Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As background for a serological definition of the unique antigens of chemically induced sarcomas, we have typed a series of fibroblast and sarcoma cell lines of BALB/c and C57BL/6 origin by cytoxicity and absorption tests for murine leukemia virus (MuLV)-related cell surface antigens and known alloantigens. 7 of the 17 cultured lines expressed the range of cell surface antigens associated with MuLV (GIX, GCSA, gp70, p30), and this was invariably associated with MuLV production. In nonproducer lines of C57BL/6 (but not BALB/c) origin, a MuLV-gp70-like molecule was found on the surface of fibroblasts and sarcoma cells. The alloantigenic phenotype of these MuLV+ and MuLV- cell lines was H-2D+, H-2K+, Thy-1.2+ or -, PC.1+ or -, Lyt-1.2-, Lyt-2.2-, Ia.7-, and TL.2-. A unique antigen was defined on the BALB/c ascites sarcoma Meth A with antisera prepared in BALB/c or (BALB/c X C57BL/6)F1 mice. Tissue culture lines derived from this tumor were MuLV-, which facilitated serological study of the antigen. Absorption analysis indicated that the antigen was restricted to Meth A; it could not be detected in normal or fetal BALB/c tissue MuLV+ or MuLV- fibroblast lines, 12 syngeneic or allogeneic sarcomas, or normal lymphoid cells from 13 different inbred mouse strains.
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PMID:Cell surface antigens of chemically induced sarcomas of the mouse. I. Murine leukemia virus-related antigens and alloantigens on cultured fibroblasts and sarcoma cells: description of a unique antigen on BALB/c Meth A sarcoma. 19 92

Antisera prepared against BALB/c Meth A sarcoma in syngeneic or compatible F1 mice recognize a protein with an apparent molecular weight of 53,000 in extracts of [35S]methionine-labeled transformed BALB/c cells. This component, designated p53, was not detected in normal adult mouse fibroblasts, lymphoid cells, or hematopoietic cells or in mouse embryo cells or 3T3 cells. An extensive variety of antisera, including alloantisera and heterologous antisera directed against structural antigens of murine leukemia viruses, was tested for reactivity with p53; other than Meth A antisera, only comparably prepared antisera against another BALB/c sarcoma, CMS4, had anti-p53 activity. All transformed mouse cells tested were found to express p53; these tests included chemically induced sarcomas, leukemias, spontaneously transformed fibroblasts, and cells transformed by simian virus 40 and murine sarcoma virus. The presence of p53 in tumors of no known viral etiology indicates coding by resident cellular genes; this does not exclude endogenous viruses as the source of coding sequences or the possibility that transforming viruses code directly for p53.
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PMID:Detection of a transformation-related antigen in chemically induced sarcomas and other transformed cells of the mouse. 22 23

The capacity of various malignant and normal mouse cells to acquire resistance to lysis by guinea pig complement during exposure to H-2 antisera in vitro at 37 degrees C (antigenic modulation) was examined. All tumors tested, including cell lines of the TL+ leukemias RADA1, ASL1, and RLmale1, the TL- leukemia EL 4, myelomas MOPC-70A and S194, and the sarcoma Meth A, failed to modulate when incubated with multispecific or monospecific H-2 antisera up to 24 hours, even though under comparable conditions thymus-leukemia (TL) antigens and surface IgG molecules modulated within several hours. Indirect sensitization of RADA1 leukemia cells with H-2 antisera followed by antiserum against mouse IgG also failed to induce H-2 antigen modulation. Normal peritoneal cells from certain mouse strains were partially modulated with H-2D-specific or H-2K-specific and monospecific antisera within several hours, but normal thymus and lymph node cells did not modulate. Modulation of peritoneal cells occurred without a complete loss of sensitizing H-2 antibody from the cell surface and required a cobra venom factor-sensitive activity that could be restored by human complement component C3. Modulation of TL antigens in vitro had previously been shown to have similar characteristics.
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PMID:Antigenic modulation in vitro. III. Failure to modulate H-2 antigens on several mouse tumors. 31 70

The rabbit heteroantisera anti-Meth A sarcoma (H-2d) (RAMA) and rabbit anti-RBL-5 leukemia (H-2b) (RAR-5) have been used to study the presence of normal strain antigens on the surface of different murine tumour cells. RAR-5 detected H-2-like structures on TLX9 (H-bb) lymphoma, however RAMA did not on LSTRA leukemia (H-2d) mastocytoma. Neither RAR-5 nor RAMA contained antibodies against non-H-2 and differentiation antigens.
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PMID:[Strain-specific antigens detected on murine tumour cells by means of rabbit heteroantisera (author's transl)]. 31 51

