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

M0use alloantisera produced against different specificities of the K, I, and D regions of the H-2 gene complex reacted as immunogenetically anticipated with normal lymphoid target cells of different haplotypes in cytotoxicity and indirect immunofluorescence tests. These same alloantisera, however, produced anomalous positive reactions when tested on cultured MCA-induced sarcoma cells from B10 background H-2 congenic mice. Absorption experiments demonstrated that the anomalous activity in these sera was directed against a tumor membrane antigen(s) which was distinct from H-2 region specificities against which the reference alloantisera were produced, and which was shared in common by multiple cultured sarcoma lines. Similar anti-tumor antibody activity could be demonstrated in the serum of older (greater than 12 weeks) but not younger normal unimmunized mice of the strains used as recipients for alloantiserum production. It is suggested that the observed anamalous anti-tumor activity in these alloantisera may be due to the presence of antibodies reactive with envelope antigens of murine leukemia virus which are expressed on sarcoma cells maintained in culture.
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PMID:Anomalous reactions of mouse alloantisera with cultured tumor cells. I. Demonstration of widespread occurrence using reference typing sera. 5 86

Methylcholanthrene-induced sarcomas of BALB/c mice express unique tumor specific transplantation antigens (TSTA), and weaker, common TSTA. Antigens of endogenous murine leukemia virus (MuLV) expressed by some of these tumors cannot completely account for these common TSTA. However, MuLV antigens on the immunizing tumor appear to increase the immunogenicity of the common TSTA.
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PMID:Unique and common tumor-specific transplantation antigens of chemically induced mouse sarcomas. 7 55

A rabbit antiserum raised by repeated immunization with BALB/c fetuses obtained at 10-14 days of gestation was used to search for oncofetal antigens (OFA) in murine sarcomas which had previously been characterized for the expression of endogenous murine leukemia virus (MuLV). Iodinated protein A from staphylococcus aureus (IPA) was used to quantitate binding of the antiserum to cultured tumor or fetal cells or to saline extracts of tumors and fetuses. Use of the "antigen" extracts facilitated the assay: the extracts bound to plastic and served as targets for the binding assay, eliminating the need to establish tumors in culture. After absorbtion in vitro and in vivo with adult tissues the rabbit antiserum bound to day 10-14 fetal cells and extract but not to endogenous MuLV (BALB virus 1). The antiserum bound equally well to MuLV-negative and MuLV-positive sublines of MCA-induced sarcomas 1420 and 1414 but not to Moloney sarcoma cells and MCA-induced sarcoma 1386. Thus, the absorbed antiserum detects a class of common cross-reacting antigens which are serologically distinct from MuLV-associated antigens.
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PMID:Expression of oncofetal antigens on murine sarcomas characterized for expression of endogenous MuLV. 8 Nov 87

Sera from C3H/HeHa mice immunized with syngeneic methylcholanthrene-induced sarcoma react with allogeneic thymus, lymphoma and leukemia cells. The presence on leukemia and lymphoma cells of H-2 specificities expressed on normal cells of other H-2 haplotypes from the one in which the tumor originates is described. It was observed that the reaction of antisera to H-2 specificities with lymphoma cells was blocked by anti-MCA sarcoma sera. The cross-reactivity between MC sarcomas, thymus, leukemia and lymphoma cells is considered to be due to antibodies against these "alien" allospecificities.
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PMID:Alien H-2 allospecificities in murine chemically-induced tumors. 9 37

The leukaemic lesions in intact and ovariectomized mice of strain ICRC, induced with 20-methylcholanthrene (20-MCA) in combination with or without hormones were investigated for the presence of mouse leukaemia virus (MuLV) by (i) bioassays and (ii) electron microscopy. The different experimental groups treated with 20-MCA were (i) intact females, (ii) ovariectomized females, (iii) ovariectomized females with pituitary graft, (iv) ovariectomized females with 10 mug oestradiol/day for 30 days and (v) ovariectomized females with 1 mug oestradiol together with 1 mg progesteron/day for 30 days. It was possible to transmit nearly all these experimentally induced leukaemias to syngeneic mice through acellular extracts, compared with very poor transmissibility of spontaneous leukaemias in the ICRC strain, indicating functional activation of viral agents on combined treatment with carcinogen and hormones. Potency of the acellular leukaemic extract from the mice of group (ii) without the ovarian hormones was much weaker than that from mice of the other experimental groups. The leukaemogenic activity of MuLV was enhanced on serial transmission in syngeneic hosts. Leukaemic lesions of ovariectomized mice treated with 20-MCA and oestradiol were also transmissible to the sucklings of allogeneic mice of strain C3H-MTV, C57-BL and Dba-MTV. The cell-free supernatant medium of the cultures of these leukaemic lesions induced leukaemias on back inoculation into syngeneic mice. Electron microscopic studies of lesions induced with carcinogen and oestradiol consistently showed abundant intracytoplasmic type A particles. Numerous intracytoplasmic type A particles as well as some type B particles were found in the leukaemic tissues of ovariectomized females treated with MCA and oestradiol combined with progesterone. Type C particles, characteristic of MuLV were seen in the leukaemic tissues of all other experimental groups. These findings indicate a significant influence of the physiological condition of the host, particularly the hormonal make up, on expression and activity of specific viral agents.
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PMID:Activation of murine leukaemia virus under different physiological conditions. 16 15

