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Article: Further observations on mechanisms of bone destruction by squamous carcinomas of the head and neck: The role of host stroma

TitleFurther observations on mechanisms of bone destruction by squamous carcinomas of the head and neck: The role of host stroma
Authors
Issue Date1983
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
Citation
British Journal Of Cancer, 1983, v. 48 n. 5, p. 697-704 How to Cite?
AbstractMechanisms of bone invasion by squamous carcinomas of the head and neck have been investigated using fresh tumours and established tumour cell lines in an in vitro bone resorption assay with 45Ca-labelled mouse calvaria. Fresh tumours regularly resorb bone in vitro. Activity is consistently reduced by indomethacin. The tumours release E 2 prostaglandins (PGE 2) in amounts sufficient to account for ~50% of the bone resorption observed. Small amounts of non-prostaglandin (indomethacin-resistant) osteolytic factors are also produced. Control non-neoplastic tissues show a variable capacity to resorb bone in vitro; PGE 2 levels in these tissues may be related to their content of inflammatory cells. Tumour cell lines also resorb bone in vitro but, for most lines, activity is not significantly blocked by indomethacin and PGE 2 levels are generally insufficient to account for the osteolysis observed. Non-prostaglandin bone resorbing factors thus predominate. It is concluded that most squamous cancers of the head and neck are osteolytic in vitro and release a mixture of prostaglandin and non-prostaglandin factors which stimulate osteoclastic bone resorption. These factors are derived from both neoplastic and stromal elements, and are 'tumour-associated' rather than 'tumour-specific'. In vitro bone resorption and prostaglandin release does not correlate with pathological features of the tumour or with post-operative survival.
Persistent Identifierhttp://hdl.handle.net/10722/149445
ISSN
2015 Impact Factor: 5.569
2015 SCImago Journal Rankings: 2.939
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTsao, SWen_US
dc.contributor.authorBurman, JFen_US
dc.contributor.authorPittam, MRen_US
dc.contributor.authorCarter, RLen_US
dc.date.accessioned2012-06-26T05:53:43Z-
dc.date.available2012-06-26T05:53:43Z-
dc.date.issued1983en_US
dc.identifier.citationBritish Journal Of Cancer, 1983, v. 48 n. 5, p. 697-704en_US
dc.identifier.issn0007-0920en_US
dc.identifier.urihttp://hdl.handle.net/10722/149445-
dc.description.abstractMechanisms of bone invasion by squamous carcinomas of the head and neck have been investigated using fresh tumours and established tumour cell lines in an in vitro bone resorption assay with 45Ca-labelled mouse calvaria. Fresh tumours regularly resorb bone in vitro. Activity is consistently reduced by indomethacin. The tumours release E 2 prostaglandins (PGE 2) in amounts sufficient to account for ~50% of the bone resorption observed. Small amounts of non-prostaglandin (indomethacin-resistant) osteolytic factors are also produced. Control non-neoplastic tissues show a variable capacity to resorb bone in vitro; PGE 2 levels in these tissues may be related to their content of inflammatory cells. Tumour cell lines also resorb bone in vitro but, for most lines, activity is not significantly blocked by indomethacin and PGE 2 levels are generally insufficient to account for the osteolysis observed. Non-prostaglandin bone resorbing factors thus predominate. It is concluded that most squamous cancers of the head and neck are osteolytic in vitro and release a mixture of prostaglandin and non-prostaglandin factors which stimulate osteoclastic bone resorption. These factors are derived from both neoplastic and stromal elements, and are 'tumour-associated' rather than 'tumour-specific'. In vitro bone resorption and prostaglandin release does not correlate with pathological features of the tumour or with post-operative survival.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjcen_US
dc.relation.ispartofBritish Journal of Canceren_US
dc.subject.meshAnimalsen_US
dc.subject.meshBone Resorption - Drug Effectsen_US
dc.subject.meshCarcinoma, Squamous Cell - Metabolism - Physiopathologyen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCulture Mediaen_US
dc.subject.meshCulture Techniquesen_US
dc.subject.meshDinoprosten_US
dc.subject.meshDinoprostoneen_US
dc.subject.meshFibroblasts - Metabolismen_US
dc.subject.meshHead And Neck Neoplasms - Metabolism - Physiopathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Balb Cen_US
dc.subject.meshProstaglandins E - Metabolismen_US
dc.subject.meshProstaglandins F - Metabolismen_US
dc.subject.meshSkin - Metabolismen_US
dc.titleFurther observations on mechanisms of bone destruction by squamous carcinomas of the head and neck: The role of host stromaen_US
dc.typeArticleen_US
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_US
dc.identifier.authorityTsao, SW=rp00399en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid6580033-
dc.identifier.scopuseid_2-s2.0-0021089530en_US
dc.identifier.volume48en_US
dc.identifier.issue5en_US
dc.identifier.spage697en_US
dc.identifier.epage704en_US
dc.identifier.isiWOS:A1983RR07700010-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridTsao, SW=7102813116en_US
dc.identifier.scopusauthoridBurman, JF=16159916300en_US
dc.identifier.scopusauthoridPittam, MR=6701621876en_US
dc.identifier.scopusauthoridCarter, RL=7402936927en_US

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