Comparing normal primary endocervical adenoepithelial cells to uninfected and influenza B virus infected human cervical adenocarcinoma HeLa cells.
Identifieur interne : 003B56 ( Main/Curation ); précédent : 003B55; suivant : 003B57Comparing normal primary endocervical adenoepithelial cells to uninfected and influenza B virus infected human cervical adenocarcinoma HeLa cells.
Auteurs : D O Sioutopoulou [Grèce] ; E T Plakokefalos ; G M Anifandis ; L D Arvanitis ; I. Venizelos ; R M Valeri ; H. Destouni ; N C VamvakopoulosSource :
- International journal of gynecological cancer : official journal of the International Gynecological Cancer Society [ 1048-891X ]
Descripteurs français
- KwdFr :
- Adénocarcinome (anatomopathologie), Adénocarcinome (métabolisme), Adénocarcinome (virologie), Cellules HeLa, Cellules cultivées, Cellules épithéliales (anatomopathologie), Cellules épithéliales (cytologie), Cellules épithéliales (métabolisme), Cellules épithéliales (virologie), Col de l'utérus (anatomopathologie), Col de l'utérus (cytologie), Col de l'utérus (métabolisme), Col de l'utérus (virologie), Femelle, Humains, Immunohistochimie, Phénotype, Titrimétrie, Tumeurs du col de l'utérus (anatomopathologie), Tumeurs du col de l'utérus (métabolisme), Tumeurs du col de l'utérus (virologie), Virus influenza B (physiologie).
- MESH :
- anatomopathologie : Adénocarcinome, Cellules épithéliales, Col de l'utérus, Tumeurs du col de l'utérus.
- cytologie : Cellules épithéliales, Col de l'utérus.
- métabolisme : Adénocarcinome, Cellules épithéliales, Col de l'utérus, Tumeurs du col de l'utérus.
- physiologie : Virus influenza B.
- virologie : Adénocarcinome, Cellules épithéliales, Col de l'utérus, Tumeurs du col de l'utérus.
- Cellules HeLa, Cellules cultivées, Femelle, Humains, Immunohistochimie, Phénotype, Titrimétrie.
English descriptors
- KwdEn :
- Adenocarcinoma (metabolism), Adenocarcinoma (pathology), Adenocarcinoma (virology), Cells, Cultured, Cervix Uteri (cytology), Cervix Uteri (metabolism), Cervix Uteri (pathology), Cervix Uteri (virology), Epithelial Cells (cytology), Epithelial Cells (metabolism), Epithelial Cells (pathology), Epithelial Cells (virology), Female, HeLa Cells, Humans, Immunohistochemistry, Influenza B virus (physiology), Phenotype, Titrimetry, Uterine Cervical Neoplasms (metabolism), Uterine Cervical Neoplasms (pathology), Uterine Cervical Neoplasms (virology).
- MESH :
- cytology : Cervix Uteri, Epithelial Cells.
- metabolism : Adenocarcinoma, Cervix Uteri, Epithelial Cells, Uterine Cervical Neoplasms.
- pathology : Adenocarcinoma, Cervix Uteri, Epithelial Cells, Uterine Cervical Neoplasms.
- physiology : Influenza B virus.
- virology : Adenocarcinoma, Cervix Uteri, Epithelial Cells, Uterine Cervical Neoplasms.
- Cells, Cultured, Female, HeLa Cells, Humans, Immunohistochemistry, Phenotype, Titrimetry.
Abstract
Human adenocarcinoma HeLa cells surviving infection with low (10(-9) units), medium (10(-6) units), and high (10(-2) units) influenza B titers were compared to their uninfected precursors and to normal endocervical adenoepithelial and metaplastic cells using Papanikolaou-staining method and immunocytochemistry. Normal primary endocervical and infected HeLa cells surviving infection shared similar morphologic, phenotypic, and divisional patterns that differed drastically from those of uninfected HeLa cells. The number of infected hosts surviving 6-7 days of viral exposure did not change during 3-week follow-up period, and their cyclin E levels suggested that they had been arrested to the G1 phase of the cell cycle by viral stress. Our findings suggest that in addition to apoptosis, nononcogenic viral stress activated the expression of endocervical metaplastic-like motifs in surviving hosts. A mechanism of cell response to nononcogenic viral stress was proposed to explain these findings. We conclude that nononcogenic respiratory viruses specifically target and eliminate abnormal cells ectopically overexpressing appropriate receptors and may complement current treatments of cervical cancer.