Complementary DNA (cDNA) synthesized by Moloney murine sarcoma virus (M-MSV) was separated into two parts, the first, termed MSV-specific cDNA, composed of nucleotide sequences found only in M-MSV viral RNA, and the second, termed MSV-MuLV common cDNA, composed of nucleotide sequences that were found in both M-MSV and murine leukemia virus (MuLV) VIRAL RNAs. RNA complementary to the MSV-specific cDNA was not found in several other MSV isolates, nor in ecotropic MuLV, mouse mammary tumor virus, or several murine xenotropic oncoviruses. Cellular DNA of several species was examined for the presence of nucleotide sequences complementary to MSV-specific cDNA. Cells transformed by M-MSV did contain MSV-specific cDNA in their DNA. Normal mouse cell DNA apparently contained the majority of MSV-specific nucleotide sequences. Cellular DNA of related species contained proportionally less MSV-specific cDNA. Hybrids of MSV-spedivic cDNA and cellular DNA of related species melted at lower temperatures than hybrids of MSV-specific cDNA and mouse cellular DNA. RNA from normal mouse adult or embryonic cells did not contain detectable nucleotide sequences complementary to MSV-specific cDNA. Transformation of cells with M-msv resulted in transcription of RNA hybridizing with MSV-specific cDNA. Methylcholanthrene-induced mouse sarcomas and cell lines derived from them did not contain RNA complementary to MSV-specific cDNA. Mouse cell lines transformed with avian sarcoma virus or Kirsten MSV-specific cDNA. RNA homologous to MSV-specific nucleotide sequences is measurably present only in cells transformed by M-MSV and not in cells transformed by other biological or chemical agents that also cause sarcomas.
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PMID:Nucleotide sequences in mouse DNA and RNA specific for Moloney sarcoma virus. 18 23

Cells from the spleens and thymuses of BALB/c mice whose Moloney sarcoma virus (MSV)-induced, primary sarcomas have regressed 2-3 months earlier ("MSV regressors") or are in the process of regressing can, when adoptively transferred to syngeneic mice given MSV at the age of 20 days, prevent the natural regression of the MSV sarcomas in the recipient mice. The cells responsible for this tumor-enhancing effect express the Thy 1 marker. They are not demonstrable in the thymuses of normal untreated mice or in mice that have either been immunized against or are bearing methylcholanthrene-induced sarcomas. The tumor-enhancing cells are not destroyed after administration of 400 rads (1 rad = 1.00 x 10(-2) J/kg) of whole body radiation. However, the effect of the irradiated cells is seen only in the presence of a nonirradiated T-cell population, represented in the thymuses of normal control mice, with which we postulate that they interact. Studies on a transplantable, chemically induced, murine leukemia virus antigen-negative sarcoma, MCA-1460, further support the concept that relatively radioresistant thymus cells from immune mice can enhance tumor outgrowth by interacting with radiosensitive T cells that are present in nonimmune mice.
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PMID:Tumor-enhancing suppressor activator T cells in spleens and thymuses of tumor immune mice. 31 60

A competition radioimmunoassay for murine leukemia virus p30 has been developed. Serial dilutions of the unknown in wells of microtiter plates are incubated with 125I-labeled p30 and goat antiserum specific for p30. Bound p30 is then removed by an immunoadsorbent specific for goat immunoglobulin, prepared from S. aureus. An internal standard of 51Cr is used to correct for volumetric errors, the amount of the labeled p30 precipitated being calculated from the 125I/51 Cr ratio of the supernatant. The assay is rapid, being completed within 2 h, precise, having a coefficient of variation less than 1%, and sensitive, being capable of detecting p30 concentrations as low as 2 ng/ml in a volume of 0.02 ml. It has been used to measure p30 levels in a series of MCA-induced fibrosarcomas of BALB/c mice.
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PMID:Radioimmunoassay of murine leukemia virus p30 using Staphylococcus aureus as immunoadsorbent. 65 2

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

DAP-IV activity (Gly-Pro-MCA hydrolysis, pH 7.8) was found in lysates of peripheral blood lymphocytes of patients with T- and B-cell forms of malignant lymphoproliferative diseases. The highest DAP-IV activity was seen in the cells of patients with a rare variant of T-cell lymphocytic leukemia (T-CLL); these cells expressed simultaneously the antigens of T helpers and T suppressors (Th and Ts) (OKT4+ and OKT8+). The DAP-IV activity about ten times less was found in the pathological cells with a phenotype of mature Th (Sezary disease), as well as in the cells expressing antigens of both Ts and natural killers (a rare variant of T-CLL). The same activity was also found in Ts (T gamma-lymphocytosis). The data obtained show that the differences in DAP-IV expression are connected with the differentiation step rather than with the belonging to a particular subpopulation of T-cells. DAP-IV activity, which was somewhat lower than that of T-cells, was found in B-lymphocytes of patients with B-CLL, hair-cellular leukemia, and non-Hodgkin's lymphoma. No correlation of DAP-IV activity with the level of E-cellular differentiation was observed.
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PMID:[Dipeptidyl aminopeptidase-IV in lymphocytes of patients with lymphoproliferative diseases]. 257 81


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