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)

Osteogenic sarcoma developed in a 14-year-old boy 13 years after he had partially recovered from chloramphenicol-induced aplastic anemia. A possible relationship is considered between aplastic anemia, chloramphenicol, testosterone, prednisone, and osteogenic sarcoma. Leukemia has been reported following chloramphenicol-induced aplastic anemia and liver tumors have been associated with testosterone therapy. Certain chemicals have caused osteogenic sarcoma in animals. Thus, we believe there are sufficient a priori reasons to question an etiologic relationship between the cause or treatment of aplastic anemia and osteogenic sarcoma.
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PMID:Osteogenic sarcoma in a patient with aplastic anemia. 26 29

Drug encapsulation in erythrocytes has been proposed to extend its biological lifetime. Molecules encapsulated this way are protected against rapid cellular metabolism and body elimination. Unfortunately, drugs such as daunorubicin cannot be efficiently entrapped in erythrocytes since drugs diffuse rapidly from the cells. In order to overcome this problem, we have covalently linked daunorubicin to erythrocyte membranes (ghosts) using two different types of linking arms: glutaraldehyde and cis-aconitic acid. Both ghost-daunorubicin conjugates were tested in vitro on mouse leukemia cells (P388D1) and on human osteosarcoma cells (CRL-1427). Results showed a better cytotoxic activity for ghost-glutaraldehyde-daunorubicin conjugate than for ghost-cis-aconityl-daunorubicin conjugate. Both conjugates were also tested in vivo on CDF1 mice bearing P388D1 cells. T/C% of 161 and 103 respectively were observed with ghost-glutaraldehyde-daunorubicin and ghost-cis-aconityl-daunorubicin conjugate at 6.0 mg/kg. Compared to free drug, the increase in survival time could be explained by a slow release of daunomycin in the circulation from the erythrocyte membranes, leading to a more complete absorption by cancer cells.
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PMID:Erythrocyte membrane-bound daunorubicin as a delivery system in anticancer treatment. 281 3

The principles of cancer chemotherapy applied to adult patients today have been substantially derived from experience of cancer in children. Studies of pediatric solid tumors also provided the first evidence that chemotherapy combined with surgery and/or radiotherapy could markedly enhance the curative potential of these local modalities. Conceptual advances in cancer chemotherapy revealed the superiority of intermittent chemotherapy over continuous low-dose therapy with respect to tumor cell kill and the recovery of normal cells. Childrens' Cancer and Leukemia Study Group of Japan applied intensive intermittent chemotherapy for maintenance therapy for leukemia, malignant lymphoma and to adjuvant chemotherapy for solid tumors. Event-free survival rate in treatment of childhood cancer by the Department of Pediatrics, Aichi Medical University, has markedly improved: ALL, 70%; malignant lymphoma, 50%; ANLL, 33%; hepato-blastoma, 100%; osteosarcoma, 65%; neuroblastoma, 54%; and rhabdomyosarcoma, 51%. The 14% rate for brain tumors was the only exception. Current Phase I and II trials based on pharmacokinetics and pharmacodynamics in children were reviewed.
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PMID:[Current status in treatment of childhood cancer]. 766 60

The human osteosarcoma cell culture HOS does not produce matrix metalloproteinases (MPs). However, after transformation with the Ki-ras oncogene, the resulting culture (KHOS) produced readily detectable MPs. The molecular weight of the major MP was 66 kDa, while the molecular weights of two other minor bands were 71 kDa and 60 kDa. The activity of all three enzymes was inactivated by treatment with ethylene diaminetetra acetic acid, indicating that they are probably MPs. The substrate preference of the 66-kDa MP (in decreasing order) was gelatin and collagens V, I, III, and IV. Treatment of the MPs with p-aminophenylmercuric acetate led to the appearance of 62-kDa activated enzyme. The MP produced by KHOS cells did not react with the monoclonal anti-rat stromelysin antibody MC. Treatment of KHOS cells with retinoic acid and dexamethasone, which are known to suppress c-fos/c-jun and AP-1, suppressed the production of the MPs. Therefore, the activation of MPs by Ki-ras in KHOS cells may involve c-fos/c-jun and the AP-1-responsive pathway.
Leukemia 1994 Apr
PMID:Activated production of metalloproteinases in Ki-ras-transformed human osteosarcoma cells. 815 1

Serum levels of interleukin-2 receptor (IL2R) were determined in children with newly diagnosed Hodgkin disease (n = 68), Wilms tumor (n = 20), osteosarcoma (n = 18), rhabdomyosarcoma (n = 18), or Ewing sarcoma (n = 15). Measurements of soluble IL2R were positively correlated with disease stage in Hodgkin disease but not in other tumors. Very high levels of soluble IL2R (> or = 5000 U/ml) were significantly associated with a poorer treatment outcome in Hodgkin disease (p = 0.006) and retained significance in a multivariate analysis (p = 0.03). The addition of soluble IL2R measurements to existing prognostic models may improve risk assignment in children with Hodgkin disease.
Leukemia 1993 Aug
PMID:Serum interleukin-2 receptor levels in Hodgkin disease and other solid tumors of childhood. 839 83

