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At least 199 records · Page 11Linked to original sources
PubMed1985

[Cationic protein content in the leukocytes of rats with Pliss' lymphosarcoma and 7,12-dimethylbenz(a)anthracene-induced sarcoma].

The level of intraleukocytic cationic proteins is studied in rats with the transplanted Pliss lymphosarcoma and sarcoma induced by 7,12-dimethylbenz(a)anthracene (DMBA). The amount of cationic proteins was found to decrease in granulocytes both of mongrel and Wistar rats with transplantable tumours. The phenomenon is typical of the rats with the DMBA-induced tumour.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

Histochemistry of normal and diseased human lymph nodes.

Gomori's metal precipitate technique was used to demonstrate the phosphatase activity of the human cervical lymph node in health and disease, using four different phosphate esters (sodium beta-glycerophosphate and adenosine triphosphate at pH 9, riboflavin 5'-phosphate at pH 9.2 and 5'-monophosphoric acid at pH 8.3). In fetal lymph nodes, using 5'-monophosphoric acid, an outstanding positive activity was noticed in the lymphatic follicles. With the other three substrates there was either no nodular reaction or just a narrow rim of positive activity around the follicles, the internodular tissue being negative with all four substrates used. With chronic non-specific lymphadenitis the enzyme hydrolysing the three substrates (beta-glycerophosphate, riboflavin 5'-phosphate and adenosine triphosphate) began to make their appearance. It seems that with lymphadenitis, a qualitative change of the phosphatase activity takes place. A special characteristic pattern of phosphatase activity has been described in both 'early' and 'caseating' tuberculous lymphadenitis. In malignant lymphomas it was noticed that no activity was encountered with any of the four substrates in reticulum cell sarcoma. However, in lymphosarcoma a positive activity was obtained when either beta-glycerophosphate or adenosine triphosphate substrates was used, to the extent that one can depend upon this characteristic phosphatase activity in differentiating between reticulum cell sarcoma and lymphosarcoma. However, no enzymatic activity was obtained when the other two phosphate esters were used.

Adenosine Triphosphate↗
PubMed1978

Antitumor tests of amygdalin in transplantable animal tumor systems.

Except for oral administration, there was no grossly observed toxicity from carefully administered high doses of amygdalin in the experimental systems used. The compound in high doses was ineffective against the DMBA-induced rat mammary carcinoma and the following transplanted experimental tumors: Sarcoma 180, plasma cell tumor LPC-1, leukemia L1210, Mecca lymphosarcoma, Ridgway osteogenic sarcoma, sarcoma T241, mammary carcinoma E0771, Taper liver tumor, Ehrlich carcinoma (solid and ascites), and Walker carcinosarcoma 256. Amygdalin did not noticeably influence the toxicity or impair the efficacy of these chemotherapeutic agents in their respective systems: Cytosine arabinoside, methotrexate, cytoxan, or 5-fluorouracil in L1210; the latter two in LPC-1; 6-mercaptopurine in Ridgway osteogenic sarcoma; estradiol-17beta or 2alpha-methyldihydrotestosterone propionate in the DMBA-induced rat mammary carcinoma.

Amygdalin↗
PubMed1977

[Several structural characteristics of vital dyes].

Lymphocytes and macrophages of normal rats, cells of lymphosarcoma and ovarian carcinoma of rats (CC strain), cells of sarcoma 37 and lymphosarcoma Nk/Ly of mice were investigated for their capacity for vital staining by 86 days in concentrations within the range of 10(-5)--3-10(-2) M. It was found that alkylation of amino groups of the basic dyes increased their capacity for penetrating the living cells and depositing in their cytoplasm in cases of thiazine, oxazine, acridine, xanthene, diazine, and triphenylmethane compounds. The acid radicals decreased the capacity of the dye to vital staining of the cells considerably. The degree of basicity of the dye molecule and its amino groups played no decisive role in the process of vital staining.

Animals↗
PubMed1976

Loss or persistence of the differentiated state of simian virus 40-induced hamster tumor cells before and after serial passage in culture.

