Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0035412 (rhabdomyosarcoma)
6,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A full-length molecular clone of human immunodeficiency virus (HIV) proviral DNA was transferred to human rhabdomyosarcoma (RD) cells by gene transfer method. RD cells released infectious virus within 12 hours after transfection and the viral particles present in the culture medium could be quantitated by monitoring reverse transcriptase activity. Chronic low level viral producer cell lines of RD were also established. Southern hybridization analysis revealed the presence of HIV sequences in transfected RD cells. Electron microscopic studies of the transfected cell revealed intracellular budding of HIV and also showed structural abnormalities such as giant cell phenotype and vacuolation. These features qualify RD cells as a useful system for studying the regulation and cytopathic effects of HIV.
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PMID:Studies on human immunodeficiency virus-induced cytopathic effects: use of human rhabdomyosarcoma (RD) cells. 335 73

Thirteen adherent human non-lymphocyte cell lines were tested for their susceptibility to infection by human immunodeficiency virus. Productive infection could be demonstrated in three of five colorectal carcinoma cell lines examined; the other eight human non-lymphocyte cell lines were uninfectible. A susceptible colon carcinoma cell line (HT29), as well as normal colonic mucosa, was shown to contain a 3.0-kilobase species of poly(A)+ CD4 RNA, whereas uninfectible colon carcinoma and rhabdomyosarcoma cell lines synthesized no detectable T4 RNA. A persistently infected colon carcinoma cell line was established that continued to produce progeny human immunodeficiency virus for more than 10 weeks postinfection.
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PMID:Productive, persistent infection of human colorectal cell lines with human immunodeficiency virus. 364 Aug 32

Human immunodeficiency virus (HIV) related cancers in children are not as common and as well described as in adults. An HIV epidemic has been prevalent in Zambia since 1983-1984. To study the effect of the epidemic on the epidemiology of cancers in children a retrospective study was undertaken at the University Teaching Hospital (UTH), Lusaka, Zambia. All the histopathological records from 1980 to 1992 were reviewed and all cases of cancers in children less than 14 years of age were analysed. In order to define the effect of the HIV epidemic, the epidemiological features of various childhood cancers occurring before (during the years 1980-1982) and after (during the years 1990-1992) the onset of the HIV epidemic were compared. A significant increase in the occurrence of total childhood cancers was found. This is mostly due to a highly significant increase in the incidence of paediatric Kaposi's sarcoma (p = 0.000016), which is causally related to HIV infection, and a significant increase in the incidence of retinoblastoma (p = 0.02), which has an unknown relation to HIV infection. Though not yet statistically significant, there has also been a gradual and sustained increase in the incidence of non-Hodgkin's lymphoma, nasopharyngeal carcinoma, and rhabdomyosarcoma. There has been a significant reduction in the incidence of Burkitt's lymphoma. A prospective in depth epidemiological study of HIV related childhood cancers in Africa is urgently needed.
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PMID:Childhood cancers in Zambia before and after the HIV epidemic. 757 50

Vpr is a virion-associated protein of human immunodeficiency type 1 (HIV-1) whose function in acquired immunodeficiency syndrome (AIDS) has been uncertain. Employing the yeast Saccharomyces cerevisiae as a model to examine the effects of HIV-1 auxiliary proteins on basic cellular functions, we found that the vpr gene caused cell growth arrest and structural defects indicated by osmotic sensitivity and gross cell enlargement. Production of various domains by gene expression showed that this effect arose from within the carboxyl-terminal third of the Vpr protein and implicated the sequence HFRIGCRHSRIG, containing two H(S/F)RIG motifs. Electroporation with a series of peptides containing these motifs caused structural defects in yeast that resulted in osmotic sensitivity. A protein with functions relating to the yeast cytoskeleton, Sac1p [Cleves, A. E., Novick, P.J. & Bankaitis, V.A. (1989) J. Cell Biol. 109, 2939-2950], shows sequence similarity to Vpr, and Vpr's effect in yeast may be to disrupt normal Sac1p functions. The Sac1p equivalent has not yet been described in mammalian cells, but in rhabdomyosarcoma and osteosarcoma cell lines Vpr also caused gross cell enlargement and replication arrest [Levy, D.N., Fernandes, L.S., Williams, W.V. & Weiner, D.B. (1993) Cell 72, 541-550]. We note that there is a correlation between the region containing the H(S/F)RIG motifs and the pathogenicity of primate lentiviruses and we suggest that the function of Vpr may be to bring about cell growth arrest and/or cytoskeletal changes as an early step in HIV-1 infection.
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PMID:A domain of human immunodeficiency virus type 1 Vpr containing repeated H(S/F)RIG amino acid motifs causes cell growth arrest and structural defects. 770 21

