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Biomedical subjects

M Zöller

Publications and source records attributed to M Zöller.

At least 163 records · Page 9Linked to original sources
PubMed1980

Organ-related and malignancy-associated reactivity of cancer patients' leucocytes: a leucocyte migration study with tumour and foetal extracts.

Leucocytes from patients with a variety of tumours including gastric, colorectal, lung, kidney and mammary cancer, were tested in the leucocyte migration test (LMT) against organ-related and non-organ-related tumour and foetal extracts. The reactivity of cancer patients' leucocytes against a panel of organ-related tumour extracts was found to be 71-93%, depending on the tumour system tested. Cross-reactivity with a panel on non-organ-related tumour extracts was found in 0-38% of patients. Corresponding patterns of reactivity were obtained by testing patients' leucocytes against human foetal organ extracts; pathological migration indices (MI) were found in 70% of tests in which patients' leucocytes were reacted with organ-related extracts, and in 16% of tests with non-organ-related extracts. The data strongly support the concept that patients' leucocytes are sensitized to cross-reactive foetal determinants of organ-related specificities. Furthermore, it is proposed that foetal extracts as inducers of lymphokine production in presensitized lymphocytes could be used efficiently and reproducibly as a source of foetal antigen, as well as in the clinical application of the LMT procedure.

Adult↗
PubMed1980

Lack of correlation between carcinoembryonic antigen content of tumor extracts and leukocyte migration reactivity of tumor patients.

Tumor extracts varying in carcinoembryonic antigen (CEA) content (0.4--2,280 ng/mg protein) did not affect the reactivity of cancer patients' leukocytes in the leukocyte migration inhibition test (LMIT). In addition, variations in the plasma CEA levels of tumor-bearing leukocyte donors did not influence the frequency of significant LMIT reactivity.

Adenocarcinoma↗
PubMed1980

Specific cytotoxicity in vitro by T-cell-enriched lymphocyte subpopulations from rats bearing chemically induced but not spontaneous tumors.

Effector cells from inbred BD X and WAB rats bearing either spontaneously arising or chemically induced tumors were cytotoxic for target cells of both kinds of tumor. The level of cytotoxicity of tumor-bearing animals regularly surmounted that of natural cytotoxicity observed in age-matched untreated controls. These findings were obtained by a visual-countin microcytotoxicity assay (48 hr) and by a 51Cr label assay (12 hr). Cytotoxicity by tumor-bearing rat effectors was directed against the homologous tumor target cell line, different tumor cells of the same inbred rat strain, tumor cells derived from allogeneic rats, and fetal fibroblasts, but not against adult fibroblasts. Separation of lymphocytes by rosetting with sheep red blood cells (SRBC) loaded with either antiimmunoglobulin or anti-SRBC or with anti-SRBC and complement revealed that cross-reactive cytotoxiciy was confined to a non-T effector cell population, which was observed with lymphocytes from rats bearing either chemically induced or spontaneous tumors. Cytotoxicity directed exclusively against the tumor of the lymphocyte donors was exerted by the T-cell-enriched fraction. This element was completely absent in lymphocytes from animals bearing spontaneous tumors, but it was detected in lymphocytes from donors with chemically induced (immunogenic) tumors.

Animals↗
PubMed1980

Characterization of natural cytotoxicity in vitro in a spontaneous rat tumor model.

Spontaneous rat tumor cells were tested in a 12-hr Cr-release assay for susceptibility or resistance to cytolysis by lymphoid effector cells from untreated rats. Most target cells were intermediate to highly susceptible (up to 85% lysis at an effector-to-target ratio of 50:1), but we observed nonsusceptible target cells, too. Cold target inhibition experiments confirmed the susceptibility classifications obtained in the direct assay. The functional properties of effector cells paralleled closely the known properties of natural killer cells. The NK responsiveness of various rat strains did not coincide with the incidence of spontaneous tumors.

Aging↗
PubMed1979

Sensitization of leukocytes of cancer patients against fetal antigens: leukocyte migration studies.

