File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Up-regulation of lysozyme production in colonic adenomas and adenocarcinomas

TitleUp-regulation of lysozyme production in colonic adenomas and adenocarcinomas
Authors
KeywordsAdenocarcinoma
Adenoma
Large intestine
Lysozyme
Issue Date1998
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HIS
Citation
Histopathology, 1998, v. 32 n. 2, p. 126-132 How to Cite?
AbstractAims: The presence of lysozyme protein in some gastric adenomas and adenocarcinomas has been well documented. There have been relatively few studies investigating the presence of lysozyme in tumours of the large intestine and they show contrasting results. We aim to investigate the cellular source and expression of lysozyme in colonic adenomas and adenocarcinomas. Methods and results: We randomly selected 29 and 27 colonic adenomas and adenocarcinomas, respectively. Using in-situ hybridization (ISH) and immunohistochemistry (IHC), we found an up-regulation of lysozyme in the dysplastic epithelium of all the adenomas studied, with more than 80% of cases expressing moderate to strong signals. Although the up-regulation of lysozyme was also observed in adenocarcinomas, only 30% of the cases showed moderate to strong signals, mostly with an uneven distribution. Down- regulation of lysozyme in the severely dysplastic and invasive foci were toted in some cases of adenoma with malignant transformation. Normal colonic glands were consistently negative for lysozyme at both the mRNA and the protein level, but inflamed and immature regenerative colonic epithelium at the crypt base showed positive signals in a similar pattern to those observed in the dysplastic epithelium of the adenomas. Conclusions: Our results confirm that colonic epithelium can produce lysozyme and its expression is up-regulated in the dysplastic epithelium in adenomas and in invasive cancer cells. It is interesting that regenerative colonic epithelium showed a similar pattern of lysozyme expression as in adenomas. The loss of lysozyme secreting phenotype in most of the invasive tumours suggests that lysozyme may not confer an advantage to tumour progression.
Persistent Identifierhttp://hdl.handle.net/10722/148116
ISSN
2015 Impact Factor: 3.425
2015 SCImago Journal Rankings: 1.488
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuen, STen_HK
dc.contributor.authorWong, MPen_HK
dc.contributor.authorChung, LPen_HK
dc.contributor.authorChan, SYen_HK
dc.contributor.authorCheung, Nen_HK
dc.contributor.authorHo, Jen_HK
dc.contributor.authorLeung, SYen_HK
dc.date.accessioned2012-05-29T06:10:56Z-
dc.date.available2012-05-29T06:10:56Z-
dc.date.issued1998en_HK
dc.identifier.citationHistopathology, 1998, v. 32 n. 2, p. 126-132en_HK
dc.identifier.issn0309-0167en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148116-
dc.description.abstractAims: The presence of lysozyme protein in some gastric adenomas and adenocarcinomas has been well documented. There have been relatively few studies investigating the presence of lysozyme in tumours of the large intestine and they show contrasting results. We aim to investigate the cellular source and expression of lysozyme in colonic adenomas and adenocarcinomas. Methods and results: We randomly selected 29 and 27 colonic adenomas and adenocarcinomas, respectively. Using in-situ hybridization (ISH) and immunohistochemistry (IHC), we found an up-regulation of lysozyme in the dysplastic epithelium of all the adenomas studied, with more than 80% of cases expressing moderate to strong signals. Although the up-regulation of lysozyme was also observed in adenocarcinomas, only 30% of the cases showed moderate to strong signals, mostly with an uneven distribution. Down- regulation of lysozyme in the severely dysplastic and invasive foci were toted in some cases of adenoma with malignant transformation. Normal colonic glands were consistently negative for lysozyme at both the mRNA and the protein level, but inflamed and immature regenerative colonic epithelium at the crypt base showed positive signals in a similar pattern to those observed in the dysplastic epithelium of the adenomas. Conclusions: Our results confirm that colonic epithelium can produce lysozyme and its expression is up-regulated in the dysplastic epithelium in adenomas and in invasive cancer cells. It is interesting that regenerative colonic epithelium showed a similar pattern of lysozyme expression as in adenomas. The loss of lysozyme secreting phenotype in most of the invasive tumours suggests that lysozyme may not confer an advantage to tumour progression.en_HK
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HISen_HK
dc.relation.ispartofHistopathologyen_HK
dc.subjectAdenocarcinomaen_HK
dc.subjectAdenomaen_HK
dc.subjectLarge intestineen_HK
dc.subjectLysozymeen_HK
dc.subject.meshAdenocarcinoma - Enzymology - Pathologyen_US
dc.subject.meshAdenoma - Enzymology - Pathologyen_US
dc.subject.meshColonic Neoplasms - Enzymology - Pathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshIn Situ Hybridizationen_US
dc.subject.meshIntestinal Mucosa - Enzymology - Pathologyen_US
dc.subject.meshMuramidase - Biosynthesis - Geneticsen_US
dc.subject.meshRna, Messenger - Biosynthesisen_US
dc.subject.meshRandom Allocationen_US
dc.subject.meshUp-Regulationen_US
dc.titleUp-regulation of lysozyme production in colonic adenomas and adenocarcinomasen_HK
dc.typeArticleen_HK
dc.identifier.emailWong, MP: mwpik@hkucc.hku.hken_HK
dc.identifier.emailChung, LP: lpchung@hkucc.hku.hken_HK
dc.identifier.emailLeung, SY: suetyi@hku.hken_HK
dc.identifier.authorityWong, MP=rp00348en_HK
dc.identifier.authorityChung, LP=rp00249en_HK
dc.identifier.authorityLeung, SY=rp00359en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1046/j.1365-2559.1998.00339.xen_HK
dc.identifier.pmid9543668-
dc.identifier.scopuseid_2-s2.0-0031906774en_HK
dc.identifier.hkuros33957en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031906774&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume32en_HK
dc.identifier.issue2en_HK
dc.identifier.spage126en_HK
dc.identifier.epage132en_HK
dc.identifier.isiWOS:000072646400005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYuen, ST=7103160927en_HK
dc.identifier.scopusauthoridWong, MP=7403907887en_HK
dc.identifier.scopusauthoridChung, LP=24315879100en_HK
dc.identifier.scopusauthoridChan, SY=7404255845en_HK
dc.identifier.scopusauthoridCheung, N=36803314200en_HK
dc.identifier.scopusauthoridHo, J=7402649983en_HK
dc.identifier.scopusauthoridLeung, SY=7202044886en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats