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)

Newcastle disease virus (NDV), strain 73-T, has previously been shown to be cytolytic to mouse tumor cells. In this study, we have evaluated the ability of NDV to replicate in and kill human tumor cells in culture and in athymic mice. Plaque assays were used to determine the cytolytic activity of NDV on six human tumor cell lines, fibrosarcoma (HT1080), osteosarcoma (KHOS), cervical carcinoma (KB8-5-11), bladder carcinoma (HCV29T), neuroblastoma (IMR32), and Wilm's tumor (G104), and on nine different normal human fibroblast lines. NDV formed plaques on all tumor cells tested as well as on chick embryo cells (CEC), the native host for NDV. Plaques did not form on any of the normal fibroblast lines. To detect NDV replication, virus yield assays were performed which measured virus particles in infected cell culture supernatants. Virus yield increased 10,000-fold within 24 hr in tumor and CEC supernatants. Titers remained near zero in normal fibroblast supernatants. In vivo tumoricidal activity was evaluated in athymic nude Balb-c mice by subcutaneous injection of 9 x 10(6) tumor cells followed by intralesional injection of either live or heat-killed NDV (1.0 x 10(6) plaque forming units [PFU]), or medium. After live NDV treatment, tumor regression occurred in 10 out of 11 mice bearing KB8-5-11 tumors, 8 out of 8 with HT-1080 tumors, and 6 out of 7 with IMR-32 tumors. After treatment with heat-killed NDV no regression occurred (P less than 0.01, Fisher's exact test). Nontumor-bearing mice injected with 1.0 x 10(8) PFU of NDV remained healthy. These results indicate that NDV efficiently and selectively replicates in and kills tumor cells, but not normal cells, and that intralesional NDV causes complete tumor regression in athymic mice with a high therapeutic index.
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PMID:Newcastle disease virus selectively kills human tumor cells. 161 12

An overview is presented of some common and uncommon non-plaque-related lesions and conditions of the periodontal tissues. Erosive lesions of the gingiva, such as lichen planus, may clinically be misdiagnosed as being the result of inflammation. Likewise, local and generalized gingival swelling may be based on non-plaque-related lesions and conditions. True leukoplakia of the gingiva is rare, but should be looked upon with suspicion. The reasons for pigmentation of the gingiva are many-fold. Especially in the maxilla, the clinician should be alert for an early malignant melanoma. A large variety of lesions may affect the periodontal bone structures, ranging from the common periapical granuloma to the rare, sometimes sclerosing, osteosarcoma. Irregular widening of the periodontal ligament and loss of the lamina dura are ominous radiographic signs.
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PMID:Non-plaque related periodontal lesions. An overview of some common and uncommon lesions. 189 Feb 25

CCC/2M, CCC/10Y and CCC/MT-2 cat kidney cells producing Japanese isolates of human T-cell leukemia virus type I (HTLVs) and HOS/PL human osteosarcoma cells producing an American isolate of HTLV were infected with vesicular stomatitis virus (VSV) to prepare VSV pseudotypes bearing envelope antigens of HTLVs. VSV propagated in CCC/2M cells contained plaque-forming fractions that were not neutralized by treatment with anti-VSV serum alone: VSV pseudotypes bearing envelope antigens of HTLV2M and CCC cat endogenous virus were formed by infection of CCC/2M cells with VSV. Japanese HTLV2M, HTLV10Y and HTLVMT-2 and American HTLVPL pseudotypes were neutralized by sera of Japanese, American and British patients with ATL. Each serum, including the serum of the patient from whom HTLV2M or HTLV10Y had been derived, gave similar antibody titers against Japanese and American HTLV pseudotypes. The HTLV pseudotypes were also neutralized by rabbit serum raised against HTLVMT-2. A rabbit antiserum against the C-terminal half of the HTLV env protein produced in E. coli also neutralized Japanese and American HTLV pseudotypes. Thus, VSV pseudotype analyses indicated that envelope antigens of HTLVs represent a single serotype worldwide. The env protein produced in E. coli may be used to raise neutralizing antibody against HTLVs.
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PMID:Human T-cell leukemia virus type I: pseudotype neutralization of Japanese and American isolates with human and rabbit sera. 241 68

