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Biomedical subjects

M Osmak

Publications and source records attributed to M Osmak.

62 records · Page 4Linked to original sources
PubMed1983

Immunotherapy of B-16 melanoma with peptidoglycan monomer.

B-16 melanoma-bearing mice received intravenously or intratumorally one or multiple injections of peptidoglycan monomer (PGM) derived from Brevibacterium divaricatum cell wall. Multiple injections of this non-toxic, water-soluble, low-molecular-weight peptidoglycan reduced the growth rate of tumor nodule on the leg, but did not significantly prolong the survival of tumor-bearing mice. One milligram of PGM administered 3 or 7 days after tumor inoculation inhibited formation of pulmonary metastases, induced either by intravenous injection of malignant cells or seeded spontaneously from tumor nodules in the legs before amputation. The inhibition reached about 50% of control values in saline-treated mice. Addition of PGM to in vitro cultures of B-16 melanoma cells did not change their growth rate. The phagocytic activity in the lungs, but not in the spleen and liver, was significantly augmented 3 and 7 days after treatment with PGM. These data indicate that the antimetastatic potency of PGM is probably due to activation of local (pulmonary) macrophages and not due to direct cytotoxic effects on B-16 melanoma cells or to activation of systemic antineoplastic defence.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1981

Absence of AET protection against fast neutrons: cellular effects.

A series of experiments has been undertaken in order to test the biological properties of neutrons produced in the cyclotron of the Institute "Ruder Bosković" (IRB) in Zagreb. Protective effect of AET (2-amino ethylisothiuronium bromide hydrobromide) on survival of L cells irradiated by fast neutrons generated in the IRB cyclotron were studied by employing the single cell clonal growth method. For comparison the protective effect of AET after gamma irradiation has also been studied. The most important findings that have emerged from these experiments can be summarized as follows: (1) Protective effect of AET was present after gamma irradiation only. (2) The degree of protection was dependent on AET concentration in the growth medium. (3) No protective effect was found after neutron irradiation. These findings are in agreement with the generally less efficient protection of this compounds after high-LET irradiation.

Animals↗
PubMedDate not supplied

Quantitative biochemical analysis of lactate dehydrogenase in human ovarian tissues: correlation with tumor grade.

In an attempt to identify glycolytic capacity of normal and neoplastic human ovary, total lactate dehydrogenase (LDH) activity was measured in tissue cytosol originating from 69 patients (18 with benign ovarian tumor, 34 with ovarian carcinoma, six with nonepithelial ovarian malignant tumors, and 11 with tumor metastatic to ovary) and compared to the LDH activity of normal ovarian tissues (n = 19). Median value of total LDH-specific activity expressed as U/mg protein was 0.546 in normal tissues, 0.584 in benign tumors, 1.071 in malignancies metastatic to ovaries, 0.872 in nonepithelial primary ovarian tumors, and 0.818 in primary carcinomas. A significant rise in LDH-specific activity was found in malignant primary and secondary tumors of epithelial and nonepithelial origin, but not in benign neoplasms, compared to the activity in normal tissue. Ovarian carcinomas of serous histologic type did not differ in LDH activity from mucinous tumors. However, poorly differentiated carcinomas (grade 3) showed significantly enhanced activity of this glycolytic enzyme when compared to its grade 1 counterpart. The subgroup of grade 1 tumors did not differ in LDH activity from normal and benign ovarian tissue. Obtained results suggest that direct correlation might exist between ovarian epithelial tumor grade and lactate dehydrogenase activity.

Adult↗
PubMedDate not supplied

Drug resistant tumor cells have increased levels of tumor markers for invasion and metastasis.

The association between drug-resistance and three markers for invasive capacity: cathepsin D (Cath D), urokinase type plasminogen activator (uPA) and inhibitor of plasminogen activator type 1 (PAI-1) was examined in nine cervical and laryngeal carcinoma cell lines resistant to different cytostatics. The level of Cath D was measured by solid phase two-site immunoradiometric assay, while uPA and PAI-1 concentrations were determined by use of ELISA. All drug resistant cell lines had increased concentration of cathepsin D. uPA levels were similar in parental and drug resistant cervical carcinoma cells, but significantly higher in all examined drug resistant laryngeal carcinoma cells. In cervical carcinoma cells, PAI-1 concentrations were similar in parental and cisplatin resistant, but significantly higher in doxorubicin resistant cells. In laryngeal carcinoma cells, no increase in concentrations of PAI-1 was determined in the three from five resistant cell lines. There was no uPA in conditioned medium of parental or drug resistant cells. PAI-1 was detected in conditioned medium. Its levels were significantly increased in the medium of two cervical and three laryngeal drug resistant carcinoma cells. Thus, our results suggest that drug-resistance may be accompanied by increased levels of tumor associated proteases and/or its inhibitor.

Antineoplastic Agents↗
PubMedDate not supplied

Drug-resistant human laryngeal carcinoma cells have increased levels of cathepsin B.

In our previous work we showed that the drug-resistance of cervical carcinoma, laryngeal carcinoma and glioblastoma cells may be accompanied by increased levels of tumor markers for invasion and metastasis (i.e. urokinase-type plasminogen activator, plasminogen activator inhibitor type 1, and/or cathepsin D). In the present study we examined the concentration of cathepsins B, L and H in three drug-resistant clones isolated from human laryngeal carcinoma (HEp2). The basal levels of cathepsins B, L and H were determined by enzyme linked immunoabsorbent assay (ELISA). Our results showed that all three clones had an increased level of cathepsin B (in two clones an almost 4-fold increase was determined). The level of cathepsin L was altered (increased) only in VK2 clone, while the levels of cathepsin H were similar in parental cells and drug-resistant clones. Thus, our results suggest that drug-resistance may be accompanied by an increased level of cathepsin B, i.e. tumor associated protease, involved in invasion and metastasis.

Biomarkers, Tumor↗
PubMedDate not supplied

Hyperthermic modulation of resistance to cis-diamminedichloroplatinum (II) in human larynx carcinoma cells.

The aim of the present study was to examine the effect of hyperthermia on cisplatin resistance in two sublines of human larynx carcinoma HEp2 cells. Hyperthermia was tumouricidal for both parental and cisplatin resistant cells, but cisplatin resistant cells were more sensitive to the heat at 43 and 44 degrees C. In combined cisplatin-hyperthermia treatment, heat chemosensitization was observed for parental, as well as for cisplatin resistant cells. At 42 degrees C, and at 43 degrees C, the thermal enhancement ratio (TER) for cisplatin toxicity was higher in resistant than in parental cells. The heating at 42 degrees C decreased the resistance factors in CA3 and CK2 cells from 2.2 and 3.5 to 1.8 and 2.2 respectively. At 43 degrees C, the resistance factors were decreased to 1.7 for CA3 cells and 2.0 for CK2 cells. The heating at 43 degrees C increased intracellular platinum accumulation in all cell lines examined. This effect was more pronounced in resistant, than in parental cells, causing complete reversal of the reduced platinum accumulation found at 37 degrees C in resistant cells. In conclusion, the resistance to cisplatin was partially reversed by hyperthermia in CA3 and CK2 cells. Increased drug accumulation was one of the mechanisms involved in hyperthermic potentiation of cisplatin toxicity and partial reversal of cisplatin resistance in human larynx carcinoma HEp2 cells.

Cell Survival↗