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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A line of AKR leukemic mouse cells cultured in vitro, designated AKR 87, was established and characterized. Two types of cells were distinguished in this line fibroblasts and lymphoblasts. The lymphoblast-like cells resembled the original tumor cells spontaneous leukemia of AKR mice. In the XC test, cells of this line reacted specifically with XC cells, forming syncytia characteristic of cells infected with mouse leukemia viruses. Ultrathin sections of cells of this line examined on the electron microscope showed presence of type C viral particles.
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PMID:AKR mouse leukemia cells in tissue culture. I. Establishment of leukemic cell line AKR 87 and its morphologic and biologic characteristics. 18 40

Inosine dialdehyde (INOX), the periodate oxidation product of inosine, inhibited the proliferation of various tumor cell lines in suspension culture in a concentration-dependent manner. A concentration of about 1 mM was required to completely inhibit the proliferation of Novikoff rat hepatoma and mouse L-cells, whereas about 0.1 mM completely inhibited the proliferation of L1210 and P388 mouse leukemia and Chinese hamster ovary cells. INOX inhibited in a similar time- and concentration-dependent manner the synthesis of protein, RNA, and DNA, as measured by the incorporation of labeled amino acid, uridine, and thymidine, into acid-insoluble material, without significantly affecting the incorporation of these precursors into the acid-soluble pool. Flow microfluorometric analyses showed that many of the INOX-treated cells became arrested in G2 + M. The results are consistent with the view that INOX affects multiple metabolic steps. The effects of INOX were quite different from those caused by typical inhibitors of ribonucleotide reductase, hydroxyurea, and 2,3-dihydro-1H-pyrazolo(2,3-a)imidazole, which very rapidly inhibited DNA synthesis and caused arrest of the cells in G1, with minimal effects on RNA and protein synthesis.
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PMID:Mechanism of action of inosine dialdehyde (NSC 118994) in the inhibition of proliferation of tumor cells in culture. 19 37

All known tumor types have been reported in the neonate. A numerical listing and discussion are beyond the scope of this review. Wells and Fraumeni give some insight into common congenital malignant neoplasms. Table 2 lists the percentage of neonatal deaths caused by type-specific cancers. Retinoblastoma is probably the most common malignant tumor in the neonate. About seven per cent of these tumors have been apparent at birth. This tumor is not discussed in either article because it is not lethal until muypes in neonatal and pediatric patients. Some congenital malformations in the in the neonate are recognized as being frankly benign (cysts), potentially malignant (teratomas), and frankly malignant (neuroblastoma). A high percentage of teratomas are benign in the newborn period. Leukemia in the newborn appears to be more aggressive yet neuroblastoma has a better prognosis. More studies are needed to help us define why the neonate does better with some tumors and worse with others. Surface cell markers on neonatal leukemia, B and T cell function studies, and other immunologic surveillance studies are needed. Study of neonatal oncology may add to our knowledge of carcinogenesis and oncogenesis in the future.
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PMID:Neonatal oncology. 19 75

Polymethylene-bis(1-nitrosourea), polymethylene-bis(1-nitroso-3-nitroguanidine), and polymethylene-bis(1-nitroso-p-toluenesulfonamide) derivatives were tested for antitumor effect against rat ascites hepatoma AH-13 and mouse leukemia L-1210. Bisnitrosoureas were effective against AH-13 and L-1210, bisnitrosoguanidines were effective against AH-13 alone, and bisnitrosotoluene-sulfonamides were ineffective against both tumor lines. Of all these compounds, 1,1'-ethylene-bis(1-nitrosourea) (EBNU) was the most effective. The antitumor effect of EBNU was compared with that of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). Intraperitoneal administration of EBNU according to the schedule, day 1, days 1 and 5, and days 1, 5, and 9 after intraperitoneal inoculation of L-1210 showed marked prolongation of host survival, although the effective doses used were a few times higher than those used in BCNU to obtain a similar effect. The minimum effective dose (MED) of EBNU on AH-13 cells was estimated as 1 mg/kg, which was 10 times less than that of BCNU, suggesting that EBNU was more effective than BCNU against AH-13.
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PMID:Antitumor effect of 1,1'-polymethylene-bis (1-nitrosourea) and related compounds. 20 35

Acetone-fixed smears of DBA/2 mouse leukemia cells that produce clusters of intracytoplasmic A-particles (pronucleocapsids of mouse mammary tumor virus) were employed as an indirect immunofluorescence system to detect the antibody to A-particles in human sera. With positive test sera, specific fluorescence was easily detectable as discrete cytoplasmic granules at the site of A-particle clusters. The antibody was found in 26 (60%) out of 43 breast cancer patient sera and 4 (25%) of 16 mammary fibroadenoma patient sera, while only 4 (11%) out of 37 control woman sera were antibody-positive. In the case of breast cancer patients, occurrence of tha antibody was not specifically related to a particular type of tumor histology. In a considerable number of positive cases, the antibody tended to disappear within various lengths of time after surgical operation of the breast cancer.
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PMID:Occurrence of antibody against intracytoplasmic A-particles of mouse mammary tumor virus in sera from breast cancer patients. 21 37

