Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-9-24
pubmed:abstractText
Carcinogenesis of cervical cancer has been investigated, and p16(INK4a) overexpression in squamous cell carcinoma of the cervix has been reported as a result of infection by human papillomavirus (HPV) (eg, HPV 16), and the consequence of the retinoblastoma (Rb) protein inactivation by HPV E7 protein. However, to our knowledge, there have been no studies on the relation between p16(INK4a) overexpression associated with HPV and small cell carcinoma of the cervix, which behaves more aggressively clinically than squamous cell carcinoma. The purpose of this study was to determine whether p16(INK4a) is overexpressed in small cell carcinoma, and if p16(INK4a) is overexpressed, the types of HPV that are related to this cancer. We reviewed 10 cases of small cell carcinoma and examined them for p16(INK4a) overexpression by immunohistochemistry. We also performed HPV typing with polymerase chain reaction (PCR)-sequencing analysis and in situ hybridization and found that p16(INK4a) was overexpressed in every case. PCR-sequencing analyses revealed that all cases were HPV-positive and that 9 cases were positive for HPV 18. Five of the 9 cases positive for HPV 18 were also positive by in situ hybridization and yielded a punctate signal, considered to represent the integrated form. In conclusion, p16(INK4a) was overexpressed and HPV 18 was frequently detected in an integrated form in small cell carcinoma. Therefore, inactivation of Rb protein by HPV 18 E7 protein may be associated with carcinogenesis of small cell carcinoma the same as inactivation of Rb protein by HPV 16 E7 protein is associated with carcinogenesis of squamous cell carcinoma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0046-8177
pubmed:author
pubmed:issnType
Print
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
778-83
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:14506638-Adult, pubmed-meshheading:14506638-Aged, pubmed-meshheading:14506638-Carcinoma, Small Cell, pubmed-meshheading:14506638-Cyclin-Dependent Kinase Inhibitor p16, pubmed-meshheading:14506638-DNA, Viral, pubmed-meshheading:14506638-Female, pubmed-meshheading:14506638-Humans, pubmed-meshheading:14506638-Immunoenzyme Techniques, pubmed-meshheading:14506638-In Situ Hybridization, pubmed-meshheading:14506638-Middle Aged, pubmed-meshheading:14506638-Neoplasm Staging, pubmed-meshheading:14506638-Papillomaviridae, pubmed-meshheading:14506638-Papillomavirus Infections, pubmed-meshheading:14506638-Polymerase Chain Reaction, pubmed-meshheading:14506638-Tumor Markers, Biological, pubmed-meshheading:14506638-Tumor Virus Infections, pubmed-meshheading:14506638-Uterine Cervical Neoplasms
pubmed:year
2003
pubmed:articleTitle
P16 overexpression and human papillomavirus infection in small cell carcinoma of the uterine cervix.
pubmed:affiliation
Department of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't