The transformed cells that arise from among the hamster epithelial and mesenchymal cells exposed to SV40 in vitro are, as a rule, fibroblastoid and pleomorphic rather than epithelioid. Moreover, the neoplasms that these transformed cells induce in the allogeneic host are spindle cell sarcomas and pleomorphic sarcomas rather than carcinomas. Since this phenomenon may result from cellular dedifferentiation in culture, to the extent that the anaplastic morphology and lack of specialized function can no longer suggest the cell or origin, we investigated the fate of the differentiated state of cells of three types of SV40-induced hamster tumors before and after serial passage in vitro. The tumors evaluated were three reticulum cell sarcomas, three osteogenic sarcomas, and two lymphosarcomas of B-cell origin. Our data demonstrate that reticulum cell sarcoma cells lose their morphological differentiation soon after the original tumors are dissociated into cell suspensions but preserve their phagocytic activity throughout their in vitro passage. Osteogenic sarcoma cells lose their differentiated phenotype and their capacity to form osteoid during but not before their serial passage in culture. Lymphosarcoma cells preserve their lymphoid morphology and their ability to produce immunoglobulin even after many in vitro passages. These results indicate that, in many types of SV40-induced tumors, neoplastic cell dedifferentiation, following serial passage in culture, is responsible to a great extent for the emergence of new cell phenotypes lacking in morphological and functional features characteristic of the cells originally transformed by SV40.

Animals↗
PubMed1977

Antitumor activity of new anthracycline antibiotics, aclacinomycin-A and its analogs, and their toxicity.

New anthracycline antibiotics have been isolated from the culture of Streptomyces galilaeus MA144-M1. Among 14 anthracycline compounds, aclacinomycin-A showed the strongest activity in inhibiting leukemia L-1210 and had lower toxicity than others. Antitumor activity of aclacinomycin-A against leukemia L-1210 and P-388, solid sarcoma-180, and lymphosarcoma 6C3HED was examined in comparison with adriamycin and daunomycin. Aclacinomycin-A showed the same degree of activity against leukemia L-1210 and P-388, when administered intraperitoneally, as daunomycin and somewhat less than adriamycin. In oral administration, aclacinomycin-A also exhibited a significant activity on leukemia L-1210. The degree of inhibition of the growth of sarcoma-180 and 6C3HED lymphosarcoma transplanted subcutaneously by aclacinomycin-A was almost the same as that of adriamycin and daunomycin, although the optimal dose was about twice more than adriamycin. Acute cardiotoxicity of aclacinomycin-A by a test using hamsters was more than 10 times lower than that of adriamycin.

Aclarubicin↗
PubMed1992

[Experience with using carminomycin in oncological clinical practice].

Carminomycin is an original antitumor antibiotic from the anthracycline group isolated at the Institute of New Antibiotics (USSR) in 1973. Pharmacological investigation of carminomycin revealed its satisfactory absorption from the gastrointestinal tract which proved to be a distinguishing property of the antibiotic as compared to other anthracyclines such as adriamycin and rubomycin. The clinical trials of carminomycin showed that it was mainly active against soft tissue sarcoma and breast cancer, lymphosarcoma, neuroblastoma, Wilms' tumor and Ewing's sarcoma in children, as well as acute leukemia. Various regimens for the antibiotic administration were applied: short-term, single and long-term. Suppression of hemopoiesis was considered as a limiting toxic effect. By the data available carminomycin had lower cardiotoxicity as compared with rubomycin and adriamycin. Development of oral carminomycin is believed promising.

Adult↗
PubMed1989

[Synthesis and antitumor properties of 3'-desamino- dimethylformamidine doxorubicin].

