Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hormone-induced alkaline phosphatases in human osteosarcoma cells (LM) were extracted and purified. Characterization of the purified enzyme showed two distinct isoenzymes. One isoenzyme was heat labile, was homoarginine inhibited, and had the electrophoretic migration of alkaline phosphatase of human osseous origin. Immunodiffusion showed that this isoenzyme reacted positively only against anti-bone alkaline phosphatase antibodies. The second isoenzyme was heat stable, was inhibited by phenylalanie, and had the same electrophoretic migration as did alkaline phosphatase extracted from mature normal human placenta. This second isoenzyme had the same antigenicity as did the normal placental enzyme. Like the D-variant placental phenotype, this second isoenzyme was inhibited by L-leucine and ethylenediaminetetraacetic acid.
Cancer Res 1978 Jan
PMID:Placenta-like alkaline phosphatases from human osteosarcoma cells. 2 98

Various agents have caused osteosarcoma in several experimental animal systems. These agents or initiators may be classified as chemicals, radiation, viruses, and miscellaneous. Zinc beryllium silicate with beryllium oxide in rabbits and FBJ virus in mice are two such initiating agents. The relevance of these animal experiments to the human situation is not known, but recent reports regarding a transmissible agent obtained from human osteosarcoma tissue suggest that a virus may be implicated. There is a theoretic indication that the various etiologic agents, including viruses, may affect the DNA of normal cells in such a way that further evolution and differentiation through several cell divisions may result in the clinical appearance of cancer.
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PMID:The etiology of osteosarcoma. A review of current considerations. 5 Aug 94

Antiserum was generated in rabbits to the RPMI 8226 tissue culture line of human myeloma cells, and its reactions with fixed smears of bone marrow aspirates from patients with multiple myeloma, macroglobulinemia, benign monoclonal gammopathy (BMG), leukemia, and nonneoplastic plasmacyosis was assessed by indirect immunofluorescence. After absorption with preparations of bone marrow from normal individuals, the antiserum reacted to a significantly higher titer with a specific subpopulation of plasma cells in smears from 81% of patients having multiple myeloma and 50% of patients having BMG than with cells in smears of bone marrow aspirates from normal individuals or patients having leukemia or nonneoplastic plasmacytosis, or than with cells in smears of peripheral blood from patients having Hodgkin's and non-Hodgkin's lymphoma. Absorption of the antiserum with RPMI 8226 cells or with a bone marrow preparation from a patient with multiple myeloma but not the Jijoye line of Burkitt's lymphoma reduced reactivity for cells in myeloma bone marrow. The antiserum reacted at a lower titer with the Jijoye and EB-3 lines of Burkitt's lymphoma, the RPMI 4098 cell line of normal human lymphocytes, and culture lines of human melanoma and osteogenic sarcoma than with the RPMI 8226 cells or bone marrow from certain patients having multiple myeloma. Approximately 50% of the cells reactive with antiserum to RPMI 8226 cells in the bone marrow of patients with multiple myeloma were not producing immunoglobulin, as assessed by double immunofluorescence assay. The data suggested that a subpopulation of plasma cells in the bone marrow of patients with multiple myeloma possesses a tumor-associated antigen.
J Natl Cancer Inst 1976 Apr
PMID:Tumor-associated antigens in human myeloma. 5 51

Sera from 8 of 9 patients with osteogenic sarcoma equally lysed autologous tissue-cultured cells of both skin and osteosarcoma in the presence of complement. Of 155 normal human sera tested, 103 (66%) lysed allogeneic normal ksin in tissue culture. These antibodies appeared more prevalent in younger (96% in ages 11-20 yr) than older (33% in ages 41-50 yr) humans. The presence of these "natural" antibodies against normal and malignant cells growing in tissue culture was possibly directed against components adsorbed to the cells during tissue culture or to "new" cell-surface antigens expressed by these cells grown in tissue culture. These non-tumor-related neoantigens on normal and malignant cells in tissue culture represented a potential source of confusion in studies of the serologic response of humans to tumors.
J Natl Cancer Inst 1977 May
PMID:Lysis of human normal and sarcoma cells in tissue culture by normal human serum: implications for experiments in human tumor immunology. 6 9