Hypertonic extracts from human fetuses (10--22 wk of gestation) were used to test the sensitizaton of leukocytes from cancer patients against fetal antigens in a direct, microcapillary tube assay system. Leukocytes were simultaneously exposed to a panel of allogeneic tumor extracts and a panel of fetal extracts. Leukocytes from 24 gastric cancer patients, 43 colorectal cancer patients, and 13 lung cancer patients were assayed with extracts obtained from gastric, colorectal, and oat cell carcinomas, respectively, and these extracts were also used with leukocytes from 41 patients bearing tumors of various other organs. Significant migration inhibition by tumor extracts was observed in 81.6% of the tests with gastric cancer, 67.4% of the tests with colorectal cancer, 69.0% of the tests with lung cancer, and 51.2% of the tests with other types of cancer. With fetal extracts, significant migration inhibition occurred in 58.3, 58.7, 59.6, and 54.9% of the tests, respectively. Reactivity against fetal extracts did not depend on the gestation age of the fetuses used for extraction. The conclusion was reached that the leukocytes of most of the cancer patients were sensitized against substances contained in fetal extracts irrespective of the type of tumor of the leukocyte donor. The cross-reactivity pattern suggested that 3-M KCl extracts of whole human fetuses contained a complex mixture of specificities related to the various fetal organs and tissues, which may have represented counterparts to most of the tumor-associated specificities.

Antigens↗
PubMed1978

High incidence of spontaneous transplantable tumours in BDX rats.

Untreated male and female BDX rats were observed over a period of 30 months for spontaneous tumours of a size suitable for transplantation. At the age of 13-30 months 60/97 animals developed tumours, 53 of which were considered as malignant, and 7 as benign tumours. The spectrum of malignant tumours included sarcomas of connective tissue and bone, skin carcinomas, tumours of the lung, the gastrointestinal tract, the genito-urinary tract, the mammary glands, the testis, the adrenal glands and also sarcomas of the neural system and malignancies of the lymphoreticular system. Out of 41 tumours implanted s.c., 34 of them could be passaged further. The primary latent period varied between 1 and 12 months.

Animals↗
PubMed1978

Radioimmunological quantitation of human group-II pepsinogens.

A solid-phase sandwich radioimmunoassay was developed to quantitate human group-II pepsinogens in plasma. The test detected pepsinogen II in a concentration range of 0.25--64.0 ng/ml using sample volumes of 125 microliter. Purified group I pepsinogens showed no response up to concentrations of 100 microgram/ml. In apparently healthy donors, we observed mean plasma concentrations of 20.3 ng/ml (males) and of 15.5 ng/ml (females).

Antibodies↗
PubMed1977

Evaluation of 51Cr release for detecting cell-mediated cytotoxic responses to solid chemically induced rat tumours.

A 51Cr-release test was developed for the detection of cell-mediated cytotoxicity against transplanted solid chemically induced rat tumours, and the findings were compared with those obtained in parallel tests using a microcytotoxicity assay. It was necessary to incorporate several modifications of the original Brunner assay (Brunner et al., 1968) in order to increase the sensitivity of the test as applied to long-term tumour lines maintained as glass-adherent cultures. These included: 1. preincubation of labelled tumour cells at 37 degrees C for 3-4 h before addition of effector cells; 2. preincubation of effector cells at 37 degrees C for 12 h before addition to target cells; 3. upon admixture of target and effector cells, intimate cell contact was established by gentle centrifugation; 4. after incubation of target and effector cells at 37 degrees C, a further incubation for 1 h at 45 degrees C was included to complete the release of 51Cr from non-viable cells. Maximal cytotoxicity of tumour-bearer effector cells was detected after 12 h incubation of lymphoid and target cells at a ratio of 200:1. Spleen cells from tumour-bearing rats during the first 2 weeks of tumour growth exhibited the same pattern of reactivity in the 51Cr-release test and the microcytotoxicity assay, although significant reduction in target-cell numbers was more frequently recorded using the microcytotoxicity assay. Tumour-bearer spleen cells showed reactivity against the homologous tumour as well as against unrelated tumours. Using either assay, pre-exposure of effector cells to 3M KC1 extracts of tumour was found to inhibit their effect on tumour cells most frequently in tests in which the effector-cell donor, soluble extract and target cell were of the same tumour line.

Animals↗
PubMed1977

Leukocyte migration studies in gastric cancer detection: an approach toward improved specificity and sensitivity.

Peripheral blood leukocytes from patients with gastric cancer and various other malignant and nonmalignant diseases and peripheral blood leukocytes from apparently healthy volunteers were tested in the leukocyte migration inhibition test with the use of 4-5 different 3 M KCl extracts of gastric cancer tissue. An operational criterion for defining sensitization of patients' leukocytes was developed; i.e., evidence in an individual sample of leukocytes of either decreased or increased migration areas (migration index less than or equal to 0.79 and larger than or equal to 1.20, respectively) with 3 or more antigen extracts. With this as an indicator of sensitization, it was found that 91% of patients with gastric cancer (39/43), comparto 5% (5/94) and 3% (1/32) of patients with nonmalignant, nongastric diseases and normal controls, respectively, were reactive. Patients with various nongastric cancers were sensitized in 36% (49/135) of cases. Gastritis and gastric, as well as duodenal, ulcer did not influence the reactivity of patients' leukocytes, but considerable sensitization was found in patients with atrophic gastritis or intestinalization. When classified in the usual manner, i.e., by considering the reaction with individual tumor extracts, the specificity and the sensitivity of the test was markedly diminished: More false negative determinations were found in the group of gastric cancer patients, and the percentage of false positives in the group of nonmalignant diseases increased. The results gave evidence of tumor-associated antigens in gastric cancer patients, against which the host elicited a cellular immune response. The high incidence of positive reactivity of leukocytes from patients with gastric cancer, together with the considerable cross-reactivity of leukocytes from patients with nongastric cancer, pointed to the expression of antigens with organ-related and widespread specificities.