Carcinogenic chemicals enhanced infection in contact-inhibited cells with mouse leukemia virus. A correlation was found between the enhancing effects and the carcinogenicities of the 40 chemicals tested. The tumor promoter 12-O-tetradecanoylphorbol-13-acetate did not enhance viral infection.
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PMID:Carcinogenic chemicals enhance mouse leukemia virus infection in contact-inhibited culture: a new simple method of screening carcinogens. 22 46

Two types of apparently spontaneous malignant alterations of fibroblastlike ST/a mouse lung cells (ST-L cells) grown in vitro are described. One type is characterized by a high tumorigenic potential of the altered cells in nonconditioned syngeneic recipients, a fibroblastlike morphology with cell surface showing very few microvilli by scanning electron-microscopy (SEM), and a growth pattern typical of nontransformed cells. These cells were described as R- cells. The other type is characterized bya low tumorigenic potential in non-conditioned, immunocompetent syngeneic recipients, rounding up of the cells which by SEM showed numerous microvilli on the surface, and a growth pattern typical of transformed cells. These cells were described as round cells or R+ cells. In immunoincompetent mice, R+ cells readily produced sarcomas, which grew faster than those produced by R- cells. Both types of ST-L cells expressed murine leukemia virus (MuLV) when tested in a peroxidase anti-p30 plaque test. The concentration of murine leukemia virus envelope glycoprotein (gp70) has previously (5) been shown to be threefold higher in R+ cells compared to R- cells. Furthermore, round-cell transformation was accompanied by the development of crossreacting rejection antigens protective against a secondary shallenge with Ehrlich ascites tumor and with syngeneic dimethylbenzanthracene induced ST/a mouse leukemia (STABAL). A similar protection was obtained by preimmunization with a cloned embryonic feral mouse cell line (SC-1) infected with ST-L virus as well as with virus-free SC-1 cells, suggesting the presence of rejection antigens both of viral (gp70) and nonviral origin.
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PMID:Comparative studies of two types of "spontaneous" malignant alteration of ST/A mouse lung fibroblasts propagated in vitro. 23 Jan 49

Perfluorinated hydrocarbon compounds (PFHC) possess unique physical properties suggesting possible usefulness in man. Their low surface tension allows free flow into tiny folds and crevices, facilitating dispersion along peritoneal surfaces affected by a tumor. These substances are also oxygen solvents. BDF1 female mice injected intraperitoneally (IP) with 10(6) P388 mouse leukemia cells were studied following treatment with preoxygenated compound 1913 and increasing doses of radiation. Preliminary results suggest increased life span compared to radiation treatment alone. Radioenhancement at high sublethal doses of whole-body radiation cannot be excluded.
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PMID:Treatment of P388 leukemia in vivo with perfluoroctylbromide and radiation: a preliminary study. 47 98

The metabolism of 9-beta-D-arabinofuranosyladenine (AraA) to arabinofuranosyladenine 5'-triphosphate (AraATP), an inhibitor of DNA synthesis, in mouse leukemia cells was examined by means of high-pressure liquid chromatography. AraATP was separated from naturally occurring nucleotides in acid-soluble extracts and quantitative measurements of AraATP levels were made. A potent inhibitor of adenosine deaminase (2'-deoxycoformycin; co-vidarabine), when used in combination with AraA in the treatment of leukemia-bearing mice, increased the formation of AraATP in mouse leukemia cells four- to five-fold over that obtained by treatment with AraA alone. By means of high-pressure liquid chromatography the half-life of AraATP in tumor cells could be measured. Results of such studies may be of value in planning chemotherapy regimens.
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PMID:Analysis by high-pressure liquid chromatography of 9-beta-D-arabinofuranosyladenine 5'-triphosphate levels in murine leukemia cells. 55 57

From the time of its inception in 1955, the Drug Development Program of the National Cancer Institute has relied primarily on transplanted rodent tumor systems in vivo for the evaluation and selection of potential antitumor agents. Although greater emphasis has been placed in recent years on rationally designed drugs, the major effort throughout the history of the program has involved the empirical screening of a wide variety of chemical structures and natural products of varying sources. The initial screening spectrum consisted of three mouse tumors, Sarcoma 180, Carcinoma 755 and Leukemia 1210, based on the retrospective analysis presented in the GELLHORN-HIRSCHBERG Report. As a result of further expermental studies and analyses, the screens changed successively to (1) L1210 plus a spectrum of mouse, rat and hamster tumors, (2) L1210 plus the rat tumor, WALKER 256, (3) L1210, plus P388 for natural products and B16 melanoma and LEWIS lung carcinoma for special studies, and finally (4) P388 as a pre-screen followed by a panel of transplanted tumors and xenografts representing the major tumor sites. The rationale underlying each of the successive changes, and results obtained with each approach, will be discussed.
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PMID:Antitumor screening procedures of the National Cancer Institute. 61 10


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