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Biomedical subjects

M Micksche

Publications and source records attributed to M Micksche.

141 records · Page 8Linked to original sources
PubMed1976

Time lapse cinematographic demonstration of humoral and cell mediated immunity in squamous cell carcinoma of the lung.

Out of 42 attempts in one case a cell line derived from biopsy material of a squamous cell carcinoma of the lung has been established. Tumor-associated-antigen could be demonstrated by indreict immunofluorescence. The effect of allogeneic cytotoxic antibodies, absorbed with normal human lung and sera, on the target cells is shown. Blood lymphocytes obtained from patients with squamous cell carcinoma of the lung proved to be cytotoxic against this cell line. The cell to cell interactions of this phenomenon and the effect of cytotoxic antibodies are shown by time lapse cinematography.

Antibody Formation↗
PubMed1975

Studies on lymphocyte sensitization to encephalitogenic protein in tumor patients.

The specific lymphocyte sensitization of patients with malignant diseases against a basic protein, isolated from human brain, was studied by the lymphocyte migration inhibition technique. A sensitization of lymphocytes of cancer patients against this encephalitogenic factor (EF) was first reported by FIELD and CASPARY in 1970. Their test system was the Macrophage-Electrophoretic-Mobility-Test (MEMT). In 17 out of 18 patients with malignant disease we found a specific inhibition or enhancement of the migration area of lymphocytes more than 15%.

Carcinoma, Bronchogenic↗
PubMed1975

[Halo Nevus (Morbus Sutton): model of an immunological tumor regression].

Spontaneous regressions of malignant tumors are rare in the history of malignant disease. In malignant melanoma immunological mechanisms were accounted for the regressions observed. By the clinical phenomenon called Halo nevus a benign pigment-cell-tumor is described which shows spontaneous involution. The characteristic feature is the depigmentation of the surrounding uninvolved skin and a centripetal progression of the tumor-regression-phenomenon. In the present study it is demonstrated by histopathological and immunological investigations that lymphocytes are responsible for this tumor-regression. Lymphocyte-reactivity of 16 patients with Sutton's disease in different stages were investigated in the microcytotoxicity-assay against culture-grown melanomatargetcells. In 11 patients a specific cell-mediated immunity against the melanoma cells could be demonstrated in vitro. 5 patients did not show any reactivity, the Halo nevus had been removed by surgery 2 years earlier. The results of the immunological assay are confirmed by histopathological light- and electron-microscopic incestigations and documented by typical examples.

Adult↗
PubMedDate not supplied

Influence of thia-benzimidazole Wy 18251 of cancer patients' lymphocyte reactivity.

The influence of thiazolobenzimidazole Wy 18251 on reactivity of cancer patients' lymphocytes was investigated. Doses of 0.2 to 20 micrograms/ml added to lymphocytes for 72 hrs did not influence spontaneous 3H-thymidine uptake nor PHA-induced blastogenic response. 50 micrograms/ml of Wy 18251 significantly enhanced blastogenic response of lymphocytes in 5 out of 8 patients. Augmentation of response to mitogens was mainly observed when PHA was added in a concentration leading to suboptimal stimulation. These results suggest that Wy 18251 is active on suboptimal stimulated lymphocytes but ineffective on unstimulated or optimal stimulated human lymphocytes. Further studies are required to give insight in this mechanism of stimulation.

Antineoplastic Agents↗
PubMedDate not supplied

Genetic polymorphisms of CYP1A1 and GSTM1 and lung cancer risk.

Susceptibility to lung cancer may, in part, be determined by interindividual differences in the cytochrome P450-catalysed bioactivation and the glutathione S-transferase-catalysed detoxification of procarcinogens. Therefore a lung cancer case-control study was set up to investigate the association of three polymorphisms of the CYP1A1 gene (CYP1A1*2A, CYP1A1*2B, CYP1A1*4) and GSTM1*0 genotype with lung cancer risk in Austrian Caucasians. Genomic DNA was isolated from the peripheral blood lymphocytes of 134 male lung cancer patients and 134 age-matched controls with nonmalignant conditions and PCR-based analyses were performed. There was no significant difference in risk between cases and controls, either for the CYP1A1*2A (OR=1.09, 95%CI=0.46-2.58), CYP1A1*2B (OR=1.09, 95%CL=0.46-2.58) or for the CYP1A1*4 polymorphism (OR=0.49, 95%CL=0.20-1.16). The prevalence of the GSTM1*0 genotype in the lung cancer group (47.8%) was comparable to that found in the control group (49.3%) and also had no effect on lung cancer risk (OR=0.94, 95%CL=0.54-1.57). Further, in a subgroup of male ever-smokers (n=126), no significant influence on the relative risk was found for these polymorphisms. Our results suggest that these investigated polymorphisms can not be considered as genetic susceptibility markers for lung cancer within the Austrian Caucasian population.

