scholarly journals Undifferentiated Pleomorphic Sarcoma and the Importance of Considering the Oncogenic and Immune-Suppressant Role of the Human T-Cell Lymphotropic Virus Type 1: A Case Report

2017 ◽  
Vol 7 ◽  
Author(s):  
Sergio Lupo ◽  
Carolina Berini ◽  
Camila Cánepa ◽  
Eduardo Santini Araujo ◽  
Mirna Biglione
2011 ◽  
Vol 286 (36) ◽  
pp. 31092-31104 ◽  
Author(s):  
Batsukh Dorjbal ◽  
David Derse ◽  
Patricia Lloyd ◽  
Ferri Soheilian ◽  
Kunio Nagashima ◽  
...  

1998 ◽  
Vol 5 (5) ◽  
pp. 721-724 ◽  
Author(s):  
Kevin R. Porter ◽  
Joao Aguiar ◽  
Allen Richards ◽  
B. Sandjaya ◽  
H. Ignatias ◽  
...  

ABSTRACT To examine the role of the Plasmodium falciparum Exp-1 blood-stage protein in producing antibodies that cross-react with human T-cell lymphotropic virus type I (HTLV-I) proteins, we studied sera from Indonesian volunteers who seroconverted to malaria after transmigrating to an area where malaria is hyperendemic. Samples from Philippine volunteers, that were used in a prior study that examined malaria antibodies that cross-react with HTLV-I proteins, were also used. Eighty-three percent of the Indonesian transmigrants developed antibodies against the malaria Exp-1 protein by 6 months postmigration. Of these malaria seroconverters, 27% developed false-positive HTLV-I enzyme immunoassay (EIA) immunoreactivity, as indicated by indeterminate HTLV-I Western blot banding patterns. Five of the six Philippine samples tested were HTLV-I EIA false positive and Western blot indeterminate. When a recombinant Exp-1 protein was used in blocking experiments, the HTLV-I Western blot immunoreactivity of sera from both groups was either completely eliminated or greatly reduced. No effect on the Western blot immunoreactivity of truly HTLV-I-positive sera was seen. To determine if immunization with the recombinant Exp-1 protein could elicit the production of HTLV-I antibodies, six mice were inoculated with the recombinant protein. Following administration of three 50-μg doses of the protein, four of the six mice developed antibodies that cross-reacted with HTLV-I proteins on Western blot. These results indicate that the immune response against the malaria Exp-1 protein may result in HTLV-I-cross-reacting antibodies that can lead to false-positive EIA and indeterminant Western blotting results.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5474-5474
Author(s):  
Ana Luisa Langanke Pedroso Meireles ◽  
Dalton Chamone ◽  
Carla Rosa Teixeira Godoy ◽  
Juliana Pereira

Abstract The role of angiogenesis in metastasis of solid tumors is well established, but not in hematologic malignancies. Marwan et al demonstrated that Human T Cell Lymphotropic Virus Type 1 (HTLV1) transformed T cells secrete vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) and induce angiogenesis in vitro. Adult T-cell leukemia-lymphoma (ATL) leukemic cells produce VEGF and bFGF proteins. Therefore, the role of angiogenesis in ATL development is under investigation. We interested whether endothelial progenitor cells (EPCs) and mature endothelial cells (ECs) contribute to tumor angiogenesis in ATL Thought, this cross-sectional study aimed at quantifying circulating endothelial cells in the blood of HTLV1 asymptomatic carriers in comparison to healthy individuals by flow cytometry. A sample of 30 HTLV1 carrier age and sex matched has been compared to the control group. We demonstrated that the EPCs values were greater in the asymptomatic HTLV1 carrier (median 0.8288 cells/mm3) rather than to the control group (median 0.4905 cells/mm3) (p = 0.035). We identified other pathway of the angiogenesis in HTLV1 carriers. However, others studies are necessary to confirm the role of EPCs in the ATL pathogenesis.


2003 ◽  
Vol 77 (13) ◽  
pp. 7291-7299 ◽  
Author(s):  
Sanae Kawata ◽  
Yasuo Ariumi ◽  
Kunitada Shimotohno

ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) Tax regulates the expression of virally encoded genes, as well as various endogenous host genes in trans. Tax-mediated regulation of gene expression is important for the immortalization of normal human T lymphocytes and the transformation of fibroblast cells, such as Rat-1 cells. Tax has the ability to transactivate p21Waf1/Cip1/Sdi1, resulting in high expression levels in HTLV-1-immortalized cells. Since p21 expression is suppressed due to methylation of the promoter region in Rat-l cell line, p21 may not be critical for the transformation of this cell line by Tax. To further understand the role of p21 for the proliferation of Tax-transformed Rat-1 cells, we examined the effect of ectopic expression of p21 in these cells. Here, we observed that p21 expression enhanced the transformation of this cell line via at least two mechanisms: (i) the enhancement of NF-κB activation and/or CREB signaling and (ii) the excitation of antiapoptotic machinery. To analyze the role of p21 that is overexpressed in HTLV-1-immortalized lymphocytes, p21 expression was suppressed by using an antisense oligonucleotide specific for p21 mRNA; these cells then became sensitive to apoptotic induction. These results suggest that p21 plays an important role in the proliferation of Tax-expressing cells through the regulation of at least two independent mechanisms.


2006 ◽  
Vol 81 (3) ◽  
pp. 1506-1510 ◽  
Author(s):  
Norihiro Takenouchi ◽  
Kathryn S. Jones ◽  
Ivonne Lisinski ◽  
Kazunori Fugo ◽  
Karen Yao ◽  
...  

ABSTRACT GLUT1 has recently been suggested to be a binding receptor for human T-cell leukemia virus type 1 (HTLV-1). We used a novel, short-term assay to define the role of GLUT1 in cell-to-cell transmission. Although increasing cell surface levels of GLUT1 enhanced HTLV-I transfer, efficient virus spread correlated largely with heparan sulfate proteoglycan (HSPG) expression on target cells. Moreover, since activated CD4+ T cells and cord blood lymphocytes that are susceptible to HTLV-1 infection expressed undetectable levels of surface GLUT1, these results indicate that GLUT1 and HSPGs are important for efficient cell-to-cell transmission of HTLV-1 but raise concerns on the role of GLUT1 as the HTLV-1 primary binding receptor.


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