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Biomedical subjects

V P Nikolin

Publications and source records attributed to V P Nikolin.

13 recordsLinked to original sources

[Effects of exogenous poly(A)+ mRNA on antigenic properties and growth of Krebs-2 tumor cells].

The treatment of Krebs-2 ascitic tumor cells (TC) with total RNA from the liver of Wistar rats (2 mg/ml) altered their antigenicity. As a result, the growth of treated TC in contrast with untreated TC was inhibited when transplanted i. m. to mice preimmunized with rat liver homogenate. Investigations of poly(A+)mRNA, rRNA and tRNA isolated from the same tissue established that the alteration of antigenicity is due to mRNA (8-24 micrograms/ml). In the cytotoxicity assay with antisera against rat Wistar antigens, the expression of rat antigens in TC treated mRNA was observed in the next cell generations.

Animals

[Suppression of tumor growth in the liver by cis-diamminedichloroplatinum as large oligolamellar liposomes prepared by freezing and thawing].

A/HeJ mice with experimental metastases of HA-1 tumor in the liver and other organs were given therapeutic doses of cisplatin, free or encapsulated in phosphatidylcholine cholesterol freeze-thawed liposomes, intravenously. Free cisplatin treatment was found to decrease the growth rate of liver metastases by half and to extend survival by 1.5 times as compared to controls. The inhibitory effect of liposome-encapsulated cisplatin on hepatic metastases growth was more pronounced than that of the free drug although it weakly affected metastatic growth in other organs.

Animals

[Interaction of the plasma membranes of the cells of tumors metastasizing to the lungs with the target organ].

Cells of lines of mice transplantable tumours metastasizing into the lung have been used: lung adenocarcinoma (AL), Lewis lung carcinoma (LL), melanoma B-16 (B-16), mammary tumour MMT-1 (MMT-1), malignant subline of L-cells (LS). Hybrid vesicles were obtained for each tumour. They contain fragments of cell plasmatic membranes (PM). It has been shown that AL-, LL-, LS- and B-16-liposomes were accumulated in lung, the trapping of AL- and LL-liposomes being higher than that of the other hybrid vesicles. Despite the similar dynamics and frequency of metastatic spreading into the lung for all tumours studied, no trapping of MMT-1-vesicles in the target-organ was observed. The role of specific interaction of tumour cells PM with the endothelium of the lung capillaries in the process of organotropic metastatic spreading is discussed.

Adenocarcinoma

[Decrease in the antimetastatic effect of vinblastine administered in liposomes].

The model of experimental metastases in the HA-1 tumour in the liver of A/He mice was used to show that the anti-tumoural effect of cis-dichlorodiamminoplatinum being used in the liposomes increases, while that of vinblastine (VB) decreases. It is suggested that the low activity of liposome-encapsulated VB as to its influence on the tumour growth in the liver is a result of preferable uptake of liposomes by Kupffer cells and hepatocytes from where VB cannot diffuse into tumour cells since it binds to intracellular tubulin.

Animals

[The immunomodulator thymalin in the experimental chemotherapy of tumors].

Experiments on inbred and noninbred mice showed thymalin to potentiate the therapeutic effect of cytostatic drugs. Thymalin treatment was followed by inhibition of tumor growth and dissemination, increase in the animal's life span and amelioration of antitumor drug-induced immunodepression.

Adjuvants, Immunologic

[Selective adhesion of tumor cells to the endothelium of the target organ in metastasis].

The fragments of cell plasma membranes of two lines of metastatic tumour of A/He mice (lung adenocarcinoma--LA-cells and hepatoma HA-1--HA-cells) were used to prepare "hybrid" vesicles (LA- and HA-liposomes). Incorporation of the fragments of LA-cells into the bilayer vesicle increased the binding of LA-liposomes with lung almost by an order of magnitude, their trapping by liver being noticeably decreased. HA-liposomes were retained in the liver in larger amounts than the model phospholipid liposomes. It is assumed that the specificity of metastatic spreading into an organ is associated with the interaction of the plasma membrane of the tumour cells with the apical membrane of the target organ endothelium.

Adenocarcinoma

[Macrophage enhancement of the immunogenicity of a suboptimal dosage of antigen-antibody complex].

Dawley mice were immunized with rabbit gamma globulin combined with allotypical antibodies, introduced alone or after preliminary incubation with syngeneic macrophages. Enhanced immune response was observed in the rats immunized both with low (0.11 mg) and high (1.1 mg) doses of the antigen with macrophages. A conclusion was made that this enhanced response had no connection with the elimination of the excess antigen by the macrophages.

Animals

Stimulation of tumor growth in mice by high doses of BCG.

The growth of Krebs-2 carcinoma in BCG-prevaccinated virgin female C57BL/6, CC57BR/M, and C3Hf mice was studied in relation to the number of living mycobacteria in the organism. When the number of mycobacteria was high, tumor growth was stimulated. After the bacteria were eliminated, tumor growth was inhibited. The effect of BCG was based, on the one hand, on the diversion of effector cells, presumably macrophages, responsible for tumor defense and, on the other hand, on the activation of the pool of these cells. The conclusions were reached that high doses of BCG may be dangerous in human cancer immunotherapy and that patients predisposed to neoplastic disease should be revaccinated with BCG.

Animals