Oral bacteria and cancer
OSCC surfaces have been reported to harbor significantly higher levels of Porphyromonas and Fusobacterium compared with contiguous healthy mucosa [3]. [...]immunohistochemistry with P. gingivalis antibodies revealed higher levels of detection and intensity of staining in gingival carcinomas compar...
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Veröffentlicht in: | PLoS pathogens 2014-03, Vol.10 (3), p.e1003933-e1003933 |
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OSCC surfaces have been reported to harbor significantly higher levels of Porphyromonas and Fusobacterium compared with contiguous healthy mucosa [3]. [...]immunohistochemistry with P. gingivalis antibodies revealed higher levels of detection and intensity of staining in gingival carcinomas compared with healthy gingival tissue, although only a small number of cases were examined [4]. MMP-9 degrades basement membrane and extracellular matrix, which promotes carcinoma cell migration and invasion, thus allowing carcinoma cells to enter the lymphatic system and blood vessels for dissemination and metastatic growth at remote sites. [...]since well-characterized virulence factors of P. gingivalis and F. nucleatum, such as the FimA and FadA adhesins, may function as effector molecules in the transition of normal epithelial cells to cancerous cells, they may provide novel targets for therapeutic intervention. |
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OSCC surfaces have been reported to harbor significantly higher levels of Porphyromonas and Fusobacterium compared with contiguous healthy mucosa [3]. [...]immunohistochemistry with P. gingivalis antibodies revealed higher levels of detection and intensity of staining in gingival carcinomas compared with healthy gingival tissue, although only a small number of cases were examined [4]. MMP-9 degrades basement membrane and extracellular matrix, which promotes carcinoma cell migration and invasion, thus allowing carcinoma cells to enter the lymphatic system and blood vessels for dissemination and metastatic growth at remote sites. [...]since well-characterized virulence factors of P. gingivalis and F. nucleatum, such as the FimA and FadA adhesins, may function as effector molecules in the transition of normal epithelial cells to cancerous cells, they may provide novel targets for therapeutic intervention.</description><identifier>ISSN: 1553-7374</identifier><identifier>ISSN: 1553-7366</identifier><identifier>EISSN: 1553-7374</identifier><identifier>DOI: 10.1371/journal.ppat.1003933</identifier><identifier>PMID: 24676390</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Apoptosis ; Bacteria ; Bacterial infections ; Cancer ; Cell cycle ; Cell division ; Cell growth ; Host-parasite relationships ; Humans ; Infections ; Kinases ; Lymphatic system ; Medical prognosis ; Medicine and Health Sciences ; Metastasis ; Microbiological research ; Mortality ; Mouth - microbiology ; Mouth cancer ; Neoplasms - microbiology ; Oncology, Experimental ; Organisms ; Pancreatic cancer ; Pearls ; Risk factors ; Studies ; Tumorigenesis ; Viral infections</subject><ispartof>PLoS pathogens, 2014-03, Vol.10 (3), p.e1003933-e1003933</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Whitmore, Lamont 2014 Whitmore, Lamont</rights><rights>2014 Whitmore, Lamont. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Whitmore SE, Lamont RJ (2014) Oral Bacteria and Cancer. PLoS Pathog 10(3): e1003933. doi:10.1371/journal.ppat.1003933</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c684t-c6d9fd7498fc80aaa3ac619ed28f8acb04db7012c3844944d6337c246ee3ff5a3</citedby><cites>FETCH-LOGICAL-c684t-c6d9fd7498fc80aaa3ac619ed28f8acb04db7012c3844944d6337c246ee3ff5a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3968118/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3968118/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24676390$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Whitmore, Sarah E</creatorcontrib><creatorcontrib>Lamont, Richard J</creatorcontrib><title>Oral bacteria and cancer</title><title>PLoS pathogens</title><addtitle>PLoS Pathog</addtitle><description>
OSCC surfaces have been reported to harbor significantly higher levels of Porphyromonas and Fusobacterium compared with contiguous healthy mucosa [3]. [...]immunohistochemistry with P. gingivalis antibodies revealed higher levels of detection and intensity of staining in gingival carcinomas compared with healthy gingival tissue, although only a small number of cases were examined [4]. MMP-9 degrades basement membrane and extracellular matrix, which promotes carcinoma cell migration and invasion, thus allowing carcinoma cells to enter the lymphatic system and blood vessels for dissemination and metastatic growth at remote sites. [...]since well-characterized virulence factors of P. gingivalis and F. nucleatum, such as the FimA and FadA adhesins, may function as effector molecules in the transition of normal epithelial cells to cancerous cells, they may provide novel targets for therapeutic intervention.