Sections were taken from the center, midzone, and margin of four human osteogenic sarcomas and one fibrosarcoma. Single-cell suspensions of tumors were examined in an indirect immunofluorescence assay with autologous or homologous anti-osteogenic sarcoma antisera as the intermediate reactant and fluorescein-labeled anti-human IgG as the final reactant. Cells were stained under conditions in which the fluorescence intensity was directly proportional to the density of the tumor-associated antigen on these cells. The density of tumor-associated antigen on cells from the center of the five tumor masses was low; cells from the midzone had intermediate levels of tumor antigen density, and cells at the margin had the highest levels. Similar preparations stained with polyspecific anti-HLA antisera did not demonstrate such a gradient. Since osteogenic sarcomas grow outward from the center, with the outer margin populated by the youngest cells, these results suggest that the oldest cells in the tumor bear the least tumor antigen, and the youngest tumor cells have the most. This is not compatible with theories which postulate that the immune system modulates the growth of a tumor so that only the least antigenic cells are allowed to grow. Alternative mechanisms are discussed.
Cancer Res 1977 Sep
PMID:Antigenic differences among osteogenic sarcoma tumor cells taken from different locations in human tumors. 6 91

The surface antigenic characteristics of human glial brain tumor (HGBT) cells were studied by complement-dependent cytotoxic antibody assays and indirect membrane immunofluorescence. Eight permanent, well-characterized cell lines derived from human gliomas were used for analysis with antisera raised by hyperimmunization of nonhuman primates (Macaca fascicularis) with glioblastoma multiforme tissue or established HGBT cells lines. Exhaustive absorption of these antisera to remove predominantly antispecies activity rendered HLA nonreactive "preabsorbed" antisera, which reacted with a large panel of gliomatous and nongliomatous human tumor cells; 1 carcinoma, 2 sarcomas, 2 melanomas, 1 neuroblastoma, and 8 HGBT cell lines. Four lymphoblastoid lines and 2 carcinomas were unreactive. After further absorption with a human osteogenic sarcoma cell line, the antisera demonstrated significant levels of reactivity for 8 tested HGBT cell lines and no longer reacted with the nongliomatous cultured tumor cells lines. Therefore, extensive absorption of nonhuman primate anti-human glioma sera removed all activity for the nongliomatous cell lines tested, but it left significant reactivity against a glial tumor cell line-associated antigen(s) present on all 8 human glioma cell lines tested.
Cancer Res 1977 Dec
PMID:Surface antigenic characteristics of human glial brain tumor cells. 7 98

Thirteen patients with osteogenic sarcoma were treated with multiple drug chemotherapy consisting of bleomycin, cyclophosphamide and dactinomycin. The dosage schedule used was: bleomycin 12 mg/m2/day, cyclophosphamide 600 mg/m2/day, and dactinomycin 450 microgram/m2/day. All drugs were given intravenously for two consecutive days. Treatment was repeated every 2 weeks. Toxicity included severe nausea and vomiting (managed with antiemetics and intravenous hydration) and manifestations of bone marrow depression. Of 13 patients, eight were previously treated with high dose methotrexate with citrovorum factor rescue, cyclophosphamide and Adriamycin. Of these eight, three patients had objective evidence of tumor regression (37.5%). Five of five previously untreated patients had objective evidence of tumor regression. The overall response rate in osteogenic sarcoma patients to BCD was 61.5%. The combination of BCD appears to be more active against osteogenic sarcoma than cyclophosphamide alone or Adriamycin alone. The relative safety with which BCD can be administered makes this combination a valuable adjunct to high dose methotrexate with citrovorum factor rescue and Adriamycin in the treatment of osteogenic sarcoma.
Cancer 1977 Dec
PMID:Combination chemotherapy with bleomycin, cyclophosphamide and dactinomycin for the treatment of osteogenic sarcoma. 7 9

