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)

Amygdalin MF was evaluated alone and in combination with an activating agent, beta-glucosidase, against three transplantable rodent tumors; Ridgway osteogenic sarcoma, Lewis lung carcinoma, and P388 leukemia. In dose-response studies up to the LD20 in normal mice, amygdalin MF alone did not demonstrate significant antitumor activity against any of these three tumor systems. Similarly, at doses not exceeding the LD10 in normal mice, amygdalin MF plus beta-glucosidase did not demonstrate antitumour activity against any of these three tumor systems. Potentiation of the lethal toxicity of amygdalin MF by beta-glucosidase was observed in all studies where the two agents were given in simultaneous combination.
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PMID:Experimental studies of the antitumor activity of amygdalin MF (NSC-15780) alone and in combination with beta-glucosidase (NSC-128056). 106 May 11

N-(Phosphonacetyl)-L-aspartate (PALA) is an analog of the transition state for the aspartate transcarbamylase reaction and has been reported previously to be a potent and specific inhibitor of de novo pyrimidine nucleotide biosynthesis. It is now shown that PALA has considerable antitumor activity against certain transplantable tumors in mice. PALA, unlike other antimetabolites, was less effective against ascitic leukemias than against two solid tumors, B16 melanoma and Lewis lung carcinoma. Another solid tumor, Ridgway osteogenic sarcoma, which is sensitivie to many established chemotherapeutic agents, did not respond to PALA. Daily or intermittent treatment with PALA did not significantly increase the life-span of mice bearing i.p. leukemia L1210. The survival time of mice bearing i.p. P388 leukemia was prolonged by PALA treatment by up to 64%. In a number of experiments mice bearing i.p. B16 melanoma survived 77 to 86% longer than did controls when treated with PALA (490 mg/kg) on Days 1, 5, and 9. Lewis lung carcinoma, a tumor refractory to most established antineoplastic agents, was highly sensitive to PALA. Treatment on Days 1, 5, and 9 following s.c. implantation of Lewis lung carcinoma was curative to 50% of the mice. If treatment was delayed until s.c. Lewis lung tumors had reached about 500 mg, PALA neither cured the mice nor produced significant tumor regression. However, extensive delay of tumor growth and prolongation of survival were still observed.
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PMID:Antitumor activity of N-(phosphonacetyl)-L-aspartic acid, a transition-state inhibitor of aspartate transcarbamylase. 106 66

The biologic activity in terms of survival of normal hematopoietic stem, osteosarcoma, and L1210 leukemia cells was determined for the following compounds:cyclophosphamide, its derivatives isophosphamide and trophosphamide, its possible metabolites nor-nitrogen mustard, hydroxylamine mustard, 4-ketocyclophosphamide, and and acrolein, and two substitutes for its primary active metabolite 4-hydroxycyclosphamide anhydro-dimer (4-hydroxy-CP-anhydro-dimer) and 4-hydroperoxycyclophosphamide (4-hydroperoxy-CP). On a molar basis none of the compounds shows a better therapeutic ratio between osteosarcoma and bone marrow stem cells than the parent compound. The therapeutic ratio between L1210 leukemia and normal cells is slightly better for 4-hydroperoxy-CP only. It may be concluded that the conversion of 4-hydroxy-CP-anhydro-dimer and 4-hydroperoxy-CP to the primary active metabolite 4-hydroxycyclophosphamide differs quantitatively. Moreover, it appears that by the use of these precursors a better therapeutic ratio might be obtained for some malignancies but not for others.
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PMID:Biologic activity of two derivatives and six possible metabolites of cyclophosphamide (NSC-26271). 106 68

Experimental data are presented which demomstrate the existence of a transmissible factor(s) in the majority of samples of leukemic bone marrow. This factor(s) is associated with the presence of a cytoplasmic antigen which can be detected by fixed immunofluorescence test with sera of patients with osteosarcoma, leukemia and some apparently normal individuals. Cultures of leukemic bone marrow carrying this factor(s) also form multinucleated cells when exposed to RD114 virus or cels. This factor(s) is transmitted into susceptible whole human embryo cells by cell-free culture fluid. Appearance of the new antigen can be detected by fixed immunofluorescence test about 6 weeks after transmission. Cultures showing the new antigen also form multinucleated cells following co-cultivation with RD114 virus or cells. Co-cultures of human osteosarcoma cells and leukemic bone marrow cells undergo morphologic as well as antigen changes after a long period of time (at least 3 months). Cell line fluids from these cultures contain a factor which induces in recipient whole human embryo cultures both the new antigen and morphological alterations resembling those observed in the co-cultures. Cell-free fluids from leukemic bone marrow and sarcoma cultures as well as from short-term co-cultures have failed to produce morphological alterations in whole human embryo cells. Extensive electron microscope studies carried out at different stages of the experiments have failed to reveal the presence of viral particles. The morphological changes resemble those induced in susceptible cells by sarcoma viruses. The described factor(s) may conceivably represent subviral components capable of biological activity. While suggestive of viral involvement in human sarcoma of bone and soft tissues, there is no definite proof of viruses being the causative agent(s) of human sarcoma. Present evidence provides only a basis for search of additional ways of treatment of human sarcoma to those of surgery and radiotherapy. Present treatment consists of chemotherapy as adjuvant treatment directed against viral markers represented by enzymes, nucleic acids and proteins of possible viral origin, resembling those already known to be present in animal bone and soft tissue sarcomas. However tenuous the contention of the possiblity of viral involvement in human osteosarcoma may appear, adjuvant therapy directed against viral markers warrants the attention of orthopedic surgeons and other clinicians.
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PMID:Transforming factors in human sarcoma cells in tissue culture. 106 98

