelium. No fluorescence is observed with antibodies to collagen type I and III. From quantitation of the incorporation of [14c]proline-labeled proteins, 1.5 to 2.5 per cent of the newly synthesized proteins are collagen. Type IV collagen from these cultures was biochemically identified on the basis of (1) the high ratio of labeled 3-hydroxyproline to 4-hydroxyproline (1:10), (2) the gel electrophoretic pattern of the collagenase-sensitive proteins precipitated with 1.7 M NaCl, (3)the failure of the collagen to bind to diethylaminoethyl-cellulose, and(4)the immunologic cross-reactivity with mouse tumor type IV is identical with that of type IV collagen from other sources. When the supportive hormones, insulin, prolactin, hydrocortisone, progesterone, and estradiol are removed from the cultures, there is a 90 per cent reduction in the amount of [3H]proline recovered in collagen synthesis coincides with only a 30 percentdrop in the growht rate and a 20 per cent drop in total protein synthesis of the sells over the 24-hour period without hormones. Pulse-chase experimout hormones. Pulse-chase experiments revealed an enhanced turnover of collagen following hormone withdrawal. This system may be an in vitro model of collagen turnover in mammary gland in involution.
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PMID:Hormonal requirements for basement membrane collagen deposition by cultured rat mammary epithelium. 39 Feb 39

Peripheral blood lymphocytes from 32 patients with malignant melanoma were tested for cell-mediated cytotoxicity (CMC) against cultured autologous melanoma cells. Effector cells were prepared from venous blood by defibrination, gel sedimentation, nylon column filtration, and lysis of remaining erythrocytes with NH4Cl. Melanoma cells prelabelled with [3H])proline were used as target cells in a 40-h assay and CMC was evaluated against standards obtained with blood lymphocytes from the least reactive normal donor. Reproducible autologous CMC was detected in 18 of 32 patients in a series of 367 total tests. CMC correlated with tumor volume (5-500 cm3) but not with tumor stage or DNCB reactivity. Preliminary results indicated that autologous CMC was not affected by treatment with DTIC, dexamethasone, intralesional BCG, radiation therapy, or partial surgical excision. Lack of consistent CMC in 14 patients could not be attributed to a measurable decrease in general immune capacity or to increased resistance of the patients' melanoma cells to CMC in general. Fibroblasts were more resistant to CMC than melanoma cells, and therefore of questionable value for defining specificity in direct tests.
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PMID:Cell-mediated cytotoxicity for cultured autologous melanoma cells. 47 90

Cells separated by enzyme treatment of the R3230AC mammary carcinoma were used to characterize the entry of proline. These cells showed minimal changes in cell viability and intracellular volume and were found to be suitable for transport studies, since the vi of proline was maintained for at least 4 h when cells were stored at 37 or 4 degrees C, or when transport was measured in the presence or absence of Na+. Proline was acitvely transported by these tumor cells, reaching a distribution ratio ([proline] intracellular/[proline] extracellular) of 20 after 2 h. Proline entry consisted of two processes, one saturable (carrier mediated) and the other, non-saturable. The carrier-mediated entry, Km - 0.83 mM and V = 151.10(-5) mumol/min per 5.10(6) cells, was Na+-dependent, sensitive to pH and metabolic inhibitors, and completely inhibited by alpha-(methylamino)-isobutyric acid (Ki = 0.34 mM). Proline entry in the absence of Na+ was 20% that in the presence of Na+ and was found to be due to a non-saturable process, since (a) vi of proline uptake in the absence of Na+ increases linearly with increasing proline concentration and (b) was not suppressed by either 20 mM alpha-(methyl-amino)-isobutyric acid, 50 mM glycine +20 mM phenylalanine, or 50 mM serine +20 mM phenylalanine when proline uptake was measured in the presence or absence of Na+. Therefore, under the conditions studied, we conclude that proline transport appears to be restricted to the A (alanine-preferring) system. Furthermore, these cells should provide a suitable model to study the effect of hormonal manipulations on the amino acid transport process.
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PMID:Characteristics of proline transport into R3230AC mammary tumor cells. 63 48

An ovarian cystadenocarcinoma-associated antigen (OCAA) was found to be common to all serous and mucinous cystadenocarcinomas of the ovary. It was apparently absent in tissues of normal reproductive organs. Furthermore, OCAA was not detected in benign ovarian serous and mucinous cyst-adenomas or in any other gynecologic or nongynecologic cancers thus far tested. The antigenic determinant of OCAA was immunologically unrelated to the carcinoembryonic antigen, other known tumor antigens, or the histocompatibility antigens. We purified and partially characterized OCAA. The antigen was a high-molecular-weight glycoprotein soluble in 0.6 M perchloric acid. It consisted of about 50-60% protein (based on dry wt). Amino acid composition in OCAA was characterized by a high percentage of threonine, serine, proline, and valine. Galactose and N-acetylglucosamine were the principal carbohydrate constituents. The antigenic activity was resistant to treatment with trypsin and protease and also to treatment with DNase, RNase, and N-acetylneuraminidase. The antigenicity was considerably reduced by mild periodate oxidation.
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PMID:Tumor-associated antigen for cystadenocarcinomas of the ovary. 82 81