Actinomycin (Act) analogs, differing in the chemical substitution(s) made at various positions in either their pentapeptide chain(s) or chromophore ring, were evaluated for their antitumor activity in mice bearing either Ridgway osteogenic sarcoma (ROS) or P388 leukemia. Of the analogs tested against advanced (2--3-g) ROS tumors, azetomicin I and Act III caused therapeutic responses which, although variable, were nevertheless indicative of antitumor activities greater than was found using Act D. Several other analogs, Act C2, 2-N-(gamma-hydroxypropyl)-Act D, Act X0delta, and azetomicin II, displayed antitumor activity in ROS-bearing mice which varied, in different experiments, from comparable to superior to that achieved using Act D. Additionally, Act Pip1beta and 3'-(4-cisCl-Pro)-Act were comparable to, and Act-2-hydroxy-C3 inferior to, Act D in activity against ROS. Both azetomicin I and II were as effective as Act D in mice bearing P388 leukemia. Moreover, a subline of P388 that is resistant to Act D was cross-resistant to both azetomicin I and II.
Cancer Treat Rep 1978 May
PMID:Comparative antitumor activity of actinomycin analogs in mice bearing Ridgway osteogenic sarcoma or P388 leukemia. 7 30

The hemacytometer leukocyte adherence inhibition (LAI) assay was investigated with respect to immunological relevance, specificity, and cellular mechanisms. Humans were immunized to keyhole limpet hemocyanin, and rats were immunized to dinitrophenyl-bovine gamma-globulin. LAI analysis disclosed classic patterns of immune response kinetics. The LAI response was dose dependent in vitro with no inhibition at relatively high antigen doses. In vitro specificity in rats was restricted to the immunizing conjugate. Cells forming spontaneous E-rosettes were required for LAI reactions. Lymphokine production required the presence of E-rosette-forming cells. E-rosette-forming cells from normal donors lost adherence in the presence of lymphokine. The requirement for T-lymphocytes was confirmed in a human osteosarcoma system using independent criteria. Thus, the hemacytometer LAI depends upon T-lymphocyte collaboration via a lymphokine. It should be distinguished from the tube and microplate variants of LAI analysis because these appear to depend upon different mechanisms.
Cancer Res 1979 Feb
PMID:Antigenic specificity and cellular mechanisms in leukocyte adherence inhibition analysis of immunity to simple proteins and hapten-protein conjugates. 8 11

From 1973--1975, 31 patients with biopsied primary osteogenic sarcoma were treated with preoperative chemotherapy followed by surgical ablation of the primary tumor. Surgery was delayed in order to obtain a custom-fitted prosthetic bone implant in an attempt to avoid amputation. Preoperative chemotherapy included high dose methotrexate (HDMTX) with citrovorum factor rescue (CFR) and adriamycin (T-5 protocol) and was administered for 3 months preoperatively and continued with the inclusion of cyclophosphamide for approximately 5 months postoperatively. At a follow-up period of 30--52 months, 23 of 31 patients (75%) are surviving (21 of 23 with no evidence of disease). Histologic examination of primary tumor removed at surgery revealed varying degrees of tumor destruction (from very little effect to no evidence of viable tumor) attributable to the effect of chemotherapy. The 21 patients that are disease-free survivors had a more complete effect of preoperative chemotherapy on the primary tumor. Some patients achieving favorable effects upon the primary tumor did so only after the dose of HDMTX was escalated to greater than the starting dose of 8 g/m2. Preoperative chemotherapy for all patients with osteogenic sarcoma would seem to offer the following advantages: 1) Evaluation of the effect of HDMTX with CFR on the primary tumor with escalation of the dose of HDMTX until a clinical response is observed, thus defining the dose of HDMTX effective in that patient, to be continued postoperatively as adjuvant therapy; 2) The early use of systemic therapy to eradicate distant microfoci of disease that will eventually kill the patient if not adequately treated by effective chemotherapy; 3) Allow more time for postoperative healing without the need to start adjuvant chemotherapy immediately; and 4) Provide the surgeon time to plan resection surgery. To date, 20 additional patients with biopsy proven osteogenic sarcoma have been treated with more aggressive preoperative chemotherapy (T-7) for approximately 2 1/2 months prior to definitive surgery (resection or amputation). Doses of HDMTX were escalated where necessary and good clinical responses were obtained in 19 of 20 patients. In the majority of patients, no evidence of viable tumor was found on histologic examination of the surgically removed primary tumor. All 20 patients are surviving free of active disease at this brief follow-up period of 4--20 months.
Cancer 1979 Jun
PMID:Primary osteogenic sarcoma: the rationale for preoperative chemotherapy and delayed surgery. 8 51


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