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V S Turusov

Publications and source records attributed to V S Turusov.

At least 55 records · Page 3Linked to original sources
PubMed1992

Metastatic capacity of Burkitt's lymphoma cell lines in nude mice.

Burkitt's lymphoma (BL) cell lines estimated in a previous study as having a high, low and no tumourigenicity (7) were intravenously (i.v.) injected into preirradiated (480 rad) nude mice. BL cell lines with a high tumourigenic potential produced metastatic tumours in the brain, spinal cord, bone marrow, stomach and kidney, but did not disseminate into the lung, liver, ovary and spleen. The survival time of the tumour bearing animals ranged from 2 to 10 weeks. The majority of mice i.v. injected with highly tumourigenic BL cell lines showed paresis or paralysis of the hind legs. This was associated with the presence of neoplastic nodules either in the brain and/or in the spinal cord. In animals with metastasis to the stomach and kidney progressive cachexia was observed. The described experimental model of metastatic BL tumours in nude mice can effectively be used for the in vivo study of new therapeutic molecules such as monoclonal antibodies coupled or not to substances, toxic to tumour cells. This model can also be useful for the identification and analysis of homing properties of BL cells and their implication in BL pathogenesis.

Animals↗
PubMed1992

Tumor induction in monkeys after administration of dimethylhydrazine.

1,2-Dimethylhydrazine (DMH) was administered subcutaneously to nine Macaca fascicularis monkeys (6 males and 3 females) at doses of 16 mg/kg body weight, three times a month for two years. Colon cancer was detected in two male monkeys after total DMH doses of 1080 and 3696 mg (528 and 400 mg/kg body wt., respectively). A uterine tumor was induced in one female monkey which received 3648 mg of DMH (608 mg/kg body wt.). Latent periods of tumor development were 34, 47 and 55 weeks, respectively. Histologically, the colon tumors had the structure of adenocarcinoma in both cases and the uterine tumor was diagnosed as fibromyoma.

1,2-Dimethylhydrazine↗
PubMed1992

Renal cell tumors induced in CBA male mice by 1,2-dimethylhydrazine.

Epithelial kidney tumors induced in CBA male mice by 1,2-dimethylhydrazine (DMH) were studied histochemically and immunohistochemically. A total of 48 tumors studied histologically were diagnosed as clear-cell, acidophilic, or mixed adenomas located in the renal cortex. Gamma-glutamyl transpeptidase (GGT) was strongly positive in normal proximal convoluted tubules, slightly positive in the cells of Bowman's capsule, and negative in 47 of 48 tumors examined. Antibodies against the new antigen obtained from the mouse liver oval cells, antigen A6, were also used. This antigen is negative in normal kidney proximal tubules but always positive in distal tubules and collecting ducts. It was also positive in all 47 GGT-negative tumors studied here. One tumor was GGT-positive and antigen A6-negative. Based on our data, it was concluded that the majority of renal cell adenomas induced by DMH in mice probably originate from the distal tubules or collecting ducts and not from the proximal tubules.

1,2-Dimethylhydrazine↗
PubMed1992

[Histogenesis of experimental renal tumors in mice].

Epithelial kidney tumours induced in CBA male mice by 1,2-dimethylhydrazine were studied histochemically and immunohistochemically. Histologically, 48 tumours studied were diagnosed as clear-cell, acidophilic or mixed adenomas located in the renal cortex. Gamma-glutamyl transpeptidase (GGT) was strongly positive in normal proximal convoluted tubules, slightly positive in the cells of Bowman capsule and negative in 47 of 48 tumours examined. Antibodies against the new antigen obtained from the mouse liver oval cells and called A6 antigen were also used. This antigen in normal kidney is negative in proximal tubules but always positive in distal tubules and collective ducts. It was also positive in all 47 GGT-negative tumours. One tumour was GGT-positive and A6 antigen-negative. The conclusion is made that the majority of renal cell adenomas in mice most likely originate from the collective duct system and not from the proximal tubules.

Adenoma↗
PubMed1991

Modifying effect of ascorbic acid and sodium ascorbate on the promoting stage of uterine sarcomogenesis induced in CBA mice by 1,2-dimethylhydrazine and estradiol-dipropionate.

Administration of estradiol-dipropionate (EP) after the cessation of 1,2-dimethylhydrazine (DMH) treatment increased the incidence of uterine sarcomas in CBA mice from 32.5 (DMH alone) to 62.5%. Ascorbic acid (AA) (0.3% in drinking water) given simultaneously with EP decreased the tumour incidence to 35%. Sodium ascorbate did not exert an inhibiting effect. AA inhibited the increase of uterine weight produced in mice by EP and did not influence the growth of mouse transplantable uterine sarcomas. The mechanisms of the antiestrogenic effects of AA are discussed.

1,2-Dimethylhydrazine↗
PubMed1991

[Mouse hepatoblastoma: comparative aspects].