Interaction of doxorubicin hydrochloride with dimethylformamide diethylacetal yielded hydrochloride of 3'-desamino-3'-dimethylformamidine doxorubicin (DFD). It was shown that with single intravenous administration to tumor-free mice DFD was 2.5 times less toxic than the initial doxorubicin. Antitumor activity of DFD was studied with respect to 6 transplantable murine tumors: lymphosarcoma LIO-1, sarcoma 180, lymphadenosis NK-Ly, Ehrlich carcinoma, hemocytoblastosis La and leukemia P-388. Selectivity of the DFD activity against all the above tumors was shown to be high and practically equal to that of doxorubicin. DFD had the highest inhibitory effect on development of Ehrlich carcinoma and lymphosarcoma LIO-1.

Amidines↗
PubMed1980

Comparison of the level of cellular retinoid-binding proteins and susceptibility to retinoid-induced growth inhibition of various neoplastic cell lines.

The presence and level of cellular retinol-binding protein (CRBP) and cellular retinoic acid-binding protein (CRABP) were determined in several neoplastic cell lines. These cells exhibited different degrees of susceptibility to growth inhibition in culture by two retinoids, retinyl acetate and retinoic acid. CRABP was detected in 10 and CRBP in 3 of the 11 tested cell lines. The levels of CRBP and CRABP were in the ranges 15-3,400 and 4-1,290 pmol per 10(9) cells, respectively, as determined by sucrose gradient centrifugation. Cell lines that contained CRABP included S91 and B16 melanomas; Mm5mT and DMBA No. 8 mammary adenocarcinomas; BW5147, BW5147.RicR, and P3 neoplastic lymphoid cells; F361.2 (a hybrid cell line obtained by fusion of MSV3T3 and BW5147); MSV3T3 sarcoma; and RAW8 lymphosarcoma. All but the last two cell lines were inhibited by retinoic acid in culture. CRBP was detected in extracts of S91, Mm5mT, and RAW8. Retinyl acetate inhibited the growth of all cell lines with the exception of RAW8, MSV3T3, and F361.2. No correlation was found between the level of either binding protein and the extent of growth inhibition by either retinyl acetate or retinoic acid. Neither of the binding proteins was detected in L1210-A5 leukemia cells, whose proliferation can be inhibited by both retinyl acetate and retinoic acid. These data indicated that screening cell lines for the presence and level of CRBP and CRABP is not sufficient to predict the susceptibility of cultured cells to growth inhibition by retinoids.

Adenocarcinoma↗
PubMed1987

Mortality among plutonium and other radiation workers at a plutonium weapons facility.

Mortality among 5,413 white males who were employed for at least two years at a plutonium weapons facility was investigated to measure risks from exposures to low levels of plutonium and external radiation. When compared with US death rates, fewer deaths than expected were found for all causes of death, all cancers, and lung cancer. No bone cancer was observed. An excess of brain tumors was found for the cohort in general. Elevated rate ratios for all causes of death and all lymphopoietic neoplasms were found when employees with plutonium body burdens greater than or equal to 2 nCi were compared with those with body burdens less than 2 nCi, while accounting for age, calendar period, and induction time. Increased rate ratios were also found for esophageal, stomach, colon, and prostate cancers, and for lymphosarcomas and reticulum cell sarcomas. No elevated rate ratios were noted for bone and liver cancers. When employees with cumulative exposures greater than or equal to 1 rem were compared with those with exposures less than 1 rem, elevated rate ratios were found for myeloid leukemia, lymphosarcoma and reticulum cell sarcoma, liver neoplasms, and unspecified brain tumors. No overall dose-response relationships were found for plutonium or external radiation exposures. Standardized rate ratios increased, however, as plutonium body burden levels increased for all causes, all cancers, and digestive cancers at five years induction time. Standardized rate ratios also increased as external radiation exposure categories increased for all lymphopoietic cancers and unspecified brain tumors for a two-year induction period. With the exception of analyses of combined categories of death, and perhaps of lung cancer, confidence limits were wide, indicating limited precision. Nevertheless, these findings suggest that increased risks for several types of cancers cannot be ruled out at this time for individuals with plutonium body burdens of greater than or equal to 2 nCi. Plutonium-burdened individuals should continue to be studied in future years.

Air Pollutants, Radioactive↗