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A Opolski

Publications and source records attributed to A Opolski.

At least 37 records · Page 2Linked to original sources
PubMed2000

The role of GABA-ergic system in human mammary gland pathology and in growth of transplantable murine mammary cancer.

In this paper we described the results of our studies on the baclophen (gamma aminobutyric acid (GABA)-B receptor agonist) inhibitory effect on the growth of experimental mammary cancer 16/C in mice and on the estimation of GABA level and GAD (glutamine acid decarboxylase--the key enzyme in GABA synthesis) activity after this treatment in mice. The experimental data are confronted with the estimation of GABA level and GAD activity in human mammary gland material taken from the patients with benign breast tumors of different pathological and age related hormonal stages. A significant inhibition of 16/C tumor growth in treated with baclophen mice was observed. Mean GABA level and GAD activity were significantly higher both in tumor and in normal tissue of baclophen treated mice in comparison to control animals. The results of clinical studies have shown that the lowest GABA level and GAD activity in tumor and normal mammary gland tissue was detected in patients in peri-menopausal stage. Both, in human and mouse material, the GABA level and GAD activity were higher in tumor than in normal tissue and there was a clear positive correlation between GABA level and GAD activity in both tissues studied. GABA level and GAD activity in tumor and in normal tissue were lower in patients with dysplasia than in patients with fibroadenoma. Considering our results, namely an inhibitory effect of GABA receptor agonist on mammary cancer growth and the correlation between GABA level and the stage of breast pathology and/or hormonal activity, it seems probable that GABA-ergic system is involved in hormonal regulation and pathogenesis of breast cancer.

Adolescent↗
PubMed2000

The library of p-nitrophenyl esters of oligopeptides as a model to study the anticancer drug-peptide conjugates activated during tumor angiogenesis.

An indexed library of oligopeptide p-nitrophenyl esters immobilized via methoxy-1,3,5-triazine scaffold on the cellulose support, was synthesized by the step by step procedure and by segment coupling, involving 2-chloro-4,6-dimethoxy-1,3,5-triazine as a condensing reagent. The substrate specificity towards homogenate supernatant of mouse lung cancer LL2 cells has been studied.

Animals↗
PubMed2000

The library of p-nitrophenyl esters of oligopeptides as a model to study the anticancer drug-peptide conjugates activated during tumor angiogenesis.

An indexed library of oligopeptide p-nitrophenyl esters immobilized via methoxy-1,3,5-triazine scaffold on the cellulose support, was synthesized by the step by step procedure and by segment coupling, involving 2-chloro-4,6-dimethoxy-1,3,5-triazine as a condensing reagent. The substrate specificity towards homogenate supernatant of mouse lung cancer LL2 cells has been studied.

Animals↗
PubMed2000

The antitumor effect of postoperative treatment with genistein alone or combined with cyclophosphamide in mice bearing transplantable tumors.

Genistein has been shown to be an inhibitor of tumor growth as well in vitro as in vivo. In addition to its antitumor effect, genistein reveals the antimetastatic and antiangiogenic properties. In this paper we described the results of our studies on the antimetastatic activity of genistein alone or combined with cyclophosphamide (CY) in mice which before this treatment were exposed to surgical excision of the primary tumor. Three transplantable subcutaneously growing mouse tumors were applied: Lewis lung cancer (LL2), B16F-10 melanoma and 16/C mammary cancer. The antitumor and antimetastatic effect was evaluated by the estimation of a number of lung colonies and a number of primary tumor recurrence as compared to the control mice exposed to the s.c. tumor extirpation only. Twenty days after the surgery, an average of 52 lung tumor colonies per mouse were detected in control mice bearing LL2 cancer. The treatment with genistein resulted in the reduction of the lung colonies to 24 per mouse. The treatment with CY reduced the number of lung colonies to 12 (p < 0.05) and combined treatment with both agents to 4 (p < 0.05). The percentage of primary tumor recurrence was 25, 86, 67 and 80% in the control, genistein treated, CY treated, and genistein + CY treated mice, respectively. Twenty days after the surgery, no lung metastases in the control mice bearing B16F-10 melanoma were observed. The percentage of primary tumor recurrence in the control, genistein treated, CY treated and genistein + CY treated mice was: 86, 29, 57 and 67% respectively. Two different protocols of the treatment with genistein were applied in 16/C mammary cancer model. In the first one genistein was injected before and in the other after surgical excision of tumor. The histological examination revealed the presence of lung metastases in all, untreated and treated, according to both protocols groups of mice. The percentage of primary tumor recurrence in the control mice, genistein treated according to the protocol I, and II was: 100, 40, and 40%, respectively.

Animals↗
PubMed1999

GABA level and GAD activity in human and mouse normal and neoplastic mammary gland.

Our studies have demonstrated that GABA (gamma-aminobutyric acid) is detectable both in mouse and in human normal mammary gland and in neoplastic alterations. We have also shown that GABA content in tumor was significantly higher than in normal tissue. The statistically significant difference in GAD (glutamine acid decarboxylase) activity between tumor and normal mammary tissue was also detected. The positive correlation between GABA content and GAD activity in tumor cells was observed both in human and in mice materials. The observed increase in GABA level and GAD activity in tumor tissue could reflect an eventual local antitumor immune response, however, a hypoxia of tumor cells could also be considered. The role of GABA, GAD and GABA-ergic receptors in cancerogenesis and in cancer progression is still to be clarified and requires further studies; however, it may indicate that the known agonists of GABA-ergic system (e.g. baclofen) can potentially modulate the tumor growth.

Adenocarcinoma↗
PubMed1998

Metastatic potential of human CX-1 colon adenocarcinoma cells is dependent on the expression of sialosyl Le(a) antigen.

Several lines of evidence indicate that sialosyl Le(a), tumor-associated carbohydrate antigen present on human colon carcinoma cells, is involved in formation of metastases. To study the role of this carbohydrate structure in development of metastases, we have used the clone of human colon carcinoma CX-1 cells transfected with antisense expression vector containing fragment of cDNA for alpha1,3/4-fucosyltransferase (FT III), which is involved in synthesis of sialosyl Le(a) tetrasaccharide. It has been reported previously that, in contrast to the parental cells, the antisense-transfected CX-1.1AS5 cells do not express sialosyl Le(a) and do not adhere to E-selectin-expressing CHO cells. In the present work we have studied the formation of liver metastases by CX-1.1AS5 cells after their orthotopic or intrasplenic implantation into athymic nu/nu mice. After orthotopic implantation of sialosyl Le(a)-negative colon carcinoma CX-1.1AS5 cells, the number of mice with liver metastases was markedly lower (21% of mice) in comparison with their number after implantation of the parental CX-1.1 cells (86% of mice). However, no differences in ability to form colonies in liver were observed between parental CX-1.1 cells and antisense-transfected CX-1.1AS5 cells after intrasplenic inoculation. The liver metastases were formed in 89% and 84% of mice, respectively. Our data support the thesis on the importance of sialosyl Le(a) antigen expression in the development of liver metastases by colon cancer cells, and indicate the role of transplantation route and primary tumor localization in formation of metastases.

Adenocarcinoma↗
PubMed1998

[The importance of angiogenesis in tumor growth dynamics].

The interactions between tumor cells and cellular compartments of direct environment, including soluble ECM factors, in the mechanisms of cancer progressive growth are discussed. Experimental data showing the role of increased apoptotic index even with unchanged proliferation rate in achieving the tumor "dormant state" are presented. The role of various molecules and factors involved in the process of tumor angiogenesis and their value as diagnostic and prognostic markers in cancer patients is discussed. The new antitumor therapeutical strategies based on an antiangiogenic activity of new potential agents are reviewed.

Animals↗
PubMed1998

GABA content and GAD activity in colon tumors taken from patients with colon cancer or from xenografted human colon cancer cells growing as s.c. tumors in athymic nu/nu mice.

