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)

Antibodies against non-histone chromosomal proteins for 89Sr-induced osteogenic sarcoma (mouse) were prepared by immunization of rabbits. The immunoreactivity of this antigen was then compared with those of non-histone chromosomal proteins from Ehrlich ascites tumor, normal mouse liver, and calf thymus by the method of quantitative microcomplement fixation. The non-histone chromosomal proteins of 98Sr-induced osteogenic sarcoma, fractionated by hydroxylapatite chromatography, exhibited significant affinity for the antibodies. Similar proteins from Ehrlich ascites tumor, normal mouse liver, or calf thymus were virtually inactive, indicating the tissue-specificity of 89Sr-induced osteogenic sarcoma proteins.
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PMID:Immunospecificity of non-histone chromosomal proteins in 89Sr-induced osteogenic sarcoma (mouse). 7 Apr 27

cDNAs which encode bone gla protein (BGP), an abundant gamma-carboxylated protein of bone, have been cloned from rat and mouse osteosarcoma cell lines. DNA sequence analysis indicates that the cDNAs code for both the 50 (rat) or 46 (mouse) amino acids of the mature proteins and a 49 amino acid leader peptide. The leader peptide of each BGP includes the expected hydrophobic signal sequence and an apparent pro sequence. Although there is no homology between the mature forms of BGP and the gamma-carboxylated clotting factors, we note that there is some homology between their leader peptides. These cDNAs have been used to examine the modulation of BGP mRNA levels by osteoblastic cells in response to hormones. The cDNAs have also allowed isolation of the human BGP gene; analysis of this gene indicates the presence of four exons. Comparison of the exon structure of the BGP gene and the Factor IX (a gamma-carboxylated clotting factor) gene suggests that the exons encoding the part of the leader peptides presumably directing gamma-carboxylation arose from a common ancestral sequence.
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PMID:Isolation of the human gene for bone gla protein utilizing mouse and rat cDNA clones. 301 68

The 8.2-kilobase (kb) unintegrated circular DNA form of the FBJ murine leukemia virus (FBJ-MLV) was linearized by cleavage at the single HindIII site, molecularly cloned into bacteriophage Charon 30, and subsequently subcloned into pBR322 (pFBJ-MLV-1). Both FBJ-MLV virion RNA and pFBJ-MLV-1 DNA were used to investigate the arrangement of helper virus sequences in the FBJ murine osteosarcoma virus genome (FBJ-MSV) by heteroduplex formation with cloned FBJ-MSV proviral DNA. The results showed that the FBJ-MSV genome contained 0.8 kb of helper virus sequence at its 5' terminus and 0.98 kb at its 3' terminus. Approximately 6.8 kb of helper virus sequence had been deleted, and 1.7 kb of unrelated sequence was inserted into the FBJ-MSV genome. This substituted region contains v-fos, the transforming gene of FBJ-MSV. Using a probe specific for v-fos, we have cloned homologous sequences (c-fos) from mouse and human chromosomal DNA. Heteroduplex analysis of FBJ-MSV DNA with these recombinant clones showed that both the c-fos(mouse) and the c-fos(human) sequences hybridized to the entire 1.7-kb v-fos region. However, five regions of homology of 0.27, 0.26, 0.14, 0.5, and 0.5 kb were separated by four regions of nonhomology of 0.76, 0.55, 0.1, and 0.1 kb from 5' to 3' with respect to the FBJ-MSV genome. The size of these sequences showed striking similarity in both c-fos(mouse) and c-fos(human).
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PMID:Structure of the FBJ murine osteosarcoma virus genome: molecular cloning of its associated helper virus and the cellular homolog of the v-fos gene from mouse and human cells. 630 48

We studied the effect of human leukocyte interferon (HuIFN-alpha) on a human osteosarcoma (OS-OH) transplanted and passed serially in athymic mice. The growth of OS-OH was strikingly inhibited by HuIFN-alpha (50,000 IU/mouse), regardless of whether the interferon treatment was initiated 24 hr after tumor inoculation or 2 weeks later, when tumors had grown to an appreciable size (4-6 mm). The antitumor effect of HuIFN-alpha was found to be dose-dependent and a daily administration of HuIFN-alpha (50,000 IU/mouse) all but completely arrested the tumor growth.
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PMID:Antitumor effect of human leukocyte interferon on human osteosarcoma transplanted into nude mice. 658 Jan 70