The effects of orchidectomy on the structure and function of lymphoid tissues in mice have been studied. Both pre- and postpuberal orchidectomy caused relative hypertrophy of the thymus. There was also an increase in size of peripheral lymph nodes to reach a sustained maximum (6 weeks). Sychronous thymectomy and orchidectomy prevented the lymph node enlargement that follows orchidectomy alone. Enlargement of the thymus was due to increased numbers of thymocytes, and it could be abrogated by administration of androgens. Orchidectomy was associated with an acceleration of rejection of skin allografts which was prevented by androgen administration and abrogated by antilymphocyte serum. The reactivity of orchidectomized mice to sheep red blood cells and the early response to oxazolone, which is limited by thymus-processed cells, was increased, whereas production of antibodies to oxazolone, skin allografts, and pneumococcal polysaccharide was unchanged. It is suggested that orchidectomy increases cell-mediated immune responses but has no direct effect upon responses that are mainly dependent on B cells. Orchidectomy prolongs the interval between the subcutaneous injection of methylcholanthrene and the appearance of subcutaneous sarcomas. In tumour transplantation experiments orchidectomy casued protection against the Meth A tumour grown in ascitic or subcutaneous form. This protection was counteracted by antilymphocyte serum and partially countered by adult thymectomy combined with orchidectomy. In contrast, the appearance in AKR mice of spontaneous leukaemia, a tumour known to be thymus dependent, was increased after orchidectomy. The results of experiments with hypopituitary mice suggested that the effects of orchidectomy on immune response result from androgen withdrawal rather than interference with the hormonal milieu.
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PMID:Orchidectomy and immune response. 78 19

Transplantability of mouse tumors superinfected with various kinds of membrane viruses was investigated in syngeneic hosts. Methylcholanthrene-induced fibrosarcomas in BALB/c mice, Meth A, and in C57BL/6 mice, BMT-, superinfected with Friend lymphatic leukemia virus in mice given neonatal injection of the virus, grew more slowly than uninfected tumors. The retardation of growths was not observed in mice that had been given injections of the virus at birth. Similarly, Meth A and a hepatoma in C3H/He mice, MH134, superinfected with Moloney murine sarcoma virus in nu/nu mice, had reduced their transplantability in respective syngeneic mice. Further, Meth A and MH134 superinfected with endogenous rat leukemia virus and human measles virus, respectively, in nu/nu mice also showed reduced transplantability, and some of the former were actually rejected by normal syngeneic hosts. On the other hand, the reduced transplantability was not found in irradiated mice, suggesting that the phenomenon was due to immunological events. However, a myelogenous leukemia in C57BL/6 mice, C1498, superinfected with Moloney sarcoma virus in nu/nu mice grew like uninfected tumor and did not show reduced transplantability at all.
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PMID:Reduced transplantability of syngenic mouse tumors superinfected with membrane viruses in nu/nu mice. 100 77

The antitumor activity of an oily formulation of SMANCS (oily SMANCS), which is a product of conjugation between a proteinaceous antitumor antibiotic neocarzinostatin and poly (styrene-co-maleic acid), after oral administration to mice inoculated with various murine tumors was investigated. BALB/c mice, inoculated either s.c. or i.p. with allogeneic (sarcoma-180) or syngeneic (RL male 1 leukemia and Meth A fibrosarcoma) tumors, were treated with oily SMANCS orally or with an aqueous formulation of SMANCS (aqueous SMANCS) i.v. or i.p. Oral administrations of oily SMANCS or i.v. administrations of aqueous SMANCS to mice bearing three types of tumors in the ascites form resulted in a weak inhibition of tumor growth as compared to the complete inhibition of these tumors by aqueous SMANCS administered i.p. In mice bearing solid tumors, tumor growth was inhibited by 63-82% when a 10 mg/kg dose of oily SMANCS was administered orally to these mice. The antitumor potential of oily SMANCS administered orally was comparable to that obtained from solid tumor-bearing mice receiving i.v. doses of aqueous SMANCS. These results suggest that the oral administration of oily SMANCS to mice bearing various solid tumors inhibits the tumor growth as effectively as aqueous SMANCS administered i.v.
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PMID:Antitumor activity of orally administered SMANCS, a polymer-conjugated protein drug, in mice bearing various murine tumors. 129 69

