scholarly journals Detection of human polyomavirus proteins, T-antigen and agnoprotein, in human tumor tissue arrays

2010 ◽  
Vol 82 (5) ◽  
pp. 806-811 ◽  
Author(s):  
Luis Del Valle ◽  
Kamel Khalili
Keyword(s):  
Tumor Tissue ◽  
Human Tumor ◽  
T Antigen ◽  
Human Polyomavirus ◽  
Tissue Arrays

T-antigen of the human polyomavirus JC attenuates faithful DNA repair by forcing nuclear interaction between IRS-1 and Rad51

2005 ◽  
Vol 206 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Joanna Trojanek ◽  
Sidney Croul ◽  
Thu Ho ◽  
Jin Ying Wang ◽  
Armine Darbinyan ◽  
...  
Keyword(s):  
Dna Repair ◽  
Nuclear Interaction ◽  
T Antigen ◽  
Human Polyomavirus ◽  
Polyomavirus Jc

scholarly journals Characterization of T Antigens, Including Middle T and Alternative T, Expressed by the Human Polyomavirus Associated with Trichodysplasia Spinulosa

2015 ◽  
Vol 89 (18) ◽  
pp. 9427-9439 ◽  
Author(s):  
Els van der Meijden ◽  
Siamaque Kazem ◽  
Christina A. Dargel ◽  
Nick van Vuren ◽  
Paul J. Hensbergen ◽  
...  
Keyword(s):  
Expression Pattern ◽  
T Antigen ◽  
Productive Infection ◽  
Human Polyomavirus ◽  
T Antigens ◽  
Viral Oncoprotein ◽  
Early Region ◽  
Alternative Mrna Splicing ◽  
Donor And Acceptor ◽  
Human Polyomaviruses

ABSTRACTThe polyomavirus tumor (T) antigens play crucial roles in viral replication, transcription, and cellular transformation. They are encoded by partially overlapping open reading frames (ORFs) located in the early region through alternative mRNA splicing. The T expression pattern of the trichodysplasia spinulosa-associated polyomavirus (TSPyV) has not been established yet, hampering further study of its pathogenic mechanisms and taxonomic relationship. Here, we characterized TSPyV T antigen expression in human cell lines transfected with the TSPyV early region. Sequencing of T antigen-encoded reverse transcription-PCR (RT-PCR) products revealed three splice donor and acceptor sites creating six mRNA splice products that potentially encode the antigens small T (ST), middle T (MT), large T (LT), tiny T, 21kT, and alternative T (ALTO). Except for 21kT, these splice products were also detected in skin of TSPyV-infected patients. At least three splice products were confirmed by Northern blotting, likely encoding LT, MT, ST, 21kT, and ALTO. Protein expression was demonstrated for LT, ALTO, and possibly MT, with LT detected in the nucleus and ALTO in the cytoplasm of transfected cells. Splice site and start codon mutations indicated that ALTO is encoded by the same splice product that encodes LT and uses internal start codons for initiation. The genuineness of ALTO was indicated by the identification of acetylated N-terminal ALTO peptides by mass spectrometry. Summarizing, TSPyV exhibits an expression pattern characterized by both MT and ALTO expression, combining features of rodent and human polyomaviruses. This unique expression pattern provides important leads for further study of polyomavirus-related disease and for an understanding of polyomavirus evolution.IMPORTANCEThe human trichodysplasia spinulosa-associated polyomavirus (TSPyV) is distinguished among polyomaviruses for combining productive infection with cell-transforming properties. In the research presented here, we further substantiate this unique position by indicating expression of both middle T antigen (MT) and alternative T antigen (ALTO) in TSPyV. So far, none of the human polyomaviruses was shown to express MT, which is considered the most important viral oncoprotein of rodent polyomaviruses. Coexpression of ALTO and MT, which involves a conserved, recently recognized overlapping ORF subject to positive selection, has not been observed before for any polyomavirus. As a result of our findings, this study provides valuable new insights into polyomavirus T gene use and expression. Obviously, these insights will be instrumental in further study and gaining an understanding of TSPyV pathogenicity. More importantly, however, they provide important leads with regard to the interrelationship, functionality, and evolution of polyomaviruses as a whole, indicating that TSPyV is a suitable model virus to study these entities further.

scholarly journals Merkel Cell Carcinoma: Recent Progress and Current Priorities on Etiology, Pathogenesis, and Clinical Management

2009 ◽  
Vol 27 (24) ◽  
pp. 4021-4026 ◽  
Author(s):  
Keyword(s):  
Cell Carcinoma ◽  
Merkel Cell Carcinoma ◽  
Clinical Management ◽  
Expression Profiles ◽  
T Antigen ◽  
Neuroendocrine Cells ◽  
Human Polyomavirus ◽  
Adjuvant Radiation ◽  
Cytokeratin 20 ◽  
Merkel Cell