The structure of 12 spontaneous hepatoblastomas found in old (average age 26.5 months) male mice is described. There were considerable strain differences in their incidence: 0.5% (1/194), 0.5% (1/194) and 5% (10/198) in strain C57B1, CBA and F1 (CBA X C57B1), respectively. This proves the importance of genetic factor the role of which in the development of human hepatoblastoma is not established so far. Mouse hepatoblastoma develops almost invariably within or adjacent to liver cell tumours (adenoma or carcinoma). There was a correlation between the incidence of liver cell tumours within a given strain treated with different doses of carcinogen but such correlation was absent in mice of different strains. Histologically and ultrastructurally, mouse hepatoblastoma corresponds to the anaplastic variant of human hepatoblastoma. As distinct from human tumour, mouse hepatoblastoma does not contain alpha-fetoprotein. One tumour was transplanted to the syngeneic host and passed 30 transplant generations retaining the structure of a primary tumour with areas of osteoid tissue and foci of squamous cell metaplasia. Mouse hepatoblastoma may be induced by carcinogens. Likewise, according to the literature, risk of hepatoblastoma is higher in children whose mothers were exposed to the potential carcinogens before or during the pregnancy.

Animals↗
PubMed1990

Increased multiplicity of lung adenomas in five generations of mice treated with benz(a)pyrene when pregnant.

The effect of benz(a)pyrene (BP) given to female mice of A strain on the 18 and 19th days of pregnancy was studied in 5 consecutive generations. As expected there was a high incidence of lung tumours (TBA%) in the F1-generation of mice treated with BP (53.9 vs. 15.4% in control in females and 77.6 vs. 8.0% in control in males). The percentage of TBA was not increased (with one exception) in both males and females of F2-F5 generations which were not directly exposed to carcinogen. Tumor multiplicity increase occurred not only in the F1 generation of BP-treated mice but in both males and females of F2-F5 generations of mice which were not in direct contact with the carcinogen. This increase was statistically significant. There was a slight negative trend within F2-F5 generation of BP-treated mice which however was not significant. Thus the transgenerational carcinogenic effect manifested in a greater tumour multiplicity persisted for four unexposed generations.

Adenocarcinoma↗
PubMed1990

Tumour incidence in the progeny of male rats exposed to ethylnitrosourea before mating.

BDVI male rats were given a single i.p. dose of 80 mg/kg b.w. ethylnitrosourea (ENU), and each rat was then mated at weeks 1, 2, 3, 4 and 5 after treatment with 3 untreated females. A decrease in the fecundity of the treated males was observed, particularly when they were mated 5 weeks after ENU treatment. The average litter size was lower in the treated group, especially for females mated in week 4. No significant differences in pre- or post-weaning mortality were noted between control and treated groups. A slight, non-significant increase in the incidence of brain tumours was observed in the progeny of treated males compared with the controls. The incidence of thyroid tumours was significantly higher in controls but this difference disappeared when adjustment was made for litter effect and intralitter dependence.

Animals↗
PubMed1990

Transplantable mouse hepatoblastoma: histologic, ultrastructural and immunohistochemical study.

Hepatoblastoma found adjacent to a liver cell adenoma in an aged (CBA x C57Bl/6)F1 male mouse was transplanted to the syngeneic host and passed through 30 generations. Histologically, tumours that grew on transplantation retained principal morphological features of the primary tumour. Transplanted tumours were negative for AFP and for antigen A6. This antigen in the normal mouse liver is found in epithelial cells lining bile ducts and ductules including the terminal Hering canals. Some of the Hering cells were consistently A6 negative under normal conditions, and the suggestion is made that these A6 negative cells might be the cells of hepatoblastoma origin.

Adenoma↗
PubMed1990

[Protein S-100 in the histological diagnosis of tumors].

Review deals with the use of the antibodies against protein S-100 in the diagnosis of tumours in man and experimental animals. Protein S-100 was first isolated from the bovine brain and then identified in glial and Schwann cells of the nervous system, epidermal Langerhans cells, myoepithelial cells of the salivary and mammary glands and in many other cells of various organs. In spite of the lack of specificity to any tissue antibodies against protein S-100 are widely used in the diagnosis of human tumours, mainly for the differentiation between neurogenic and soft tissue tumours (positive response to S-100 protein is regularly observed in benign schwannomas, neurofibromas and granular cell tumours while fibroblastic tumours are S100-negative), for the differentiation between nonpigmented melanomas (positive) and anaplastic carcinomas (negative). The knowledge of S-100 protein distribution in normal organ facilitates the establishment of the tumour origin. Antibodies against S-100 protein allowed one to establish the neurogenic origin of some rat soft tissue tumours which were considered otherwise to be of mesenchymal origin and gave additional proof of the neurogenic origin of the rat endocardial tumours.

Animals↗
PubMed1990

[1,2-dimethylhydrazine induction of epithelial tumors of the kidneys in CBA strain mice].

