Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035412 (rhabdomyosarcoma)
 6,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The production of a cytotoxic factor synthesized by human haemic killer cells growing in vitro is described. The factor can be found extra- and intra-cellularly. It is released from the cells by an apocrine form of secretion, illustrated by light and electron micrographs. The culture fluid from 14C-labelled killer cells reveals numerous radioactive bands following SDS-gel electrophoresis. The killing factor is precipitated by 30 to 60% saturation of ammonium sulphate. Cultures of human rhabdomyosarcoma and osteosarcoma cells are more susceptible to the killer cells than normal human dermal or lung fibroblasts. During contact or killer with target cells a higher level of cytotoxic activity can be detected in the culture fluid. The cell-killing activity is completely inactivated by 30 min at 60 degrees C, but it is not absorbed by target cells during 1 h of incubation. The cytotoxic factor is unlikely to be an interferon since it did not prevent the replication of a wide range of viruses and only a low level of interferon could be detected in the culture medium. The introduction of Strep. faecalis into cultures of killer cells caused their transformation into immunoblast-like cells, indicating their lymphoid origin. The cells did not phagocytose the microorganism. When the humoral factor was injected into fibro-sarcoma-bearing mice approximately 50% survived, whereas all control animals died.
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PMID:A humoral cytotoxic substance produced by a human killer cell line. 41 8

Rhabdomyosarcoma (TE) and cervical carcinoma (MS) cells 24 h previously brought from medium with a PO2 of 18 kilo Pascal (kPa) (ambient air) to PO2 of 6 or 3 Kpa (in vivo physiologic values) were infected with Sendai virus, and the interferon (IFN) and virus production was followed in the ensuing 24 h period. With TE cells the IFN production decreased when moving from 18 to 6 Kpa and ceased completely at 3 Kpa, while the virus production responded inversely. MS cells produced most IFN at the lowest oxygen tension, and virus production was only moderately affected. Growth for three months at the three different oxygen tensions prior to infection reduced the difference in IFN production at the different oxygen tensions. On the same target cells different human virus responded in different ways to the tested oxygen tensions. It is concluded that mimicking the in vivo situations might require primary cultures of virus and cells to be started and passaged at in vivo physiological oxygen tensions.
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PMID:In vitro interferon and virus production at in vivo physiologic oxygen tensions. 172 24

The effects of carcinogenic nickel [(Ni) CAS: 7440-02-0] and Ni compounds on the natural killer (NK) cell activity of rat peripheral blood mononuclear cells (PBMCs) were studied. Rhabdomyosarcomas were locally induced by one im injection of Ni or Ni subsulfide [(Ni3S2) CAS: 12035-72-2] dust in the hind leg of WAG rats. A weakly tumorigenic dose of 5 mg Ni3S2 (tumor incidence, 2%) induced a transient decrease of PBMC NK activity against YAC-1 cells in vitro (from the 17th to the 23d wk after Ni3S2 inoculation), which could be restored by in vivo injections of partially purified rat fibroblastic interferon (IFN). Injection of 20 mg Ni (tumor incidence, 47.5%) produced a long-lasting depression of NK cell activity (from the 8th to the 23d wk). In vivo chronic IFN treatment of the Ni-injected rats neither restored NK cell activity nor affected the tumor incidence. However, NK cells of Ni-treated animals responded normally to IFN in vitro. Prospective analysis of individual NK cell responses showed that a persistent depression of basal NK cell activity was restricted to rats that subsequently developed a tumor. In these animals the time between carcinogen treatment and clinical detection of the primary tumor was positively correlated with the mean level of NK cell activity (3-4 determinations/rat). Admixture of manganese to Ni inhibited the development of tumors and also prevented the depression of NK cell activity produced by Ni alone. Noncarcinogenic Ni oxide stimulated NK cell activity. These results point out the possible involvement of NK cells in resistance to Ni-induced carcinogenesis.
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PMID:Inhibition of rat natural killer cell function by carcinogenic nickel compounds: preventive action of manganese. 243 44