(-)-(R)-2-Aminomethylpyrrolidine(1,1-cyclobutanedicarboxylato++ +)platinum(II) monohydrate (DWA2114R), cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II) (CBDCA) and cis-diamminedichloroplatinum(II) (CDDP) were compared for their antitumor effects and nephrotoxicity-inducing activities at the same dosage (1/8, 1/4, 1/3, 1/2, 2/3 or 3/4 of the LD10 or LD10) on the basis of their intravenous lethal doses in mice. DWA2114R was effective against murine tumor lines, Colon 26 and Colon 38 carcinomas, M5076 ovarian sarcoma and P388 L1210 leukemias, implanted subcutaneously (s.c.). Triple injection every other day of DWA2114R was more effective than a single injection at each sublethal dose. The antitumor effects of DWA2114R against these tumors were more effective than or were similar to those of CBDCA and CDDP. The antitumor effect against CDDP-resistant L1210 leukemia implanted s.c. was only observed in the treatment of DWA2114R, but not in CBDCA and CDDP. No excellent antitumor effects of three platinum complexes were observed against Lewis lung carcinoma and B16 melanoma implanted s.c. even at triple injection every other day, and no effect was obtained against Meth-A fibrosarcoma under similar conditions. While the treatment of CDDP showed marked increases in levels of blood urea nitrogen and of urinary protein and sugar at effective doses in the antitumor evaluations, the treatment of DWA2114R as well as CBDCA showed no increase in these parameters. These results indicate that DWA2114R represents a desirable second generation antitumor platinum complex.
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PMID:Antitumor effects of three platinum complexes, (-)-(R)-2-aminomethylpyrrolidine(1,1-cyclobutanedicarboxylato)-platinum (II) monohydrate (DWA2114R), cis-diammine-(1,1-cyclobutanedicarboxylato)platinum(II) (CBDCA) and cis-diamminedichloroplatinum(II) (CDDP), in mice. 156 81

The intraperitoneal administration of human recombinant granulocyte colony-stimulating factor (G-CSF) enhanced the growth of intradermally inoculated tumor in mice; in a Meth A fibrosarcoma model, G-CSF administration significantly shortened the latency before tumor appearance, accelerated the increase of tumor size, shortened the survival time of tumor-bearing mice and increased the incidence of lethal tumor growth. A similar growth-enhancing effect of G-CSF was observed in models employing Meth 1 fibrosarcoma, colon carcinoma 26, and L1210 leukemia, although not all the effects were statistically significant. In vitro study showed that G-CSF did not enhance Meth A growth in suspension culture or in soft agar. These data suggest that G-CSF enhances the Meth A growth not directly but through the mediation of host factors. The accumulation of neutrophils was histologically observed in the tumor nodule, the blood, and the spleen in mice given G-CSF repeatedly. The spleen cells and the peripheral blood leukocytes of G-CSF-injected mice enhanced Meth A growth in vitro as compared with those of mice injected with physiological saline. These results suggest the possibility that the in vivo growth of tumor cells was enhanced by G-CSF-induced overproduction of cells including neutrophils.
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PMID:In vivo tumor growth enhancement by granulocyte colony-stimulating factor. 171 Jun 15

We previously demonstrated that a tumor cytotoxic factor(F-TCF) purified from the culture broth of human embryonic lung diploid fibroblast, IMR-90 cells was one of the human hepatocyte growth factors (hHGFs). In the present report, we demonstrate its biological functions. F-TCF showed moderate cytotoxicity on human tumor cell lines KB, BG-1, MCF-7 and Hs913 T, and strong cytotoxicity on mouse tumor cell lines Sarcoma 180, Meth A sarcoma and P388. On the contrary, F-TCF was a potent mitogen not only for adult rat hepatocytes, but also for human endothelial cells, HUVEC and human melanocytes. Moreover, F-TCF induced the differentiation of premyelocyte leukemia, HL-60 cells into morphologically granulocyte-like cells. These biological functions suggest that F-TCF is an effector molecule responsible for inflammation and repair in injured tissues including tumor and liver.
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PMID:A fibroblast-derived tumor cytotoxic factor/F-TCF (hepatocyte growth factor/HGF) has multiple functions in vitro. 183 76


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