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Biomedical subjects

S Gundersen

Publications and source records attributed to S Gundersen.

69 records · Page 4Linked to original sources
PubMed1983

Natural killer cell activity is closely associated with a growth-inhibitory serum protein with protease-like activity.

A correlation between natural killer (NK) cell activity and growth inhibition (GI), as measured in an in vitro assay with B16 melanoma cells, mediated by a serum growth-inhibitory factor (GIF), among various strains of mice has been demonstrated. Beige mice (bg/bg), known to express low NK-activity, were also low in GIF activity and showed increased susceptibility to both B16 melanoma cells and another solid tumor (Lewis lung carcinoma) in vivo. In vivo treatment with various protease inhibitors that reduced NK-activity, also reduced growth inhibition mediated by GIF. Protease inhibitors that did not affect NK-activity did not affect GIF either. All of 4 B16 melanoma clones selected against GIF in vitro and resistant to GIF showed both resistance to NK-cells in vitro and increased growth potential in vivo. However, P-815, an NK-resistant cell line, was sensitive to GIF.

Animals↗
PubMed1983

Purification and characterization of a mouse serum protein with growth inhibitory properties in vitro against tumor cell lines.

A factor which is responsible for the growth inhibitory properties of certain mouse sera and related to NK-activity, has been studied. The factor was isolated from hybrid B6D2F1 (C57Bl/6 x DBA/2) serum, which is histo-compatible with the mouse tumour (B16 melanoma) used and has high NK-activity. Growth inhibitory activity was measured in an in vitro assay. It was independent of complement activation. The responsive factor was isolated and characterized by ion exchange chromatography. Concanavalin A affinity chromatography, gel filtration and iso-electric focusing. It appears to be a protein and had been labelled growth-inhibitory factor (GIF). It has a molecular weight of 230 000-260 000 daltons and an iso-electric point in the pH range 4.6-5.0. It was not retained on Concanavalin A columns.

Animals↗
PubMed1981

Cellular and humoral factors in host susceptibility to Lewis lung carcinoma.

Cellular and humoral anti-tumour reactivity in strains of mice highly susceptible (C57Bl/6) or less susceptible (C57Cl/6 x DBA/2 = B6D2F1) to Lewis lung carcinoma (LLC) was investigated. Natural killer cell activity in a 51Cr release assay against this tumour could be demonstrated with a good correlation to in vivo susceptibility. This has not been demonstrated earlier for solid, spontaneous tumours. T-cell deficiency (congenital athymic (nude mice)) did not affect the cumulative incidence of tumour take. However, the number of lung metastases was significantly reduced in nude mice. Treatment with antilymphocyte serum (ALS) increased the susceptibility to LLC in both strains. In a soft agar colony assay a marked reduction in the number of colonies was observed when tumour cells were incubated with serum from B6D2F1 mice as compared to serum from C57Bl/6 mice, prior to seeding. Apparently naturally occurring cellular, as well as humoral effector mechanisms are involved in host resistance to Lewis lung carcinoma in the mouse.

Animals↗
PubMed1981

Inhibitory effect on tumour colony formation of mouse serum associated with tumour resistance in vivo in semi syngeneic mice.

Differences in tumour susceptibility between strains of mice (C57Bl/6 and C57Bl/6 X DBA/2 = B6D2F1) could be demonstrated for several tumours of C57Bl origin, both solid tumours (B16 melanoma and Lewis lung carcinoma) and lymphomas (RBL-5, 136-3 and ALC). Serum from mice with high tumour resistance in vivo (B6D2F1) showed an inhibitory effect on tumour colony formation in a soft agar colony assay. Serum from mice with lower tumour resistance (C57Bl/6) had no effect. When other F1 hybrids of C57Bl/6 parental origin were tested, the same correlation between in vitro inhibition of tumour colony formation and in vivo susceptibility was found. The serum factor was species non-specific, since the activity was expressed against in vitro grown cell lines of human origin. The tumour colony inhibitory activity was heat sensitive (56 degrees C for 30 minutes), precipitable by (NH4)2SO4, and not removed by adsorption on tumour cells. These results demonstrate the existance of a naturally-occurring humoral tumerostatic factor(s) which correlates to in vivo susceptibility to tumour cells. Its relationship to NK cell activity is discussed.

Animals↗
PubMed1981

Growth inhibitory effect of mouse serum on eukaryotic cells in a micro assay.

Inhibition of cell growth by B6D2F1 (C57Bl/6 X DBA/2) mouse serum in tissue culture wells confirming previous findings in the soft agar tumour colony assay is reported. The assay was time saving, more sensitive, and the amount of mouse serum used could in each experiment be reduced by 95%. In addition non-neoplastic cells ordinarily not forming colonies in the soft agar assay could be tested. Such cells were less sensitive to the growth inhibitory effect when compared to neoplastic cells.

Animals↗
PubMed1979

Treatment of micrometastases from Lewis lung carcinoma with abrin and cyclophosphamide, given singly and in combination.

