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Article: p53 oncoprotein accumulation in adenoid cystic carcinoma of parotid and palatine salivary glands

Titlep53 oncoprotein accumulation in adenoid cystic carcinoma of parotid and palatine salivary glands
Authors
KeywordsAdenoid cystic carcinoma
Histopathology
p53
Prognosis
Salivary gland neoplasm
Issue Date1997
PublisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/00313025.asp
Citation
Pathology, 1997, v. 29 n. 2, p. 154-158 How to Cite?
AbstractPrevious studies have suggested that alterations of the p53 gene are the most common genetic abnormality in human cancer. The aims of the present study were to evaluate p53 protein (p53P) immunostaining in adenoid cystic carcinoma (ACC) of the salivary gland and to correlate the expression with patient survival. A total of 27 cases of ACC in the parotid gland (n = 12) and the minor palatine glands (n = 15) were studied, with ten cases each of normal parotid and palatine glands as non-neoplastic controls. Staining was performed with mouse monoclonal antibody DO-7 against p53 (Dako, USA) using the ABC method. Stained nuclei irrespective of intensity or frequency were considered as positive. The frequency of positive nuclei was evaluated as the p53P index (p53PI), the percentage of the total nuclei in the reference epithelium. Clinical survival data were available for patients for periods up to 156 months. Our data showed that no normal tissues showed immunoreactivity with p53P in their nuclei. Thirteen of 15 (87%) cases of palatal and two of 12 (17%) cases of parotid neoplasms stained with p53P and the p53PI ranged from 0.01 to 10%. The number of p53P positive tumors was significantly higher in palatal than in parotid neoplasms, suggesting that palatal ACCs may be more aggressive in comparison with parotid ACCs. Our data also showed that the number of p53P positive tumors was significantly increased in patients who died of tumors than in patients with no evidence of disease at the end of the follow-up period between 60 to 156 months. These results suggest that p53P may be involved in the development of salivary gland ACCs and that p53P analysis may be a useful indicator of poor prognosis.
Persistent Identifierhttp://hdl.handle.net/10722/67451
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 0.919
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhu, QRen_HK
dc.contributor.authorWhite, FHen_HK
dc.contributor.authorTipoe, GLen_HK
dc.date.accessioned2010-09-06T05:55:15Z-
dc.date.available2010-09-06T05:55:15Z-
dc.date.issued1997en_HK
dc.identifier.citationPathology, 1997, v. 29 n. 2, p. 154-158en_HK
dc.identifier.issn0031-3025en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67451-
dc.description.abstractPrevious studies have suggested that alterations of the p53 gene are the most common genetic abnormality in human cancer. The aims of the present study were to evaluate p53 protein (p53P) immunostaining in adenoid cystic carcinoma (ACC) of the salivary gland and to correlate the expression with patient survival. A total of 27 cases of ACC in the parotid gland (n = 12) and the minor palatine glands (n = 15) were studied, with ten cases each of normal parotid and palatine glands as non-neoplastic controls. Staining was performed with mouse monoclonal antibody DO-7 against p53 (Dako, USA) using the ABC method. Stained nuclei irrespective of intensity or frequency were considered as positive. The frequency of positive nuclei was evaluated as the p53P index (p53PI), the percentage of the total nuclei in the reference epithelium. Clinical survival data were available for patients for periods up to 156 months. Our data showed that no normal tissues showed immunoreactivity with p53P in their nuclei. Thirteen of 15 (87%) cases of palatal and two of 12 (17%) cases of parotid neoplasms stained with p53P and the p53PI ranged from 0.01 to 10%. The number of p53P positive tumors was significantly higher in palatal than in parotid neoplasms, suggesting that palatal ACCs may be more aggressive in comparison with parotid ACCs. Our data also showed that the number of p53P positive tumors was significantly increased in patients who died of tumors than in patients with no evidence of disease at the end of the follow-up period between 60 to 156 months. These results suggest that p53P may be involved in the development of salivary gland ACCs and that p53P analysis may be a useful indicator of poor prognosis.en_HK
dc.languageengen_HK
dc.publisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/00313025.aspen_HK
dc.relation.ispartofPathologyen_HK
dc.rightsPathology. Copyright © Informa Healthcare.en_HK
dc.subjectAdenoid cystic carcinoma-
dc.subjectHistopathology-
dc.subjectp53-
dc.subjectPrognosis-
dc.subjectSalivary gland neoplasm-
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshCarcinoma, Adenoid Cystic - metabolism - mortalityen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshSalivary Gland Neoplasms - metabolism - mortalityen_HK
dc.subject.meshSurvival Rateen_HK
dc.subject.meshTumor Suppressor Protein p53 - metabolismen_HK
dc.titlep53 oncoprotein accumulation in adenoid cystic carcinoma of parotid and palatine salivary glandsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0031-3025&volume=29&spage=154&epage=158&date=1997&atitle=p53+Oncoprotein+accumulation+in+adenoid+cystic+carcinoma+of+parotid+and+palatine+salivary+glandsen_HK
dc.identifier.emailTipoe, GL:tgeorge@hkucc.hku.hken_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1080/00313029700169784en_HK
dc.identifier.pmid9213334-
dc.identifier.scopuseid_2-s2.0-0030739001en_HK
dc.identifier.hkuros23617en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030739001&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue2en_HK
dc.identifier.spage154en_HK
dc.identifier.epage158en_HK
dc.identifier.isiWOS:A1997XH82100007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridZhu, QR=16026167700en_HK
dc.identifier.scopusauthoridWhite, FH=7202578907en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.issnl0031-3025-

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