A significantly high GABA level and GAD activity was found in human colon cancer tissue as compared with normal macroscopically unchanged human colon wall taken from the same patients. Similarly in athymic nu/nu mice transplanted with human colon adenocarcinoma cells established in in vitro culture (line CX-2) the high level of GABA accompanied by high GAD activity was found in subcutaneously growing tumors as compared with the unchanged colon wall and unchanged skin tissue from the same tumor bearing mice. Interestingly, the level of GAD activity in the macroscopically unchanged colon tissue of mice transplanted with tumor cells were increased in comparison with normal colon of healthy control mice. For the skin, only GAD activity was higher in the material coming from tumor bearing mice than in the material from normal control mice, whereas GABA level was even lower in the skin of tumor inoculated mice compared with control group. An increase in GABA level and in GAD activity can perhaps reflect a local immune response to the neoplastic process. The observed direction of GABA metabolism in tumor of the colon indicates a possibility to interfere in this process using the agonists of the GABA-ergic system.

Adenocarcinoma↗
PubMed1992

Localization of the conformational alteration of MHC molecules induced by the association of mouse class I heavy chain with a xenogeneic beta 2-microglobulin.

Changes in the antigenicity of major histocompatibility complex (MHC) class I molecules resulting from the association of bovine beta 2-microglobulin (beta 2-m) with mouse class I heavy chains were investigated. Mice (H-2b) were immunized with syngeneic Concanavalin A (Con A) blasts induced in the presence of fetal calf serum (FCS) in conditions allowing exchange between mouse and bovine beta 2-microglobulin (beta 2-m). Spleen cells from hyperimmunized mice were fused with myeloma cells and two monoclonal antibodies which required for their reactivity the presence of FCS have been further studied. One of them (CAB 297) recognized a determinant of bovine beta 2-m which is present on free molecules in solution as well as when they are associated with either mouse or bovine class I heavy chains. In contrast, the second monoclonal antibody (CBB 70) did not react with free bovine beta 2-m molecules, nor with beta 2-m associated with bovine class I heavy chains. It did react with cells of some H-2 haplotypes (b, f, p and r) but only when their class I heavy chains are associated with bovine or with human beta 2-m. Therefore, expression of the CBB 70 defined antigenic determinant requires both xenogeneic beta 2-m and class I heavy chain of a given H-2 molecule. In order to precisely localize the antigenic determinant defined by this monoclonal antibody and therefore the region altered by the association of class I heavy chain with xenogeneic beta 2-m, we made use of exon shuffled class I molecules. The results indicate that changes induced by the association of bovine beta 2-m with H-2 class I heavy chain affect the conformation of the alpha 2 domain. These studies illustrate that MHC class I molecules exhibit a considerable conformational flexibility which could influence their ability to bind and present various peptides to the T-cell receptor.

Animals↗
PubMed1987

Induction of H-2-specific antibodies by injections of syngeneic Sendai virus-coated cells.

The capacity of the B cell immunoglobulin receptor to recognize complexes of Sendai viral and H-2b antigens was investigated by studying the antibody response to injections of syngeneic Sendai virus-coated (SV+) spleen cells in C57BL/6 (B6) mice. Almost all mice produced alloreactive anti-H2 lymphocytotoxic antibodies. In contrast, such antibodies were found very exceptionally in mice injected with normal (SV-) cells or with Sendai virus (SV) only. The reaction pattern of the cytotoxic antibodies induced was variable and ranged from almost anti-private to widely cross-reactive serotypes. The results of reactions on H-2-congenic, -recombinant and -mutant mouse strains, and of capping and immunoprecipitation experiments showed that the cytotoxic antibodies were directed against H-2 class I molecules. The anti-H-2 antibodies exhibited enhanced binding for SV+ target cells, but absorption experiments showed that this was not the result of cross-reactions with cell surface Sendai viral determinants or with a molecular complex of H-2 plus SV. This conclusion was supported by the observation that syngeneic SV+ cells were not the predominant targets for the induced lymphocytotoxic antibodies. Our results do not support the existence of MHC-restricted antiviral antibodies, but show the induction of anti-class I H-2 alloantibodies by injections with syngeneic SV-coated cells. We present a model for regular induction of anti-H-2 antibodies without intentional alloimmunization.

Animals↗
PubMed1987

Genetic monitoring of inbred mouse strains maintained at the Bhabha Atomic Research Centre, Bombay: serological typing for H-2 haplotypes and lymphocyte differentiation markers.