A 13-year-old boy developed an osteogenic sarcoma of the right humerus ten years after treatment for bilateral retinoblastoma. The bilateral retinoblastoma has been managed with enucleation of one eye and successful treatment of the solitary tumor in the other eye with a single application of a local 10-mm round cobalt plaque. Patients with bilateral retinoblastoma have a significant (15 to 20%) chance of developing a second, nonocular, neoplasm. These neoplasms have occurred from one to 42 years after the treatment for retinoblastoma. The most common of these tumors is an osteogenic sarcoma; it may occur after external beam irradiation, local cobalt plaque, or no irradiation. The tumors may be in the skull or at distant sites whether or not these patients receive radiation.
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PMID:Osteogenic sarcoma of the humerus after cobalt plaque treatment for retinoblastoma. 693 20

Recombinant adenovirus Ad5CMV-p53 induced a strong cytocidal effect in Saos-LM2 cells. This cell line, derived from human osteosarcoma Saos-2 cells, has a homozygous deletion of the p53 gene. By using immunocytochemical and Western blot analyses, we demonstrated that Ad5CMV-p53 effectively infected Saos-LM2 cells at multiplicities of infection of 10 to 50 plaque-forming units/cell and mediated a high-level expression of the exogenous wild-type p53 protein in the cells. Growth of the infected cells was greatly suppressed whereas that of mock- or control virus-infected cells was not. Because wild-type p53 induces apoptosis in certain types of cells, we studied DNA fragmentation in situ in the Ad5CMV-p53-infected Saos-LM2 cells by terminal deoxynucleotidyl transferase assays, which yielded positive nuclear staining. Further analysis of the Ad5CMV-p53-infected Saos-LM2 cells by light and electron microscopy demonstrated that the cells underwent the characteristic morphological changes of apoptosis such as plasma-membrane blebbing, nuclear condensation, and fragmentation. These changes were not observed in mock- or control virus-infected cells. Our results on Saos-LM2 cells indicate that apoptosis induced by Ad5CMV-p53 may be one of the mechanisms underlying the cytocidal effect of Ad5CMV-p53.
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PMID:Apoptosis induced in human osteosarcoma cells is one of the mechanisms for the cytocidal effect of Ad5CMV-p53. 762 Dec 57

We have developed a differential screening technique, single plate one transfer (SPOT), that allows the easy detection of mRNAs induced only 2-fold to 3-fold or less above background. As a model system, we looked at the induction of mRNA by parathyroid hormone (PTH) in ROS 17/2.8 rat osteosarcoma cells. The basis for this technique is to symmetrically spot in quadruplicate, on a single plate, a large number of potentially positive plaques obtained from a primary, conventional screen. We then do only one transfer from this plate in order that there will be minimal variability in DNA transfer. This filter is cut into symmetrical strips so that all clones are multiply represented on each strip. These strips are then hybridized with different probes. Since each strip contains an approximately identical amount of DNA per plaque, it is possible to accurately detect mRNAs that are induced only slightly above background. Additionally, the large sizes of the DNA plaques, as well as spotting each clone serially, contribute to the sensitivity of the technique.
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PMID:SPOT: an improved differential screening protocol that allows the detection of marginally induced mRNAs. 845 47

The treatment modalities and prognosis of 636 retinoblastoma (RB) cases diagnosed and treated in our specialist center between 1963 and 1994 were evaluated. Patient age ranged from 20 days to 16 years, the mean age being 2.2 years (26.4 months). Of the 636 cases, 441 were unilateral and 195 were bilateral. Enucleation was the most frequent treatment employed in unilateral RB patients (412 cases). Follow-up treatment included exenteration (48 cases), radiotherapy (154 cases) and chemotherapy (108 cases) for cases with optic nerve invasion and/or orbital recurrence following enucleation. Seventeen cases displayed massive proptosis, ocular damage and blindness at initial presentation and underwent exenteration as the initial treatment. Two cases were subjected to external beam radiotherapy without invasive surgical procedures. Ten cases regressed spontaneously without treatment. For bilateral cases, the most frequent treatment used was enucleation for one eye and radiotherapy for the other (132 cases). Adjuvant treatment included exenteration (9 cases) and chemotherapy (50 cases) depending on orbital recurrence and/or systemic metastasis. Spontaneous bilateral regression was noted in one case. Six cases underwent bilateral external beam radiotherapy without surgery. One eye of the remaining 56 bilateral cases underwent enucleation. The treatment for the contralateral eyes included cryotherapy in 14 cases, enucleation in 11 cases, Cobalt plaque (Co plaque) therapy in 10 cases, photocoagulation in 6 cases and exenteration in one case. No treatment was undertaken in the contralateral eyes of 14 cases. Secondary treatment modalities employed in these 56 bilateral cases were radiotherapy (11 cases), chemotherapy (8 cases), Co plaque (8 cases) and exenteration (5 cases). Treatment complications were detected in 25 cases followed for at least 18 months. Eighteen cases had radiation cataracts and 6 of these 18 patients underwent intraocular lens implantation. Post-radiation orbital malignancy (osteosarcoma) was noted in two cases aged 14 and 15 years. Phthisis bulbi was observed in three cases and radiation keratitis in two cases. The overall survival rate was 82.2% after a mean follow-up of 5 years. The survival rate of unilateral cases was 82.8% and that of bilateral cases was 81.1% at 5 years.
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PMID:Retinoblastoma in Turkey--treatment and prognosis. 873 6