Adenocarcinoma↗
PubMedDate not supplied

Hyperthermia increases the susceptibility of chondro- and osteosarcoma cells to natural killer cell-mediated lysis.

As an adjuvant to chemotherapy hyperthermia has proven to be successful as a treatment for osteo- and chondrosarcoma patients. The aim of this study was to investigate whether hyperthermia could increase cellular expression of heat-shock-protein 72 in human osteo- and chondrosarcoma cells and how heat treatment would affect their susceptibility to natural killer cell (NK-cell)-mediated lysis. About 5-10% of the peripheral mononuclear blood cells (PBMC) in the human peripheral blood are natural killer cells (NK-cells). Natural cytotoxicity, mediated by NK-cells, is believed to play an important role in host defense against cancer. The exact mechanisms of recognition of target cells and subsequent NK-cell activation are not yet known. NK-cells, isolated from the peripheral blood of healthy donors, were enriched by magnetic cell-separation to a purity of 85-97%, assessed by FACS-analysis. The susceptibility of heat-treated (42.5 degrees C, 90 minutes) and untreated osteosarcoma (MG63) and chondrosarcoma (HTB94) cell lines to NK-killing was determined by a release assay of lactate dehydrogenase (LDH). Lysis by NK-cells was increased by heat treatment of the target cells from 16.6% + 4.5% to 33% + 15%, p=0.035, for osteosarcoma cells, (E/T ratio of 5:1) and from 13.7% + 3.1% to 27.9% + 16.9%, p=0.021, (E/T ratio of 20:1) for chondrosarcoma cells. An increased expression of HSP72 of chondro- and osteosarcoma cells after heat treatment was detected by the Western blot technique. The results of this study show that hyperthermia increases HSP72 expression in osteo- and chondrosarcoma cells and their susceptibility to NK-cell-mediated lysis. These findings may lead to new therapeutic strategies, using hyperthermia to improve immunological defense against chondro- and osteosarcoma cells.

Bone Neoplasms↗
PubMedDate not supplied

Production of polypeptide regulatory factors by human melanoma cells.

Peptide regulatory factors, i.e. cytokines, are released spontaneously or upon induction by melanoma cells in culture. Among these cytokines there are factors such as Il-1, IL-6, IL-8, IL-10 as well as TGF-beta 1 which are basically acting as immunoregulatory molecules. However, their contribution to an augmentation and/or suppression of local or systemic immune response against melanoma cells in situ has not yet been elucidated. On the other hand, some of these molecules, e.g. IL-6 and TGF-beta 1, are growth inhibitors, especially in the early phases of melanoma development. During tumor progression, resistance to the inhibitory effect of these cytokines seems to take place. Whether this resistance is due to an excessive production of these cytokines or a downregulation or blockade of receptors is still controversial. The aberrant expression of bFGF in melanoma cells explains how melanoma cells in vitro and probably also in vivo acquire growth autonomy and the capacity of metastasis formation. The expression of bFGF by human melanoma cells and its activity as autocrine growth regulator imply that agents which interfere with heparin-binding growth factors such as Suramin or pentosan sulfate may be of clinical usefulness. Additionally, these latter agents have been shown to be potent anti-angiogenic factors. Their clinical efficacy, however, has to be established in phase I and II studies.

Cell Division↗
PubMedDate not supplied

Modification of growth in small heat shock (hsp27) gene transfected breast carcinoma.

The role of hsp27 in the regulation of cell growth has been investigated in the breast cancer cell line MDA-MB-23 1. Cells were co-transfected with an expression vector carrying the human hsp27 gene (pSG-2711) and a plasmid conferring neomycin resistance (pWlneo). Transfected cells were selected for neomycin resistance. Stable transfectants were used as a pooled population for further experiments, since single-cell colonies were not able to grow into mass culture under continuous selection pressure. Over-expression of hsp27 was analysed by immunohistochemistry and immunoblotting. Cells only transfected for neomycin were used as control cells. The growth rate of the transfected cell line was determined whether overexpression of hsp27 directly influences the growth properties of the cells. Growth analysis of transfected cell lines in vitro revealed a lower proliferation rate of the hsp27 overexpressing cells compared to controls. These data suggest that hsp27 is involved in downregulation of cell proliferation in this human breast cancer cell line.

Breast Neoplasms↗