Purpose To expedite improved understanding, diagnosis, treatment, and prevention of Merkel cell carcinoma (MCC), a rare malignancy of cutaneous neuroendocrine cells that has a 28% 2-year mortality rate. Methods This article summarizes a workshop that discussed the state-of-the-art research and priorities for research on MCC and on a new human polyomavirus (ie, MCPyV) recently discovered in 80% of MCC tumors. Results Normal Merkel cells are widely distributed in the epidermis near the end of nerve axons and may function as mechanoreceptors or chemoreceptors. Malignant MCC cells typically stain for cytokeratin 20 as well as for other epithelial and neuroendocrine markers. MCC subtypes, which are based on histology, on cell line growth properties, and on gene expression profiles, have been reported but have not been linked to prognosis. Clinical management has been empiric. MCPyV is clonally integrated at various sites in the human genome of MCC tumors, with truncating mutations in the viral, large T antigen gene that interrupt viral replication. MCPyV seroprevalence may be high, as with previously known human polyomaviruses. MCC risk is increased 11-fold with AIDS and with other cell-mediated immune deficiencies, B-cell neoplasms, and ultraviolet radiation exposure. Conclusion Development and validation of a range quantitative polymerase chain reaction and serologic assays for detection of MCPyV, as well as an infectious clone of the virus, would clarify the fundamental biology, natural history, and epidemiology of the virus, of MCC, and of other diseases. Contingent on standardized histologic diagnosis and staging of MCC, consortia are needed to clarify the risks and benefits of sentinel lymph node biopsy, adjuvant radiation therapy, and salvage therapies; consortia are needed also for epidemiologic studies of MCC etiology.

A report of sex chromatin in human tumor tissue culture

1958 ◽  
Vol 15 (1) ◽  
pp. 244-246 ◽  
Author(s):  
E.V. Orsi ◽  
H.B. Ritter
Keyword(s):  
Tissue Culture ◽  
Tumor Tissue ◽  
Human Tumor ◽  
Sex Chromatin

scholarly journals Human Tumor Tissue-Based 3D In Vitro Invasion Assays

2018 ◽  
pp. 213-221 ◽  
Author(s):  
Pirjo Åström ◽  
Ritva Heljasvaara ◽  
Pia Nyberg ◽  
Ahmed Al-Samadi ◽  
Tuula Salo
Keyword(s):  
Tumor Tissue ◽  
Human Tumor ◽  
In Vitro Invasion ◽  
Invasion Assays

scholarly journals SLMP53-1 Inhibits Tumor Cell Growth through Regulation of Glucose Metabolism and Angiogenesis in a P53-Dependent Manner

2020 ◽  
Vol 21 (2) ◽  
pp. 596 ◽  
Author(s):  
Helena Ramos ◽  
Juliana Calheiros ◽  
Joana Almeida ◽  
Valentina Barcherini ◽  
Sónia Santos ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Cytochrome C ◽  
Cancer Cells ◽  
Cytochrome C Oxidase ◽  
Tumor Tissue ◽  
Human Tumor ◽  
Dichloroacetic Acid ◽  
Dependent Manner ◽  
Glucose Transporter 1 ◽  
Expression Levels

The Warburg effect is an emerging hallmark of cancer, which has the tumor suppressor p53 as its major regulator. Herein, we unveiled that p53 activation by (S)-tryptophanol-derived oxazoloisoindolinone (SLMP53-1) mediated the reprograming of glucose metabolism in cancer cells and xenograft human tumor tissue, interfering with angiogenesis and migration. Particularly, we showed that SLMP53-1 regulated glycolysis by downregulating glucose transporter 1 (GLUT1), hexokinase-2 (HK2), and phosphofructokinase-2 isoform 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase-3 (PFKFB3) (key glycolytic enzymes), while upregulating the mitochondrial markers synthesis of cytochrome c oxidase 2 (SCO2), cytochrome c oxidase subunit 4 (COX4), and OXPHOS mitochondrial complexes. SLMP53-1 also downregulated the monocarboxylate transporter 4 (MCT4), causing the subsequent reduction of lactate export by cancer cells. Besides the acidification of the extracellular environment, SLMP53-1 further increased E-cadherin and reduced metalloproteinase-9 (MMP-9) expression levels in both cancer cells and xenograft human tumor tissue, which suggested the interference of SLMP53-1 in extracellular matrix remodeling and epithelial-to-mesenchymal transition. Consistently, SLMP53-1 depleted angiogenesis, decreasing endothelial cell tube formation and vascular endothelial growth factor (VEGF) expression levels. SLMP53-1 also exhibited synergistic growth inhibitory activity in combination with the metabolic modulator dichloroacetic acid. These data reinforce the promising application of the p53-activating agent SLMP53-1 in cancer therapy, by targeting p53-mediated pathways of growth and dissemination.

Development of therapeutic vaccines by direct modification of cell membranes from surgically removed human tumor tissue with immunostimulatory molecules

Vaccine ◽  
2001 ◽  
Vol 19 (15-16) ◽  
pp. 2029-2038 ◽  
Author(s):  
Neil J Poloso ◽  
Shanmugam Nagarajan ◽  
Gary W Bumgarner ◽  
Periasamy Selvaraj
Keyword(s):  
Cell Membranes ◽  
Tumor Tissue ◽  
Human Tumor ◽  
Therapeutic Vaccines ◽  
Direct Modification
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