Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-3-5
pubmed:abstractText
Cells expressing high-risk human papillomavirus (HPV) E7 protein display impaired checkpoint control after DNA damage and exhibit elevated rates of mutagenesis. Repression of HPV E7 expression results in the subsequent accumulation of hypophosphorylated retinoblastoma protein and repression of the Cdc25A genes. No study has been conducted to elucidate the role of Cdc25A in the development and progression of human oral carcinomas. To confirm Cdc25A protein expression together with HPV, immunohistochemistry, Western blotting, polymerase chain reaction (PCR), and reverse transcriptase (RT)-PCR were performed using various histological subtypes of oral carcinomas. Cdc25A protein was localized predominantly in the cell nuclei in carcinomas, and high expression was found in 54% of primary tumors. HPV-16 E7 was not found in non-neoplastic oral tissues, whereas it was observed in eight (36%) of 22 oral carcinomas. We found a significant correlation between Cdc25A over-expression and HPV-16 E7 positive carcinomas. There was a strong positive correlation between Cdc25A over-expression and tumor size and TNM stage. This study suggests that Cdc25A is likely to be an important mediator in the progression of oral tumors, and HPV-16 E7 may be a sensitive indicator of the involvement of viral oncogenes in oral carcinogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0945-6317
pubmed:author
pubmed:issnType
Print
pubmed:volume
450
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
65-71
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
High-risk human papillomavirus type 16 E7 oncogene associates with Cdc25A over-expression in oral squamous cell carcinoma.
pubmed:affiliation
Department of Dental and Medical Biochemistry, Graduate School of Biomedical Sciences, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima, 734-8553, Japan. bhawal2002@yahoo.co.in
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't