The effect of the plant toxin abrin and of cyclophosphamide given as adjuvant chemotherapy after irradiation of the primary tumor was studied in mice bearing intramuscularly growing Lewis lung carcinoma. The chemotherapy was given immediately after irradiation performed 9 days after inoculation of 10(5) tumor cells. The drugs were given in bolus injections either as single agents or concurrently. The therapeutic effect was assessed by recording the appearance of lung metastases on day 21 or the number of long-term survivors, i.e. animals alive at day 60. In the control group 21 +/- 3.4 (SD) macroscopic lung colonies was recorded on day 21. Mean survival time was 25.5 days with none of the mice alive at day 60. The optimal abrin dose (612.5 ng/kg IV) reduced the number of lung metastases to 2.6 +/- 0.8 and yielded 37% long-term survivors (11/30). The optimal dose of cyclophosphamide (150 mg/kg IP) reduced the number of lung colonies to less than 1 and yielded 61% survivors (14/23). Small to moderate doses of abrin significantly potentiated the therapeutic effect of cyclophosphamide without increasing the toxicity. The best results (18/20 or 90% long-term survivors) were obtained when the optimal dose of cyclophosphamide, 150 mg/kg, was combined with 350 ng/kg of abrin. The results obtained in this highly resistant tumor suggest that combinations of the two drugs may be useful also in other tumor types.

Abrin↗
PubMed1978

Left anterior hemiblock in acute myocardial infarction. Incidence and clinical significance in relation to the presence of bundle branch block and to the absence of intraventricular conduction defects.

The incidence of intraventricular conduction defects was examined retrospectively in 449 consecutive patients with acute myocardial infarction (AMI). The incidence of left anterior hemiblock (LAH), right bundle branch block (RBBB), left bundle branch block (LBBB) and RBBB+LAH was 12.2, 4.2, 3.8 and 2.5%, respectively. At least 24 patients (5.8%) developed LAH as a result of the AMI. LAH was present in 20% (33/164) of patients with anterior infarction, in 14% (18/131) of those with infarction of undetermined localization, and in 3% (4/143) of patients with diaphragm infarction. The incidence of complete atrioventricular (AV) block in patients with LAH was 6% and in patients with no intraventicular conduction defects 7%. In patients with RBBB, RBBB+LAH and LBBB, the incidence of complete AV block was 37, 45 and 18%, respectively. Severe pump failure occurred with the same low incidence in patients with LAH as in patients without intraventricular conduction defects, but was much more common in patients with complete bundle branch block (BBB). The mortality rate for patients with LAH was 22% and for patients with no intraventricular conduction defects 21%. In patients with RBBB, RBBB+LAH and LBBB, the mortality rates were 53, 55 and 53%, respectively. Patients with complete BBB had a higher age and a higher incidence of previous AMI than the others. Compared to patients with no intraventricular conduction defects, the presence of LAH did not increase the mortality rate, or the risk of developing severe heart failure or complete AV block, in contrast to the serious prognosis in patients with complete BBB.

Acute Disease↗
PubMed1977

Blood B and T lymphocytes and in vitro cellular immune reactivity in untreated human malignant lymphomas and other malignant tumors.

Peripheral blood lymphocytes and their in vitro reactivity have been recorded prior to treatment in 18 patients with Hodgkins disease, 11 with lymposarcoma, 13 with reticulosarcoma, 20 with various solid tumors and 37 normal control persons. The mean total numbers of lymphocytes, those of T lymphocytes,and the mean reactivity to PHA and ConA were reduced in all groups except lymphosarcoma, although with varying degrees of statistical significance. The percentages of T and B lymphocytes appeared to be normal in all groups, but the ranges of values were somewhat greater than among the normal controls. The mean total numbers of B lymphocytes were normal in all patient groups. All reductions seemed to be more pronounced in patients with disseminated than in those with localized disease, but none of these differences was statistically significant. All patient groups appeared to have reduced reactivity in MLC, while the ability to stimulate control lymphocytes was nearly normal. The results fail to indicate an in vitro immunological abberation specific to Hodgkin's disease. It seems that human malignant, neoplastic diseases are associated with a relatively selective reduction of the total numbers and reactivity of blood T lymphocytes. Various explanations of the reactivity impairment are proposed. The pathogenesis of the reduction of the total number of blood T lymphocytes remains obscure.

Adult↗
PubMedDate not supplied

Efficacy of pamidronate in breast cancer with bone metastases: a randomized, double-blind placebo-controlled multicenter study.

PURPOSE: To evaluate the efficacy of pamidronate 60 mg i.v. q 4 weeks in women with advanced breast cancer with skeletal metastases. PATIENTS AND METHODS: 404 woman with skeletal metastases from breast cancer in Sweden and Norway were included in a randomized, placebo-controlled, multicenter study. Except for the study medication, other palliative treatment was chosen at the discretion of the physician. Skeletal related events, i.e. increased pain, treatment of hypercalcemia, pathologic fractures of long bones or pelvis, paralyses due to vertebral compression, palliative radiotherapy for skeletal metastases, surgery on bone and change of antitumor therapy were recorded every third month as well as a self-estimated pain-score using visual Analog Scales and analgesic consumption. RESULTS: There was a significantly increased time to progression of pain (p < 0.01), to hypercalcemic events (p < 0.05) as well as for the cumulative number of skeletal related events (p < 0.01) in favor for the pamidronate group. No statistically significant reduction of pathologic fractures of long bones or pelvis, or pareses due to vertebral compression occurred. No statistically significant differences were found for the need of radiotherapy and surgery on bone. The pamidronate group faired better regarding performance status (p < 0.05). There was a statistically not significant lower consumption of opioid analgesics in the pamidronate group (p = 0.14). CONCLUSION: Pamidronate 60 mg i.v. q 4 weeks reduces skeletal events and improves the quality of life in women with bone metastases from breast cancer.

Antineoplastic Agents↗