DOI: 10.1111/j.1525-1438.2006.00731.x
PubMed: 17177842
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pubmed:17177842Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenocarcinoma (metabolism)</term>
<term>Adenocarcinoma (pathology)</term>
<term>Adenocarcinoma (virology)</term>
<term>Cells, Cultured</term>
<term>Cervix Uteri (cytology)</term>
<term>Cervix Uteri (metabolism)</term>
<term>Cervix Uteri (pathology)</term>
<term>Cervix Uteri (virology)</term>
<term>Epithelial Cells (cytology)</term>
<term>Epithelial Cells (metabolism)</term>
<term>Epithelial Cells (pathology)</term>
<term>Epithelial Cells (virology)</term>
<term>Female</term>
<term>HeLa Cells</term>
<term>Humans</term>
<term>Immunohistochemistry</term>
<term>Influenza B virus (physiology)</term>
<term>Phenotype</term>
<term>Titrimetry</term>
<term>Uterine Cervical Neoplasms (metabolism)</term>
<term>Uterine Cervical Neoplasms (pathology)</term>
<term>Uterine Cervical Neoplasms (virology)</term>
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<term>Adénocarcinome (métabolisme)</term>
<term>Adénocarcinome (virologie)</term>
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<term>Cellules cultivées</term>
<term>Cellules épithéliales (anatomopathologie)</term>
<term>Cellules épithéliales (cytologie)</term>
<term>Cellules épithéliales (métabolisme)</term>
<term>Cellules épithéliales (virologie)</term>
<term>Col de l'utérus (anatomopathologie)</term>
<term>Col de l'utérus (cytologie)</term>
<term>Col de l'utérus (métabolisme)</term>
<term>Col de l'utérus (virologie)</term>
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<term>Humains</term>
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<term>Phénotype</term>
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<term>Tumeurs du col de l'utérus (virologie)</term>
<term>Virus influenza B (physiologie)</term>
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<term>Cellules épithéliales</term>
<term>Col de l'utérus</term>
<term>Tumeurs du col de l'utérus</term>
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<term>Col de l'utérus</term>
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<term>Epithelial Cells</term>
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<term>Cervix Uteri</term>
<term>Epithelial Cells</term>
<term>Uterine Cervical Neoplasms</term>
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<term>Cellules épithéliales</term>
<term>Col de l'utérus</term>
<term>Tumeurs du col de l'utérus</term>
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<term>Epithelial Cells</term>
<term>Uterine Cervical Neoplasms</term>
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<term>Cellules épithéliales</term>
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<term>Phenotype</term>
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<front><div type="abstract" xml:lang="en">Human adenocarcinoma HeLa cells surviving infection with low (10(-9) units), medium (10(-6) units), and high (10(-2) units) influenza B titers were compared to their uninfected precursors and to normal endocervical adenoepithelial and metaplastic cells using Papanikolaou-staining method and immunocytochemistry. Normal primary endocervical and infected HeLa cells surviving infection shared similar morphologic, phenotypic, and divisional patterns that differed drastically from those of uninfected HeLa cells. The number of infected hosts surviving 6-7 days of viral exposure did not change during 3-week follow-up period, and their cyclin E levels suggested that they had been arrested to the G1 phase of the cell cycle by viral stress. Our findings suggest that in addition to apoptosis, nononcogenic viral stress activated the expression of endocervical metaplastic-like motifs in surviving hosts. A mechanism of cell response to nononcogenic viral stress was proposed to explain these findings. We conclude that nononcogenic respiratory viruses specifically target and eliminate abnormal cells ectopically overexpressing appropriate receptors and may complement current treatments of cervical cancer.</div>
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