Linked Life Data

11564582

Source:http://linkedlifedata.com/resource/pubmed/id/11564582

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2001-9-20
pubmed:abstractText
Abnormal amplification of epidermal growth factor receptor (EGFR) gene has been reported widely in various human tumors. However, the status of amplification of this gene in the process of carcinogenesis is not clearly defined. We used competitive polymerase chain reaction (PCR) to study whether EGFR gene is amplified and the degree of amplification in pre-malignant and malignant oral epithelial lesions, and also examined the relationship between EGFR gene aberration and the development of squamous cell carcinoma (SCC). Genomic DNA was extracted from paraffin sections of 17 cases of oral epithelial dysplasia (ED), four cases of carcinoma in situ (CIS), and 20 cases of untreated primary SCC. The extracted DNA was subjected to competitive PCR to amplify EGFR gene. Amplification of the EGFR gene was observed in three cases (17%) of ED, one case of CIS and four cases (20%) of SCC. In cases showing EGFR gene amplification, the degree of amplification was low in ED and CIS cases, whereas it was extremely high in SCC cases. These results suggest that amplification of EGFR gene occurs in the relatively early stage of the development of oral SCC. However, a high level of EGFR gene accumulation probably plays an important role in the progression to invasive cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1368-8375
pubmed:author
pubmed:issnType
Print
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
599-604
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Quantitation of epidermal growth factor receptor gene amplification by competitive polymerase chain reaction in pre-malignant and malignant oral epithelial lesions.
pubmed:affiliation
Department of Oral Pathology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700-8525, Japan. jin@dent.okayama-u.ac.jp
pubmed:publicationType
Journal Article