Comparing normal primary endocervical adenoepithelial cells to uninfected and influenza B virus infected human cervical adenocarcinoma HeLa cells.
Identifieur interne : 000815 ( PubMed/Corpus ); précédent : 000814; suivant : 000816Comparing normal primary endocervical adenoepithelial cells to uninfected and influenza B virus infected human cervical adenocarcinoma HeLa cells.
Auteurs : D O Sioutopoulou ; 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 ]
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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Venizelos</name></author><author><name sortKey="Valeri, R M" sort="Valeri, R M" uniqKey="Valeri R" first="R M" last="Valeri">R M Valeri</name></author><author><name sortKey="Destouni, H" sort="Destouni, H" uniqKey="Destouni H" first="H" last="Destouni">H. Destouni</name></author><author><name sortKey="Vamvakopoulos, N C" sort="Vamvakopoulos, N C" uniqKey="Vamvakopoulos N" first="N C" last="Vamvakopoulos">N C Vamvakopoulos</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="????"><PubDate><MedlineDate>2006 Nov-Dec</MedlineDate></PubDate></date><idno type="RBID">pubmed:17177842</idno><idno type="pmid">17177842</idno><idno type="doi">10.1111/j.1525-1438.2006.00731.x</idno><idno type="wicri:Area/PubMed/Corpus">000815</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000815</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Comparing normal primary endocervical adenoepithelial cells to uninfected and influenza B virus infected human cervical adenocarcinoma HeLa cells.</title><author><name sortKey="Sioutopoulou, D O" sort="Sioutopoulou, D O" uniqKey="Sioutopoulou D" first="D O" last="Sioutopoulou">D O Sioutopoulou</name><affiliation><nlm:affiliation>Department of Biology and Genetics, University of Thessalia Medical School, Larisa, Greece.</nlm:affiliation></affiliation></author><author><name sortKey="Plakokefalos, E T" sort="Plakokefalos, E T" uniqKey="Plakokefalos E" first="E T" last="Plakokefalos">E T Plakokefalos</name></author><author><name sortKey="Anifandis, G M" sort="Anifandis, G M" uniqKey="Anifandis G" first="G M" last="Anifandis">G M Anifandis</name></author><author><name sortKey="Arvanitis, L D" sort="Arvanitis, L D" uniqKey="Arvanitis L" first="L D" last="Arvanitis">L D Arvanitis</name></author><author><name sortKey="Venizelos, I" sort="Venizelos, I" uniqKey="Venizelos I" first="I" last="Venizelos">I. Venizelos</name></author><author><name sortKey="Valeri, R M" sort="Valeri, R M" uniqKey="Valeri R" first="R M" last="Valeri">R M Valeri</name></author><author><name sortKey="Destouni, H" sort="Destouni, H" uniqKey="Destouni H" first="H" last="Destouni">H. Destouni</name></author><author><name sortKey="Vamvakopoulos, N C" sort="Vamvakopoulos, N C" uniqKey="Vamvakopoulos N" first="N C" last="Vamvakopoulos">N C Vamvakopoulos</name></author></analytic><series><title level="j">International journal of gynecological cancer : official journal of the International Gynecological Cancer Society</title><idno type="ISSN">1048-891X</idno></series></biblStruct></sourceDesc></fileDesc><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></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Cervix Uteri</term><term>Epithelial Cells</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adenocarcinoma</term><term>Cervix Uteri</term><term>Epithelial Cells</term><term>Uterine Cervical Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Adenocarcinoma</term><term>Cervix Uteri</term><term>Epithelial Cells</term><term>Uterine Cervical Neoplasms</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza B virus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Adenocarcinoma</term><term>Cervix Uteri</term><term>Epithelial Cells</term><term>Uterine Cervical Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cells, Cultured</term><term>Female</term><term>HeLa Cells</term><term>Humans</term><term>Immunohistochemistry</term><term>Phenotype</term><term>Titrimetry</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17177842</PMID><DateCompleted><Year>2007</Year><Month>02</Month><Day>23</Day></DateCompleted><DateRevised><Year>2018</Year><Month>10</Month><Day>30</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1048-891X</ISSN><JournalIssue CitedMedium="Print"><Volume>16</Volume><Issue>6</Issue><PubDate><MedlineDate>2006 Nov-Dec</MedlineDate></PubDate></JournalIssue><Title>International journal of gynecological cancer : official journal of the International Gynecological Cancer Society</Title><ISOAbbreviation>Int. J. Gynecol. Cancer</ISOAbbreviation></Journal><ArticleTitle>Comparing normal primary endocervical adenoepithelial cells to uninfected and influenza B virus infected human cervical adenocarcinoma HeLa cells.</ArticleTitle><Pagination><MedlinePgn>2032-8</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sioutopoulou</LastName><ForeName>D O</ForeName><Initials>DO</Initials><AffiliationInfo><Affiliation>Department of Biology and Genetics, University of Thessalia Medical School, Larisa, Greece.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Plakokefalos</LastName><ForeName>E T</ForeName><Initials>ET</Initials></Author><Author ValidYN="Y"><LastName>Anifandis</LastName><ForeName>G M</ForeName><Initials>GM</Initials></Author><Author ValidYN="Y"><LastName>Arvanitis</LastName><ForeName>L D</ForeName><Initials>LD</Initials></Author><Author ValidYN="Y"><LastName>Venizelos</LastName><ForeName>I</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Valeri</LastName><ForeName>R M</ForeName><Initials>RM</Initials></Author><Author ValidYN="Y"><LastName>Destouni</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Vamvakopoulos</LastName><ForeName>N C</ForeName><Initials>NC</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Int J Gynecol Cancer</MedlineTA><NlmUniqueID>9111626</NlmUniqueID><ISSNLinking>1048-891X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000230" MajorTopicYN="N">Adenocarcinoma</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002584" MajorTopicYN="N">Cervix Uteri</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006367" MajorTopicYN="N">HeLa Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009981" MajorTopicYN="N">Influenza B virus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017186" MajorTopicYN="N">Titrimetry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002583" MajorTopicYN="N">Uterine Cervical Neoplasms</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>12</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>2</Month><Day>24</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>12</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17177842</ArticleId><ArticleId IdType="pii">IJG731</ArticleId><ArticleId IdType="doi">10.1111/j.1525-1438.2006.00731.x</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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