Adult↗
PubMed1977

A modified leucocyte migration assay as indicator of malignant and non-malignant gastric mucosal alteration.

When gastric cancer patients' leucocytes were exposed to a panel of tumour extracts, leucocyte migration reactivity was "positive" before operation (90% of cases), it declined after surgery and it reappeared in patients with local recurrence or metastases. In patients with non-malignant gastric diseases, "positive" reactivity against tumour extracts was associated almost exclusively with atrophic gastritis with and without intestinal metaplasia (24/43 cases). "Positive" patients also showed a pathological migration index with an extract of normal gastric mucosa.

Adult↗
PubMed1976

Purification of human gastric proteases by immunoadsorbents. Pepsinogen I group.

Human pepsinogen I group was purified by immunoadsorption techniques. Gastric mucosal extracts containing the pepsinogen I group and the pepsinogen II group and concentrated urine containing only pepsinogen I group were separated by DEAE-ion-exchange chromatography to remove the bulk of human serum protein. Fractions displaying proteolytic activity were further purified by adsorption on an anti-pepsinogen I group Sepharose immunoadsorbent column. After desorption, gastric pepsinogen I group was separated from pepsinogen II group. Trace amounts of contaminating protein were removed from preparations from gastric mucosal extracts and urine by passage over an anti-human serum immunoadsorbent column. The purity of pepsinogen I group from both sources was assessed by electrophoretic and immunological criteria. The isolated pepsinogen I group from gastric mucosal extracts and urine were by biochemical and immunochemical criteria identical with each other and with the pepsinogen I group in the unfractionated starting materials. By agarose enzyme electrophoresis four bands were detected and it was determined that the proteases of the pepsinogen I group express the same individual antigenic determinant.

Adult↗
PubMed1976

Inhibition of cell-mediated cytotoxicity to chemically induced rat tumours by soluble tumour and embryo cell extracts.

When lymph-node and spleen cells from rats bearing or immunized against aminoazo dye-induced rat hepatomas or 3-methylcholanthrene-induced rat sarcomas were pretreated with 3 M KCl extracts of these tumors, their cytotoxicity for cultured cells from the corresponding tumour was specificially inhibited. In cross-test combinations of target tumour and tumour-bearer effector-cell donor, tumour extracts only inhibited cytotoxic responses when they were derived from the tumour homologous to the target-cell and not when the extract was from the tumour borne by the effector-cell donor. One component of the tumour-bearer cytotoxic response was shown to be directed against tumour-associated embryonic antigens since soluble extracts of embryos or tumour extracts containing embryonic antigens inhibited tumour-bearer cell-mediated cytotoxicity in both specific and cross-test combinations of target tumour and effector cells. These findings are discussed in relation to tumour antigen expression and the immune responses that these tumour-associated antigens may evoke in tumour-bearing rats.

Animals↗
PubMed1975

Cell-mediated cytotoxicity to chemically-induced rat tumours.

Cell-mediated immune reactions against carcinogen-induced rat tumours were demonstrated by the in vitro microcytotoxicity test. Lymph-node cells from syngeneic rats immunized against individual aminoazo-dye-induced hepatomas or 3-methylcholanthrene-induced sarcomas were cytotoxic for cells of the immunizing tumour compared with the effects of normal lymph-node cells. Only a low level of cross-reactivity was detectable against target cells derived from otherr tumours. Conversely, lymph-node cells from tumour -bearing rats were cross-reactive against a range of tumour cells, suggesting that the tumour-bearer was sensitized against a common antigen(s) as well as the individually specific antigen associated with these tumours. Lymph-node cells were reactive at an early time (from day 2) after tumour implantation and their cytotoxic potential persisted until terminal stages of tumour growth. Spleen cells from tumour-bearer and tumour-immune donors also exhibited comparable cytotoxic reactivities of the same specificity as that shown by lymph-node cell preparations. These findings are discussed in relation to the development of cell-mediated immune responses in the tumour-bearing rat and in immunized rats which are capable of rejecting transplanted tumour cells.

Animals↗