The human rhabdomyosarcoma cell line RD-114 is partially responsive to interferons (IFNs). In these cells, alpha interferon (IFN-alpha) or gamma interferon (IFN-gamma) inhibits the replication of some viruses but not of others. Similarly, some of the IFN-inducible mRNAs are induced poorly, whereas others are induced well. Here we report the isolation of clonal derivatives of this line which display different spectra of responses to IFNs. Among the eight extensively characterized clonal lines, one, C10, did not respond to IFN-alpha or IFN-gamma at all. Retrovirus production by each of the seven other lines was inhibited by both IFN-alpha and IFN-gamma. Replication of vesicular stomatitis virus was inhibited strongly by IFN-alpha in clone B1 but not in others, whereas it was not appreciably affected by IFN-gamma in any clone. Replication of encephalomyocarditis virus was inhibited strongly by IFN-gamma in clones A1, A2, A3, B3, and B8 and by IFN-alpha in clone A2. Neither IFN inhibited the multiplication of these clones greatly, although their doubling times were slightly increased. Five mRNAs were induced by IFNs to varying degrees in the seven clones. mRNA 2A was most strongly induced by IFN-gamma in clone A3. mRNA 1-8 was strongly induced by IFN-alpha in clone A1 and by either IFN in clones A2 and A3. The highest concentrations of 2',5'-oligoadenylate synthetase mRNA, mRNA 561, and mRNA 6-16 were in IFN-alpha-treated clones A1 and A2. These results demonstrated the existence of clonal heterogeneity in IFN responses in a cell line and strengthened the view that IFN treatment of cells generates multiple signals leading to a variety of IFN-induced phenotypes.
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PMID:Clonal derivatives of the RD-114 cell line differ in their antiviral and gene-inducing responses to interferons. 244 Oct 75

The mechanism of human peripheral blood monocyte-mediated cytotoxicity was investigated using the HT-29 human colon adenocarcinoma line, A673 human rhabdomyosarcoma line, and A375 human melanoma line as target cells. Pretreatment of these target cells with 100 U/ml of recombinant human interferon (IFN)-gamma for 48 hr increased their susceptibility to monocyte killing. Increased susceptibility to the lytic action was particularly pronounced at low effector/target cell ratios. Unlike IFN-gamma human IFN-alpha did not potentiate monocyte cytotoxicity, and pretreatment of HT-29 with IFN-alpha also had virtually no effect on their susceptibility to monocyte killing. However, IFN-gamma appeared to prime either monocytes or target cells to become responsive to IFN-alpha. Our data suggest that IFN-gamma can promote the killing of tumor cells by monocytes through two separate actions, one on the monocyte and one on the target cell.
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PMID:Interferon-gamma enhances target cell sensitivity to monocyte killing. 309

Two types of growth-modulating factors were derived from the serum-free conditioned media of a human rhabdomyosarcoma cell line, A673. One type, Mr 18,000 to 22,000, competes for binding to epidermal growth factor receptors and enhances the growth of normal and tumor cells in soft agar. It has all of the biological properties ascribed to transforming growth factor type alpha (TGF alpha). A673 cells also produce factors which inhibit the growth of human tumor cells in soft agar and in monolayer cultures. These tumor cell growth-inhibiting factors (TIFs) are acid- and heat-stable peptides. The major TIF activities have molecular weights in the ranges of greater than 28,000, 18,000 to 22,000, 10,000 to 16,000, and 5,000 to 10,000 and do not possess the antiviral activity associated with interferon. Partially purified preparations of TIF-1 (Mr 10,000 to 16,000) inhibit the growth of all human tumor cell lines tested and stimulate the growth of normal human fibroblasts and epithelial cells in monolayer cultures. The growth of human lung carcinoma A549 cells in soft agar, which was enhanced by treatment with TGF alpha from A673-conditioned media, was inhibited by treatment with TIF-1 derived from the same media. The ratio of the two types of tumor cell-derived, growth-modulating factors (TIFs and TGF alpha), which are antagonistic in their biological effects, may determine the capacity of tumor cells for anchorage-independent growth.
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PMID:Isolation of tumor cell growth-inhibiting factors from a human rhabdomyosarcoma cell line. 385 21