A radiation- and chemotherapy-resistant murine osteosarcoma was used to investigate the effect of local hyperthermia (42.5 +/-0.1 degrees, 30 min) alone and in combination with cyclophosphamide. The cytotoxicity of cyclophosphamide on murine osteosarcoma was established previously in our laboratory. Local hyperthermia (42.5 +/- 0.1 degree, 30 min) had little or no effect on the 16-day-old (206 X 10(6) osteosarcoma tumor cells/mouse) tumor as shown by the changes in the tumor cell marker, alkaline phosphatase. A 2.5 +/- 3.5% reduction in the number of tumor cells was seen. Large tumors treated at 21 days postimplantation (357 X 10(6) tumor cells) showed a reduction of 24 +/- 14%. The effect of combination treatment with cyclophosphamide and hyperthermia produced greater reduction in the numbers of tumor cells than did either treatment used alone.
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PMID:Reduction of tumor burden in a murine osteosarcoma following hyperthermia combined with cyclophosphamide. 658 5

Neem seed preparations contain not only azadirachtin as the active insect antifeedant or growth regulator but also a variety of their limonoids, some of which are cytotoxic to N1E-115 neuroblastoma (mouse), 143B.TK- osteosarcoma (human) and Sf9 (insect) cultured cell lines. The most potent of these limonoids is nimbolide with an IC50 ranging from 4 to 10 microM, and averaging 6 microM for the three cell lines. Other limonoids of decreasing potency and their average IC50 values (microM) are epoxyazadiradione 27 microM, salannin 112 microM, and nimbin, deacetylnimbin and azadirachtin each >200 microM (practically nontoxic). Nimbolide at 10 microM acts rapidly in the neuroblastoma cells to induce blebbing associated with disruption of plasma membranes almost instantaneously and 50% loss of cell viability with 30 min. At 5 microM nimbolide, the cells become elongated and assume a neuronal shape accompanied by spikes and lamellipodia within 1-2 hr followed shortly thereafter by extensive cytological changes and and vacuolization associated with irreversible processess leading to cell death. Calcium is apparently not involved the cytotoxic effect since a calcium-free medium, leading to profound morpholigical changes, does not alter the sensitivity to nimbolide. In contrast, epoxyazadiradione requires higher concentrations and a few hr for 50 % viability loss without major morphological changes, indicating a difference in mode of action for nimbolide and epoxyazadiradione. and epoxyazadiradione.
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PMID:Cytotoxicity of nimbolide, epoxyazadiradione and other limonoids from neem insecticide. 862 60

To examine the usefulness of interleukin-18 (IL-18) in the treatment of osteosarcomas, the effect of IL-18 on the growth of Dunn osteosarcoma cells was investigated. Daily intraperitoneal (i.p.) injection of mouse recombinant IL-18 (2 microg/mouse) suppressed the growth of Dunn osteosarcoma cells transplanted subcutaneously (s.c.) into syngeneic C3H mice. This IL-18-induced suppression was not affected by simultaneous treatment with anti-asialo GM1 serum, which inactivates natural killer (NK) cells. However, IL-18 failed to suppress the growth of Dunn osteosarcoma cells transplanted into BALB/c-nude mice devoid of T lymphocytes or C3H-gld/gld mice deficient in functional Fas ligand (FasL). IL-18 also failed to suppress the growth of Dunn osteosarcoma cells in vitro, although expression of IL-18 receptor mRNA and MyD88 mRNA as well as Fas mRNA was detected by reverse transcriptase-polymerase chain reaction (RT-PCR). On the other hand, antimouse Fas antibody showed cytotoxicity against Dunn osteosarcoma cells in a dose-dependent manner in vitro. In addition, treatment of C3H mice with IL-18 enhanced the cytotoxic activity of CD8(+) T lymphocytes against Dunn osteosarcoma cells. These results indicate that IL-18 inhibits the growth of Dunn osteosarcoma cells in vivo by enhancing the cytotoxic activity of CD8(+) T lymphocytes through the FasL-Fas system.
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PMID:Inhibition by interleukin-18 of the growth of Dunn osteosarcoma cells. 1503 49