Membrane proteins (MP) obtained from the human mesenchymal rhabdomyosarcoma cell line RD were coated on 96-well polystyrene microplates and tested for their ability to bind human immunodeficiency virus type 1 (HIV-1). The virus bound to MP was detected by solid phase assay. Anti-human CD4 monoclonal antibodies directed against the HIV-1 gp120 binding site of the CD4 receptor did not inhibit viral binding to MP. HIV-1 specific polypeptides were recovered from coated MP to microplates by a modification of the solid phase immunoisolation technique and shown by immunoblotting analysis using a high titer of biotinylated human anti-HIV-1 IgG. Together these findings provide evidence that HIV-1 binding to RD cell surfaces can proceed via a mechanism other than those mediated by the CD4 receptor.
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PMID:Evidence that membrane proteins of rhabdomyosarcoma cell line RD bind human immunodeficiency virus type 1 (HIV-1). 822 22

In a review of 8724 de novo malignancies that occurred in 8191 organ allograft recipients sarcomas were 7.4% of cancers. Kaposi's sarcoma (KS) made up 5.7%, and other sarcomas (OS) 1.7% a much higher proportion than in the general population. KS was most common in Arab, black, Italian, Jewish, or Greek patients. In 60% of patients with KS the lesions were confined to the skin and/or oropharynx while 40% involved internal organs and/or lymph nodes. Complete remissions following various treatments occurred in 53% of the former group and 27% of the latter. In both groups 32% and 60% of remissions, respectively, occurred when the only treatment was reduction or cessation of immunosuppressive therapy. However, this treatment caused impaired function or allograft loss from rejection in 22 of 34 kidney recipients. Recurrent KS occurred in 5% of patients in remission when immunosuppressive therapy was resumed. Nine of 114 patients (8%) tested for human immunodeficiency virus were positive. Most OS arose in internal organs or soft tissues. The major types were fibrous histiocytoma (20 patients), leiomyosarcoma (15), fibrosarcoma (12), rhabdomyosarcoma (9), hemangiosarcoma (8), undifferentiated sarcoma (7) and mesothelioma (6). Several unusual features were noted. Remarkably, 10 of 105 (10%) sarcomas occurred adjacent to or in a renal (6) or hepatic (4) allograft. Leiomyosarcomas are rare in children, yet 5 of 15 (33%) occurred in pediatric patients. Three hemangiosarcomas occurred in forearms at sites of arteriovenous fistulas used for pretransplant hemodialysis access. One leiomyosarcoma and one fibrosarcoma occurred in previously irradiated areas. One patient with mesothelioma had a history of asbestos exposure and two others had possible exposure.
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PMID:Sarcomas in organ allograft recipients. 854 79

The vif gene of the human immunodeficiency virus (HIV-1) is required for productive virus infection of primary blood mononuclear cells (PBMCs) and macrophages in vitro. Replication of HIV-1 vif- mutants in T-lymphoid cell lines varies and is dependent on the cell line used for virus production. To further understand the role of Vif in HIV-1 infection, we constructed to vif deletion mutants from a molecular clone derived from an African patient (HIV-1Zr6). Cell-free Zr6 vif- virus pools made from transfected rhabdomyosarcoma (RD) cells do not replicate when added to cultures of stimulated PBMCs. However, vif mutants were able to spread from transfected RD cells to PBMCs if cell-to-cell contact was permitted. By Western blot analysis, viral structural proteins expressed after transfection of RD cells by wild-type or vif mutant proviruses were indistinguishable. However, binding of vif mutants to PBMCs or to purified CD4 and virus internalization were significantly reduced when compared with wild-type virus. The defects in cell-free infection, CD4 binding, and internalization were rescued by transcomplementation using a vif expression plasmid. Our results suggest a novel level at which the HIV-1 vif gene product acts to enhance cell-free infection and indicate that vif plays an important role in promoting HIV-1 binding and internalization. Combined with the previous reports of vif's effect at other steps in infection, this suggests that vif is a pleuripotent gene product that affects multiple stages of the infective process.
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PMID:Cell-free HIV-1Zr6 vif mutants are defective in binding to peripheral blood mononuclear cells and in internalization. 892 9