Loss of the p16INK4A gene by homozygous deletions or point mutations is attributed to the development of many types of cancers including leukemia. T cell acute lymphoblastic leukemias (T-ALLs) and B-cell ALLs show a remarkable rate of 75 and 20% homozygous deletion of this gene, respectively. Restoration of p16 expression in p16-deficient solid tumor cell lines results in a dramatic reduction of growth and maligant phenotype. To test the hypothesis that p16INK4A suppresses the growth of p16-deficient leukemias, we utilized a retroviral system to restore wild-type (wt) or mutant p16 protein expression. We tested the efficacy of our system by expressing the wt or mutant p16 genes in the osteosarcoma cell line, U20S, which lacks p16 and retains functional retinoblastoma protein (pRb). The wt p16 protein formed complexes with both cyclin-dependent kinases (CDK) 4 and 6 and inhibited U20S growth by 30-fold. The p16 mutants E120K and R144C formed complexes with CDK4 and CDK6 in cells and inhibited cell growth as effectively as wt p16 (20-fold) while the mutant proteins that did not complex with detectable levels of CDK4 or CDK6 only inhibited growth 0.25- and five-fold (G101W and D141, respectively) or not at all (H83Y and DA4). The COOH-terminal 'tail' of the wt p16 protein (amino acid residues 141-156), missing in mutant D141, enhanced the growth suppressive capability of p16. The amino acid substitutions in mutants G101W and H83Y not only disrupted CDK4 and CDK6 binding, but decreased the protein half-lives by two- and three-fold, respectively, compared to wt p16. The wt, but not mutant p16 genes, effectively inhibited the growth of T cell acute lymphoblastic (CEM) and myeloid leukemia (NB-4 and K562) cell lines that lacked the p16 gene, but retained functional pRb. Growth of the T-ALL cell line, HSB-2, which lacked both p16 and pRb, was not inhibited, indicating the growth suppression involved the pRb pathway. These results define regions critical for the function of p16 and demonstrate that restoration of wt p16 expression in p16-deficient leukemias significantly reverted their transformed phenotype and inhibited their growth.
Leukemia 1997 Oct
PMID:Inhibition of growth of human leukemia cell lines by retrovirally expressed wild-type p16INK4A. 932 88

Human T cell leukemia virus type I (HTLV-I) or its transcriptional transactivator, Tax1, was introduced into a human osteosarcoma cell line, HOS, and a Moloney murine sarcoma virus-positive HOS cell line, S+L-HOS. These HTLV-I- or Tax1-expressing cells were injected subcutaneously into nude mice to investigate the effects of HTLV-I on their tumorigenicities. HOS cells did not form any tumors even in the presence of HTLV-I or Tax1. S+L-HOS cells did form small tumors in two-thirds of nude mice. Infection of S+L-HOS cells with HTLV-I, or transduction of Tax1 into S+L-HOS cells markedly facilitated the tumor formation, and the tumor-bearing mice showed marked splenomegaly and neutrophilia. Elevated levels of granulocyte colony-stimulating factor (G-CSF) were detected in sera of these mice and also in the culture supernatants of Tax1-expressing human cells, suggesting that G-CSF in the mouse sera was produced by the human cells. In sera of some mice with splenomegaly and neutrophilia, high levels of murine granulocyte-macrophage colony-stimulating factor (mGM-CSF) were observed, suggesting that Tax1 produced by human cells induced mouse cells to produce mGM-CSF. Only S+L-HOS cell lines expressing Tax1 showed high tumorigenicity in nude mice. Thus, this system will be a useful model of tumor formation, splenomegaly and neutrophilia dependent on Tax1.
Leukemia 2000 Aug
PMID:Rapid tumor formation and development of neutrophilia and splenomegaly in nude mice transplanted with human cells expressing human T cell leukemia virus type I or Tax1. 1094 44

Complementary medicine using natural product as antitumor is on the rise. Much research has been performed on Tualang Honey and it was shown to have therapeutic potential in wound healing, and antimicrobial activity and be antiproliferative against several cancer models such as human osteosarcoma (HOS), human breast (MCF-7 and MDA-MB-231), and cervical (HeLa) cancer cell lines. To date, there was limited study on antileukemic properties of Tualang (Koompassia excelsa) Honey. The aim of this study was to evaluate the antileukemic effect of Tualang Honey on acute and chronic leukemia cell lines. Leukemia cell lines (K562 and MV4-11) and human mononuclear cell isolated from peripheral blood were grown in RPM1 1640 culture medium. The cells were incubated with increasing concentrations of Tualang Honey. After incubation, the evaluation of viability and apoptosis was performed. The morphological changes of leukemia cells were the presence of cytoplasmic blebs followed by apoptotic bodies and round shape of cells. IC50 against K562 and MV4-11 was determined. Tualang Honey gave 53.9% and 50.6% apoptosis activity on K562 and MV4-11, respectively, while on human mononuclear cell it was 37.4%. Tualang Honey has the apoptosis-inducing ability for acute and chronic myeloid leukemia (K562 and MV4-11) cell lines.
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PMID:Antileukemic Effect of Tualang Honey on Acute and Chronic Leukemia Cell Lines. 2661 81