Since 1970, we have carried out cancer chemotherapy and immunotherapy in cooperation with Japanese scientists, particularly Prof. H. Umezawa, who has generously supplied bleomycin, peplomycin, acalcinomycin A (ACM), THP-adriamycin (THP), neothramycin and bestatin. Malignant tumors curable by pharmacotherapy are polycythemia vera (CR 100%), acute lymphoid leukemia (ALL) (CR 80%), Burkitt tumor (CR 80 or 50%), Hodgkin disease (CR 80%), chorioepithelioma (CR 80%), testicular cancer (CR 80%), ovary cancer of children (CR 80%), Wilms renal cancer (CR 60%), rhabdomyosarcoma (CR 75%), osteosarcoma (CR 60%), Ewing tumor (CR 60%), brain tumor of children (CR greater than 50%), testicular embryonal cancer of children (CR greater than 50%), acute myeloid leukemia (AML) (CR 50%), non-Hodgkin lymphoma (NHL) (CR 50%), ovary cancer of adults (CR 40%), small cell lung cancer (CR 20%) and breast cancer. Our experimental and/or clinical experience with ACM, THP, methoxy-9-ellipticine lactate, navelbine, 4-demethyl-epipodophyllotoxin-beta-d-ethyledene glucoside, bestatin and interferon is presented. ACM is effective against AML, ALL, NHL, Burkitt tumor, breast cancer. We have comparatively investigated cardiac and dermal toxicity of 12 kinds of anthracycline antibiotics and mitoxantrone, using golden hamsters. Of the drugs examined, ACM, THP, AD-32 and AD-143 cause much less cardiomyopathy and alopecia than the other agents. The results have been confirmed by electron microscopic studies. Bestatin is an immunorestorator, which recovers immunological functions decreased in aged animals. We hope that cancer chemotherapy and immunotherapy will progress in future and contribute to cure of neoplasms. Japanese scientists have been making a great contribution in the field of cancer pharmacotherapy, and we are eager to cooperate with Japanese scientists in cancer treatment studies.
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PMID:[Japanese-French cooperation in tumor pharmacotherapy: 1970-1990]. 619 71

The anti-viral and anti-cell fusion actions of human gamma interferon (IFN) were examined on human rhabdomyosarcoma cells and compared with the actions of IFN-alpha. Treatment of A204 and RD114-C1 cells with IFN-gamma resulted in significant inhibition of retrovirus production and cell fusions which were induced by Sendai virus, but IFN-gamma did not induce 2'-5' oligoadenylate (2-5A) synthetase or dsRNA-dependent protein kinase, and failed to inhibit EMC virus replication in RD114-C1 cells as previously observed on IFN-alpha treatment (Tomita, Y. et al. (1982) Virology 120, 258-263). Although IFN-gamma induced 56K protein more strongly than IFN-alpha in human transformed HEp-2, HeLa, RSa, IFr, and A204 cells, no significant induction of this protein was observed in RD114-C1 cells after IFN-alpha or IFN-gamma treatment. Specific bindings of 125I-labeled human IFN-alpha A to HeLa, A204 and RD114-C1 cell surfaces showed that the numbers of the binding sites on RD114-C1 cells were reduced to less than 22% of those on A204 cells. These results suggest that RD114-C1 cells exhibit a reduced number of receptors for IFN on the cell surface and that the receptors are functional for the expression of the anti-retrovirus and anti-cell fusion actions of IFN, but are not enough in number for expression of the anti-EMC virus action of IFN.
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PMID:Expression of the anti-retrovirus action of interferon in human cells which exhibit a reduced number of receptors for interferon. 620 79

Highly purified natural or recombinant human immune interferon (IFN-gamma) was found to be directly cytolytic to certain tumor cell lines in vitro. Out of 5 human tumor cell lines and one normal fibroblast line tested, the colon adenocarcinoma line HT-29 and the rhabdomyosarcoma line A673 were highly sensitive to cytolysis by interferon, as determined by 125I-iododeoxyuridine release in a 72 h microcytotoxicity assay. Cytolysis was marked at IFN-gamma concentrations of less than I U/ml, and it reached a near-maximal level at 6.4 U/ml. A synergistic cytolysis on HT-29 cells of IFN-gamma and 5-fluorouracil (5-FU) was observed at 5-FU concentrations ranging from 64 to 640 micrograms/ml. In contrast, no synergism was observed between IFN-gamma and mitomycin C. The direct cytolytic activity and synergistic cytolysis with 5-FU of the IFN-gamma preparations used in the present study were abolished completely by treatment with a neutralizing monoclonal antibody specific for human IFN-gamma.
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PMID:Cytolytic activity of interferon-gamma and its synergism with 5-fluorouracil. 643 83

Alpha and beta interferon were tested for antitumor activity and clinical toxicity in 15 children suffering from cancer. The drug was administered IV, IM, IT or intralesionally daily in the majority of cases in total doses of 18 X 10(6) to 9,634 X 10(5) IU. Major toxicities were a flulike syndrome, elevation of transaminase activity and leukopenia. A minor response (less than 50%) was observed in one patient with glioblastoma, treated by intrathecal administration, and an objective local response was noted in one rhabdomyosarcoma patient with multiple subcutaneous metastases, who was treated by intralesional administration. CNS leukemia in two patients improved without hematological response. Further trials are warranted.
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PMID:[Clinical experience with alpha and beta interferon in childhood cancer]. 659 60


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