When the causes of death were determined in 18 relations of a child with Fanconi's anaemia 10 deaths were found to be due to carcinoma of various organs. Cases of osteogenic sarcoma, leukaemia, and Marfan's syndrome were also discovered among relatives. The family was from a remote community in the hebrides and there was considerable intermarriage. Suggestive evidence of heterozygosity was found by chromosome analysis.
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PMID:Familial cancer on a Scottish island. 106 48

Medium-sized peptides isolated from normal humans urine were tested for their effect on DNA, RNA, and protein synthesis, and mitosis, in tissue culture of human myeloblastic leukemia, osteosarcoma, and HeLa cells. Two types of antineoplastic peptides were found. One type consists of strongly acidic peptides (probably sulfated glycopeptides) which act specifically on different kinds of neoplasma. The other type comprises slightly acidic and neutral peptides, and has broad specificity. The active peptides produce up to 97% inhibition of DNA synthesis and mitosis in the neoplastic cells in tissue culture. The peptide fraction which has broad specificity was tested in different concentrations and gave good dose-response relationship.
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PMID:Biological active peptides in human urine: III. Inhibitors of the growth of human leukemia, osteosarcoma, and HeLa cells. 106 15

Three groups (15 in each) of 3-month-old mice were injected intraperitoneally with 0-5 muCi 226Ra. They were male and female C3H/H and female CBA/H. The groups were matched by similar controls that were not injected. Osteosarcomas were found in 14/15 of the female C3H/H mice--animals known to carry mammary-tumour viruses in milk--compared with 6/15 in their male counterparts. In CBA/H female mice, which have a very low incidence of both mammary tumours and leukaemia, osteo-sarcomas developed in 7/15 of the animals. The CBA/H mice lived about 5-8 months longer and revealed their osteosarcomas at a correspondingly later time than C3H/H mice. Virus particles were observed in each of the three mammary tumours and in 15 out of the 17 osteosarcomas examined by electron microscopy. No definitive statement can be made from this experiment whether or not osteosarcoma was caused by a virus; but the results suggest that viruses may be a contributory factor in the development of osteosarcoma in these animals.
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PMID:Viruses in osteosarcomas induced by 226Ra. A study of the induction of bone tumours in mice. 108 Oct 88

The two-drug combination of cyclophosphamide plus adriamycin was found to be therapeutically potentiating against four different C3H mammary tumor lines, the B16 melanoma, the Ridgway osteogenic sarcoma, and the P388 leukemia. The potentiation was not schedule dependent.
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PMID:Cyclophosphamide-adriamycin combination chemotherapy of transplantable murine tumors. 113 24

The clinical manifestations of Gardner's syndrome were studied in 280 patients from 11 families. Forty-five per cent of the patients at risk inherited the syndrome. Forty-one patients had carcinoma of the intestine develop, with only a 27 per cent survival rate for this type cancer. Eight per cent of the patients with the syndrome showed peritoneal fibrosis and fibrous tumors. They also had carcinomas of the ampulla of Vater, liver, bldder and ovary develop as well as osteogenic sarcoma. The patients without the syndrome had carcinomas of the pancreas and breast develop as well as melanoma and leukemia. Twelve of the 16 patients having had a colectomy and ileoproctostomy showed regression of the remaining polyps of the rectum.
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PMID:Gardner's syndrome. 115 13

More than 200 nitro compounds, most of them nitroaniline derivatives substituted with one or more radicals having a basic reaction, were prepared and investigated as to their therapeutic activity against bacteria, fungi, protozoa, helminths, viruses and tumors. Several mono-nitrobenzenes with a radical having a basic reaction showed weak in-vitro activity against gram-positive bacteria and against Crocker's sarcoma 180; they also showed systemic activity against nematodes (Aspiculuris tetraptera) and viruses. The majority of therapeutically active compounds with pronounced in-vivo activity against Trichomonas fetus, Entamoeba histolytica, Schistosoma mansoni, cestodes, nematodes (Ancylostoma caninum), viruses (influenza, MHV, SAV and EMC) and various types of carcinoma (Ehrlich's carcinoma, leukemia 1210, Crocker's sarcoma 180) were dinitrobenzene derivatives with one radical having a basic reaction and electropositive groups or unreactive or reactive chlorine atom, and di-nitrobenzene with two equal or two different radicals having a basic reaction. Compound No. 70 revealed a marked in-vitro activity against fungi (Trichophyton; Microsporum, Candida albicans). Other nitro compounds such as bis-mono- and bis-dinitrobenzene derivatives likewise showed a systemic action against E. histolytica, viruses and, in particular, carcinoma (Crocker's sarcoma 180, Ridgway's osteosarcoma). Oxygen and sulfur analogue compounds as well as compounds produced by reduction also possessed a distinct activity against E. histolytica and viruses. On the basis of the present results particularly the dinitrobenzenes substituted with two radicals having a basic reaction include a number which have in common that a structure/activity relationship is recognizable in respect of E. histolytica, Schistosoma mansoni and different types of viruses. The activity against viruses in this class of compounds is probably due to an increased interferon production in the host animal. Whether the mechanism of action is the same against E. histolytica or Schistosoma mansoni has not been determined so far. A tumorigenic effect was observed mainly in those di-nitrobenzenes which are classed as alkylating compounds. Because of the small chemotherapeutic index the trials were not continued with the most effective compounds mentioned.
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PMID:[Chemotherapeutic effects of nitro compounds. 1. Nitroanilines]. 124 9


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