Seven inbred mouse strains, AKR, CBA, C3H, C57BL/6, C57BR/cd, DBA/2 and Swiss, maintained at the Bhabha Atomic Research Centre, Bombay (designated Bh) were monitored for compatibility with standard strains as well as for genetical homogeneity. For this purpose, five individual mice from each strain were typed serologically for H-2 class I and class II antigens and for lymphocyte differentiation markers, Thy-2, Lyt-1, Lyt-2, TL and Ly-10. In this latter testing, 15 inbred strains from the Institute of Immunology and Experimental Therapy, Wrocław (designated Iiw) were included. Results revealed that none of the tested strains deviated from the reactivity pattern of standard strains described in the literature. No evidence of genetic contamination was found in any strain. In the course of these studies, several interesting observations were made: (1) Swiss/Bh strain is an intra H-2 recombinant, probably KdAbEbDbTlab, (2) C3H/Bh and C3H/Iiw are Ly-10a and Ly-10b, respectively (3) some (CBA, C3H, DBA/2 and GR/S) but not C58/Ly-2a strains cross reacted with high concentration of anti Lyt-2.2 monoclonal antibody HO.2.2.

Animals↗
PubMed1987

Crossreactivity of anti Lyt-2.2 monoclonal antibody with some Lyt-2.2-negative mouse strains.

We observed that thymocytes from some Ly-2a (i.e., Lyt-2.2-) mouse strains crossreacted with high concentrations of anti Lyt-2.2 monoclonal antibody HO.2.2, whereas other Ly-2a strains were clearly negative. Inbred strains from two breeding colonies (Wrocław and Bombay) exhibited the same pattern of reactivity with HO.2.2. The nature of crossreacting antigen is discussed.

Animals↗
PubMed1986

Polymorphic and autoreactive H-2-specific monoclonal antibody isolated after injections of syngeneic Sendai virus-coated lymphocytes.

An H-2-specific monoclonal antibody (mAb Q-1) was obtained from B10.Q (H-2q) mice injected with syngeneic Sendai virus-coated cells. The IgM monoclonal antibody recognizes the public determinant H-2.25 shared by H-2k (Kk) and H-2r haplotypes and cross-reacts with H-2d, H-2s, H-2p, and H-2q cells, the latter being the haplotype of the challenged B-cell donor. The binding of mAb Q-1 to H-2d, H-2s, H-2q, and H-2p cells was lower than to H-2k and H-2r and of decreasing affinity but could be clearly distinguished from the negative reactions with H-2b and H-2f cells. MAb Q-1 distinguishes between Sendai virus-coated and uncoated lymphocytes only cells with low-affinity binding. On virus-coated or infected (H-2p, H-2q, H-2d, H-2s) cells lysis was stronger than on normal lymphocytes. We interpret the enhanced lysis of Sendai virus-positive cells by mAb Q-1 to be due to recognition of a modified exposure of public H-2 determinants induced by Sendai virus.

Animals↗
PubMed1986

Serological analysis of H-2 antigens expression on the cell surface of drug- and lectin-resistant mouse tumor cells.

The results of studies on the H-2 antigens expression on L1210 and P388 mouse lymphoma cells and their drug-resistant sublines as well as on Lewis lung carcinoma (LL2) cells and their wheat germ agglutinin-resistant variants (LL(2)5 and LL(2)8) are presented. The results revealed no qualitative alterations in H-2 antigens expression on cells of L1210 and P388 leukemias and their drug-resistant sublines. However, as determined by cytotoxic assay the increase relative to parental lines in the expression of normal H-2d antigens on cells of both drug-resistant sublines was observed. Using quantitative absorption assay in addition to differentiate quantitative expression of normal H-2b antigens, the presence of alien H-2k and H-2d specificities on lectin-resistant cells of Lewis lung carcinoma was detected.

Animals↗
PubMed1986

Serological analysis of H-2 antigens expression on the cell surface of selected mouse tumors.

Studies on histocompatibility antigens expression on different selected mouse tumor cells revealed very variable pattern. No qualitative alterations in H-2 antigens expression on the cells of the following tumors: RL male 1 and MP26a of BALB/c (H-2d) mice, ASL-1 and RADA-1 of A (H-2a) mice, EL-4 and E male G2 of C57B1/6 (H-2b) mice, K36 and AKSL-4 of AKR (H-2k) mice could be detected. However, the quantitative differences in H-2 antigens expression on some of these tumors were observed.

Animals↗