It has been reported that DNA of SV40, a virus of Asian macaques that is tumorigenic for rodents and can transform human cells in vitro, is present in pleural mesotheliomas and in several other cancers. To verify these observations, we tested paraffin sections from mesothelioma tissues of 50 patients for SV40 DNA using PCR with two separate sets of primers. The analytic sensitivity for detection of SV40 DNA was 1-10 genome copies. We also tested the specimens for beta-globin by PCR to assess the suitability of the specimen DNAs for amplification. beta-Globin amplification was detected in 48 of the 50 specimens, but SV40 DNA was not detected in any tumors, with either of two SV40 primer sets. Furthermore, sera from 34 additional patients with mesothelioma, 33 patients with osteosarcoma (another cancer reported to be SV40-related) and 35 controls were tested for SV40 antibodies by a plaque neutralization assay. The serological data, like the DNA results, did not support an association of SV40 with mesothelioma or with osteosarcoma; antibodies to SV40 were detected in three mesothelioma patients, in one osteosarcoma patient, and in one control. These findings call into question the association of SV40 with mesothelioma.
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PMID:Simian virus 40 and pleural mesothelioma in humans. 878 45

We examined the phenotype of a herpes simplex virus (HSV) type 1 mutant (V422) in which the C-terminal acidic activation domain of the virion transactivator VP16 is truncated at residue 422. The efficiency of plaque formation by V422 on Vero cells was boosted by approximately 100-fold by including hexamethylene bis-acetimide (HMBA) in the growth medium, as previously observed with the in1814 VP16 linker insertion mutant isolated by Preston and colleagues. V422 displayed severely reduced levels of the immediate-early transcripts encoding ICP0 and ICP4 during infection in the presence of cycloheximide, and this defect was partially overcome by the addition of HMBA. The defect in plaque formation exhibited by V422 and in 1814 was efficiently complemented in U2OS osteosarcoma cells, which had previously been shown to complement ICP0 null mutations. Taken in combination, these data confirm the key role of VP16 in triggering the onset of the HSV lytic cycle.
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PMID:Truncation of the C-terminal acidic transcriptional activation domain of herpes simplex virus VP16 produces a phenotype similar to that of the in1814 linker insertion mutation. 922 15

The relationship between cell morphology and cell metabolism and the role of mechanical load in bone remodeling is well known. Mechanical stimulation induces changes in the shape of osteoblasts, probably mediated by reorganization of focal contacts. We studied the influence of gravity (Gz) variations occurring during parabolic flight on osteoblast focal adhesion of ROS 17/2.8 osteosarcoma cells subjected to 15 or 30 parabolic flights. Significant flight-induced shape changes consisted of decreased cell area associated with focal contact plaque reorganization. Identical durations of continuous mechanical stress induced by centrifugation (2 Gz) or clinorotation (Gz randomization) had no major effect on cell focal adhesion. ROS 17/2.8 G2/M synchronization by treatment with nocodazole inhibited the flight-induced decrease in adhesion parameters. We concluded that ROS 17/2.8 cells are sensitive to Gz switches and that their adaptation is at least dependent on microtubule function.
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PMID:Effects of intermittent or continuous gravitational stresses on cell-matrix adhesion: quantitative analysis of focal contacts in osteoblastic ROS 17/2.8 cells. 934 86


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