</description><subject>Apoptosis</subject><subject>Bacteria</subject><subject>Bacterial infections</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell division</subject><subject>Cell growth</subject><subject>Host-parasite relationships</subject><subject>Humans</subject><subject>Infections</subject><subject>Kinases</subject><subject>Lymphatic system</subject><subject>Medical prognosis</subject><subject>Medicine and Health Sciences</subject><subject>Metastasis</subject><subject>Microbiological research</subject><subject>Mortality</subject><subject>Mouth - microbiology</subject><subject>Mouth cancer</subject><subject>Neoplasms - microbiology</subject><subject>Oncology, Experimental</subject><subject>Organisms</subject><subject>Pancreatic cancer</subject><subject>Pearls</subject><subject>Risk factors</subject><subject>Studies</subject><subject>Tumorigenesis</subject><subject>Viral infections</subject><issn>1553-7374</issn><issn>1553-7366</issn><issn>1553-7374</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNqVksuLFDEQxhtR3HX17kF0wIseZkx1pfO4CMviY2Bxwcc5VCfpsYeezmzSLfrfm9npXbbBiwSSUPl9X1WSKooXwFaAEt5twxh76lb7PQ0rYAw14oPiFKoKlxIlf3hvf1I8SWnLGAcE8bg4KbmQAjU7LZ5fReoWNdnBx5YW1LuFpd76-LR41FCX_LNpPSt-fPzw_eLz8vLq0_ri_HJpheJDnp1unORaNVYxIkKyArR3pWoU2ZpxV0sGpUXFuebcCURpc37vsWkqwrPi1dF334VkpkslAxUIWUGpIRPrI-ECbc0-tjuKf0yg1twEQtwYikNrO28ccJJ1LoB8xbFSWa2x1FJZBVjyKnu9n7KN9c476_sh339mOj_p259mE34Z1EIBqGzwZjKI4Xr0aTC7NlnfddT7MN7UnXMqKMuMvj6iG8qltX0TsqM94OYchUCuuGSZWv2DysP5XWtD75s2x2eCtzNBZgb_e9jQmJJZf_v6H-yXOcuPrI0hpeibu1cBZg4dd_s55tBxZuq4LHt5_0XvRLcthn8BVCPOsg</recordid><startdate>20140301</startdate><enddate>20140301</enddate><creator>Whitmore, Sarah E</creator><creator>Lamont, Richard J</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISN</scope><scope>ISR</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140301</creationdate><title>Oral bacteria and cancer</title><author>Whitmore, Sarah E ; Lamont, Richard J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c684t-c6d9fd7498fc80aaa3ac619ed28f8acb04db7012c3844944d6337c246ee3ff5a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Apoptosis</topic><topic>Bacteria</topic><topic>Bacterial infections</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell division</topic><topic>Cell growth</topic><topic>Host-parasite relationships</topic><topic>Humans</topic><topic>Infections</topic><topic>Kinases</topic><topic>Lymphatic system</topic><topic>Medical prognosis</topic><topic>Medicine and Health Sciences</topic><topic>Metastasis</topic><topic>Microbiological research</topic><topic>Mortality</topic><topic>Mouth - microbiology</topic><topic>Mouth cancer</topic><topic>Neoplasms - microbiology</topic><topic>Oncology, Experimental</topic><topic>Organisms</topic><topic>Pancreatic cancer</topic><topic>Pearls</topic><topic>Risk factors</topic><topic>Studies</topic><topic>Tumorigenesis</topic><topic>Viral infections</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Whitmore, Sarah E</creatorcontrib><creatorcontrib>Lamont, Richard J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Canada</collection><collection>Gale In Context: Science</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS pathogens</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Whitmore, Sarah E</au><au>Lamont, Richard J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oral bacteria and cancer</atitle><jtitle>PLoS pathogens</jtitle><addtitle>PLoS Pathog</addtitle><date>2014-03-01</date><risdate>2014</risdate><volume>10</volume><issue>3</issue><spage>e1003933</spage><epage>e1003933</epage><pages>e1003933-e1003933</pages><issn>1553-7374</issn><issn>1553-7366</issn><eissn>1553-7374</eissn><abstract>
OSCC surfaces have been reported to harbor significantly higher levels of Porphyromonas and Fusobacterium compared with contiguous healthy mucosa [3]. [...]immunohistochemistry with P. gingivalis antibodies revealed higher levels of detection and intensity of staining in gingival carcinomas compared with healthy gingival tissue, although only a small number of cases were examined [4]. MMP-9 degrades basement membrane and extracellular matrix, which promotes carcinoma cell migration and invasion, thus allowing carcinoma cells to enter the lymphatic system and blood vessels for dissemination and metastatic growth at remote sites. [...]since well-characterized virulence factors of P. gingivalis and F. nucleatum, such as the FimA and FadA adhesins, may function as effector molecules in the transition of normal epithelial cells to cancerous cells, they may provide novel targets for therapeutic intervention.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24676390</pmid><doi>10.1371/journal.ppat.1003933</doi><oa>free_for_read</oa></addata></record> |
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subjects | Apoptosis Bacteria Bacterial infections Cancer Cell cycle Cell division Cell growth Host-parasite relationships Humans Infections Kinases Lymphatic system Medical prognosis Medicine and Health Sciences Metastasis Microbiological research Mortality Mouth - microbiology Mouth cancer Neoplasms - microbiology Oncology, Experimental Organisms Pancreatic cancer Pearls Risk factors Studies Tumorigenesis Viral infections |
title | Oral bacteria and cancer |
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