CXCR4 (also termed fusin, LESTR, or HUMSTR) is a member of the G-protein-coupled chemokine receptor family with seven membrane-spanning domains. CXCR4 acts as a coreceptor for syncytium-inducing human immunodeficiency virus type 1 (HIV-1) strains, conferring entry into CD4+ cells. We show here that a novel mouse monoclonal antibody (12G5) that recognizes CXCR4 blocked cell-to-cell fusion and cell free-virus infection of CXCR4+ CD4+ RD rhabdomyosarcoma cells by seven HIV-1 and HIV-2 strains that had various cell tropisms for different CD4+ human cell types. Yet the majority of the members of the same virus panel resisted 12G5 inhibition on T-cell lines. When inhibition was observed on these cell types, it was both cell type and virus strain dependent. In at least one situation, 12G5 failed to block LAI infection of cells expressing CXCR4 as the only available coreceptor. Our observations suggest that CXCR4 could be processed or presented differently depending on the cell type, allowing some strains to evade 12G5 inhibition. Alternatively, since several of the viruses could infect certain CXCR4- CD4+ cell lines, it is conceivable that alternative coreceptors are active, enabling individual HIV strains to choose between compatible coreceptors during entry into cells. Moreover, the strain dependency of 12G5 inhibition implies that the interaction of different HIVs with CXCR4 varies.
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PMID:Inhibition of human immunodeficiency virus fusion by a monoclonal antibody to a coreceptor (CXCR4) is both cell type and virus strain dependent. 899 2

We have previously reported that the human immunodeficiency virus type 1 (HIV-1) regulatory gene vpr induces differentiation of rhabdomyosarcoma (embryonal muscle tumor cell line) cells, an effect that is accompanied by reduced proliferative capacity of the transfected cells. In this report, we examine the effect of Vpr expression on several different tumor cell lines derived from unique lineages. These tumor cells display different patterns of modulated oncogenes including both ras and p53 mutations. Here we demonstrate that the growth of tumor cells in vitro and in vivo is arrested by the expression of HIV-1 Vpr. Expression of Vpr in several human tumor cell lines upon transfection resulted in an accumulation of cells in the G2/M phase of cell cycle with altered cellular morphology, including an increase in adherence, and growth arrest, consistent with a differentiated phenotype. Vpr expression in B78/H1 cells results in a marked reduction in colony formation in vitro and an associated reduction in melanin synthesis by the cells. Vpr-transfected melanoma cells inoculated into syngenic C57BL/6 mice showed a markedly reduced ability to form tumors in vivo. These results suggest that this retroviral regulatory gene has broad tumor suppressor effects, likely mediated by transcriptional regulation of the state of the host cell.
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PMID:In vitro and in vivo tumor growth suppression by HIV-1 Vpr. 905 34

Cervicothoracic lesions are not uncommon in children. All cervicothoracic lesions except superficial lesions extend from the neck to the thorax through the thoracic inlet. Evaluation of this area involves multiple imaging modalities: plain radiography, ultrasonography, nuclear medicine, computed tomography, and magnetic resonance (MR) imaging. However, MR imaging is the method of choice for assessing the full extents of cervicothoracic lesions and their relationships to neurovascular structures. Cervicothoracic lesions can be classified as congenital lesions, inflammatory lesions, benign tumors, malignant tumors, and traumatic lesions. Lymphangioma is the most common cervicothoracic mass in children; other congenital lesions include hemangioma, thymic cyst, and vascular anomalies. Inflammatory adenopathy reactive to tuberculosis, mononucleosis, tularemia, cat-scratch fever, infection with human immunodeficiency virus, or other upper respiratory tract infections can manifest as cervicothoracic lesions; tuberculous abscesses and abscesses of other origins can also be seen. Lipoma, lipoblastoma, aggressive fibromatosis, and nerve sheath tumors (either isolated lesions or those associated with neurofibromatosis) can also occur as cervicothoracic masses. Malignant cervicothoracic tumors include lymphoma, thyroid carcinoma, neuroblastoma, and chest wall tumors (rhabdomyosarcoma, Ewing sarcoma, and neuroectodermal tumor). Traumatic cervicothoracic lesions include pneumomediastinum of traumatic origin, traumatic pharyngeal pseudodiverticulum, esophageal foreign-body granuloma, and cervicothoracic hematoma.
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PMID:Cervicothoracic lesions in infants and children. 1033 90


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