The results of experiments on the 1,2-dimethylhydrazine (DMH) induction of epithelial renal tumours in CBA male mice are presented. The dose-response study shows a sharp increase (from 5 to 75%) of the epithelial renal tumour incidence in the range of 2, 4 and 8 injections of DMH. Higher doses induce a decrease of the tumour incidence due to the early death caused by other tumours. DMH is shown to be the most powerful renal carcinogen in mice. Serial sacrifice of mice after 5 injections of DMH is a convenient model for the study of renal carcinogenesis in mice. Main histological types of epithelial renal tumours are illustrated.

1,2-Dimethylhydrazine↗
PubMed1990

[Morphogenesis and histogenesis of experimental malignant hemangioendothelioma].

Film preparations, various histological stains, autohistoradiography and electron microscopy were used to study morphologic changes occurring in the course of formation of vascular kidney tumors in male CBA mice after subcutaneous injection of 1.2-dimethylhydrazine. Twenty-thirty animals were examined every 4 weeks up to 45-50 weeks. In mice, renal capsule (site of malignant hemangioendothelioma growth) is avascular. Blood vessels developed due to "formation of lumen" in bands of anastomosed cells. Endothelium of the newly formed vessels originated from multipotent mesenchymal cells. Also, intracytoplasmic formation of vascular lumens was observed. The initial neoplastic vascular structure (telangiectases) were registered after 20-30 weeks. They were composed of markedly atypical cells characterized by columnar shape, high nucleo-cytoplasmic ratio and high proliferative activity. Further progression was associated with the development of cavernous hemangioma-like tumors bearing cytologic signs of malignancy as well as well- and poorly-differentiated hemangioendotheliomas.

1,2-Dimethylhydrazine↗
PubMed1990

[The inhibitory effect of ascorbic acid on the estrogen-stimulated promotion of uterine sarcoma development in mice].

The administration of estradiol propionate after the discontinuation of 1,2-dimethylhydrazine (DMH) treatment increased the incidence of uterine sarcoma in CBA mice from 32.5 (DMH alone) to 62.5%. The addition of the ascorbic acid (0.3% solution in drinking water) to estradiol propionate was followed by a decrease in the tumor incidence to 35%, i. e. the acid levelled the promoting effect of estradiol propionate almost completely. Sodium ascorbate did not share that effect. Mechanisms underlying the antiestrogenic effect of the ascorbic acid are discussed.

1,2-Dimethylhydrazine↗
PubMed1989

[Protein S-100 in spontaneous soft tissue and peripheral nerve neoplasms in rats].

16 spontaneous tumors of the peripheral nerves and 18 spontaneous tumors of mesenchymal origin in BDVI rats were studied by peroxidase-antiperoxidase method using anti-serum (DAKOPATT) against protein S-100. The majority of spontaneous peripheral nerve tumors were of cystic histological structure identical to that of cystic neurinomas induced in rats by ethylnitrosourea and almost all of these tumors were S-100 protein positive. The incidence of spontaneous neurinomas in BDVI rats was in some experiments as high as 5%. All tumors of mesenchymal origin (except one lipoma) were S-100 protein negative: 2 fibromas, 6 fibrosarcomas, 3 malignant fibrous histiocytomas, one rhabdomyosarcoma and one hemangioendothelioma. S-100 protein is found, as in human pathology, useful for distinguishing tumors of schwann cell and mesenchymal origin in rats.

Animals↗
PubMed1989

Review of experiments on multigeneration carcinogenicity: of design, experimental models and analyses.

It is widely accepted that parental exposure to a carcinogen may result in an increased risk for cancer in otherwise untreated offspring. Results of a new experiment and a review of published studies on multigeneration carcinogenesis are presented and discussed on the basis of the animal model used and of the design and analysis of the individual experiments. Several of the studies indicate an effect of multigenerational carcinogenesis, characterized by one or more of the following: an increase in tumour incidence (either specific to the carcinogen used or spontaneous, or neither spontaneous nor specific); an increase in tumour multiplicity; or transmission of the initiated state through germ cells. In several other well-conducted experiments, either no multigeneration effect was observed or the results were ambiguous. The clearest, most consistent results are obtained in experiments on mice. The published results, however, cannot preclude the possibility that the observed increases are due to a genetic predisposition rather than to induction of an oncogenic mutation in the germ cells. The studies reviewed here indicate that mothers and fathers may differ in transmission efficiency, but it would be premature to draw definitive conclusions. More work is needed in this field, but it appears that mice may be a more sensitive animal model for the study of multigeneration carcinogenesis experiments than rats. In future studies of this effect, experimental designs which allow for assessment of the relative efficiency of transmission through the mother and the father should be implemented. Care should also be taken to plan experiments that are large enough, and to retain all pertinent information, in particular litter information, in order that clear conclusions can be drawn from the results.

Animals↗