Εμφάνιση απλής εγγραφής

dc.creatorSioutopoulou, D. O.en
dc.creatorPlakokefalos, E.en
dc.creatorArvanitis, L.en
dc.creatorAthanassiou, E.en
dc.creatorVenizelos, J.en
dc.creatorKaplanis, K.en
dc.creatorDestouni, C.en
dc.creatorNomikos, I.en
dc.creatorSatra, M.en
dc.creatorVamvakopoulos, N. C.en
dc.date.accessioned2015-11-23T10:47:24Z
dc.date.available2015-11-23T10:47:24Z
dc.date.issued2008
dc.identifier10.1016/j.prp.2007.11.010
dc.identifier.issn0344-0338
dc.identifier.urihttp://hdl.handle.net/11615/33051
dc.description.abstractWe infected HeLa cells with low (10(-9) units), medium (10(-6) units), and high (10(-2) units) influenza B titers and compared the resulting human papilloma virus (HPV), retinoic acid receptor a subunit (RAR alpha) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA content of surviving infected hosts with that of their uninfected precursors by semi-quantitative reverse transcriptase/polymerase chain reaction amplification (RT/PCR). This comparison revealed a moderate and drastic dependence of HPV and RARa mRNA content, respectively, but a complete independence of GAPDH mRNA expression on viral titer. A mechanism of adoptive replacement of tolerable cellular with viral gene expression was proposed to explain these findings. We conclude that the reported ability of influenza B viruses to specifically target and eliminate the cervical adenocarcinoma HeLa cell line studied may find practical applications in biological cancer management. (C) 2008 Published by Elsevier GmbH.en
dc.sourcePathology Research and Practiceen
dc.source.uri<Go to ISI>://WOS:000255888200006
dc.subjectHeLa cellsen
dc.subjectinfluenza B virusen
dc.subjectphenotypic conversionen
dc.subjectinfecteden
dc.subjectnormal-like cellsen
dc.subjectHUMAN PAPILLOMAVIRUSESen
dc.subjectSOUTHERN GREECEen
dc.subjectHEMAGGLUTININen
dc.subjectSPECIFICITYen
dc.subjectAPOPTOSISen
dc.subjectACIDen
dc.subjectBETAen
dc.subjectPathologyen
dc.titleOn the mechanism of phenotypic conversion of human cervical adenocarcinoma HeLa cells surviving infection by influenza B virus: Potential implications for biological management of adenocarcinomasen
dc.typejournalArticleen


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