We compared three ddifferent isotopic assays of cell-mediated cytotoxicity under identical test conditions: 51Cr, 125iododeoxyuridine, and [3H]proline release assays. We made these comparisons both in a syngeneic mouse tumor system and an allogeneic system. It was found that several parameters could affect considerably the results obtained with these tests, such as: baseline controls, preparation of target cells, and methods of calculation. In comparison of three different baseline controls, the normal control gave the most consistent results, whereas the other two controls (autologous and medium controls) gave varying results depending upon the condition of the target cells. For use as target cells, established tissue culture cells were usually superior because of a much lower spontaneous release of the isotope, when compared to fresh ascites tumor cells or short-term tissue culture cells. The advantage of established culture cells was particularly noted in isotopic assays with prolonged incubation (20-40 hr). In addition, the methods used for calculation were also shown to affect the apparent outcome of the results.
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PMID:Comparison of three isotopic assays of cell-mediated cytotoxicity against mouse tumor cells. I. Basic parameters: baseline controls, target cells, and methods of calculation. 83 80

Three assays of cell-mediated cytotoxicity in mice, involving release of either 51Cr (CRA), 125iododeoxyuridine (IRA), or [3H]proline (PRA), were compared under identical test conditions. Experiments were performed with effector cells from mice immunized with FBL-3 tumor cells, a syngeneic Friend virus-induced leukemia, or with allogeneic normal spleen cells. With established tissue culture cells as targets, similar results were obtained in all three assays. The cytotoxicity produced by cells from in vivo-immunized mice and the induction of cytotoxicity in vitro were T-cell-dependent. When short-term culture target cells were used, the IRA gave a more selective pattern of cytotoxicity than did the other two assays. However, when remaining target cells at the end of the assay were treated with trypsin, higher levels of 125iododeoxyuridine (125IUDR) release were seen, and the results were then comparable to those in the CRA and PRA. These results indicated that 125IUDR, a nuclear label, could only be released after lysis of cells. In contrast, 51Cr or [3H]proline, which are cytoplasmic labels, could also be released from damaged but unlysed cells. These fundamental differences could give different results in these assays, which could determine their correlation with in vivo transplantation immunity.
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PMID:Comparison of three isotopic assays of cell-mediated cytotoxicity against mouse tumor cells. II. Sensitivity and specificity of the assays and characteristics of effector and sensitizing cells. 83 81

The effect of surgical removal of tumors on cytotoxicity reactions was studied in Lewis-Wister inbred rats bearing a transplantable methylcholanthrene-induced sarcoma (MCI). Lymphocyte cytotoxicity and the effect of the serum in blocking (decreasing) or potentiating (increasing) lymphocyte cytotoxicity were studied using MCI tissue culture cells, prelabeled with 3H-proline, as target cells. After surgical removal of the tumors, tumor nodules were again palpable in all rats by the seventh day after surgery and regrew at an accelerated rate. In control rats bearing the MCI sarcoma, serum blocking activity appeared between the 8th and 13th days and completely inhibited lymphocyte cytotoxicity until death of the animals. Surgical removal of the tumors resulted in a decrease in lymphocyte cytotoxicity and complete absence of serum blocking activity for at least 7 days. By the 13th day, when tumors were again growing rapidly, lymphocyte cytotoxicity had increased markedly, and blocking activity again appeared in the serum.
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PMID:The effect of surgical removal of a rat sarcoma on lymphocyte cytotoxicity. 87 96

In vitro cell-mediated cytotoxicity (CMC) for [3H]proline-labeled target cells was demonstrated with the use of unfractionated populations of regional lymph node, spleen, and peritoneal cells (RLNC's, SPC's, PC's, respectively) from C57BL/6 and strain A mice. Syngeneic and allogeneic hosts were immunized sc or ip with C1300 tumor or syngeneic SPC's. The syngeneic and allogeneic host effector lymphoid cells showed various degrees of cytotoxicity for C1300 target cells 3-9 days after one immunization with C1300, whereas the effector lymphoid cells of hosts immunized with syngeneic SPC's generally showed less CMC for C1300 and frequently increased the growth of C1300 target cells when compared to C1300 targets plus media controls. Effector cells obtained from lymphoid organs in the region nearest the immunization (i.e., RLNC from sc-inoculated hosts) demonstrated significantly more CMC than did effector cells from more remote lymphoid organs. The PC's and SPC's of C1300 ip hyperimmunized allogeneic hosts produced greater CMC than did those of mice immunized once. This was not observed if syngeneic C1300 or SPC's were used as hyperimmunizing antigens. The CMC of nonimmunized host effector lymphoid cells for syngeneic labeled target cells was demonstrated.
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PMID:Immune responses to mouse neuroblastoma C1300. I. Preliminary observations on cell-mediated immune responses. 90 96

Three in vivo techniques were used to establish the specificity of tumor immunity induced after sensitization of F344 rats to syngeneic MCA-induced sarcomas: (1) post-excision resistance to tumor challenge, (2) passive tumor neutralization (the Winn test), and (3) concomitant immunity. In general, these assays revealed unique non-cross-reactive antigens associated with each of three sarcomas, FMF1, FMM2, and FMM3. However, spleen cells from tumor-sensitized rats did not demonstrate cell-mediated cytotoxicity in vitro corresponding to the specificity of tumor resistance in vivo. In the (3H)-proline cytotoxicity assay, spleen cells from FMM3 tumor-bearing rats or from FMM3 tumor-immune rats were not selectively cytotoxic for cultured FMM3 target cells. Parallel analysis of spleen cells from normal or FMM3-sensitized rats using the Winn assay and the (3H)-proline assay revealed that (1) spleen cell cytotoxicity in vitro did not correlate with effective tumor protection in vivo; and (2) normal spleen cells were cytotoxic against cultured sarcoma target cells in vitro and inhibited tumor growth in vivo. Thus, passive tumor protection by normal spleen cells in vivo corresponded with the demonstration of natural cytotoxicity in vitro, but induced specific anti-tumor reactivity was observed only in vivo.
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PMID:Immunity to MCA-induced rat sarcomas: analysis of in vivo and in vitro results. 92 92


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