RGD Reference Report - Senescence and apoptosis in carcinogenesis of cervical squamous carcinoma. - Rat Genome Database

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Senescence and apoptosis in carcinogenesis of cervical squamous carcinoma.

Authors: Feng, W  Xiao, J  Zhang, Z  Rosen, DG  Brown, RE  Liu, J  Duan, X 
Citation: Feng W, etal., Mod Pathol. 2007 Sep;20(9):961-6. Epub 2007 Jul 13.
RGD ID: 2289695
Pubmed: PMID:17632454   (View Abstract at PubMed)
DOI: DOI:10.1038/modpathol.3800927   (Journal Full-text)

Senescence and apoptosis are two key mechanisms that protect against cancer development. Many cell cycle regulators, such as p14(ARF), p15(INK4b) and p16(INK4a), are important in G1 cell cycle arrest and oncogene-induced senescence. The bcl-2 protein is one of the key components that control apoptosis, while the p53 protein plays key roles in both mechanisms. The genes of these key regulator proteins are often mutated or deleted in various malignancies. It is unknown how senescence and apoptosis are regulated in one of the most common tumors of the female genital tract, cervical squamous cell carcinoma (SCC). In this study the, expression of senescence, apoptosis and proliferation markers in normal cervical epithelium, cervical intraepithelial neoplasia (CIN) and SCC are characterized via immunohistochemical staining for p14(ARF), p15(INK4b), p16(INK4a), bcl-2, p53 and Ki-67 in tissue microarray blocks containing 20 samples each of normal cervix, moderate-to-severe cervical dysplasia (CIN II-III) and invasive SCC. Samples are derived from 60 total cases of cervical biopsies and cervical conizations. Results showed that the proliferation marker, Ki-67, is markedly increased, and the senescence markers, p15(INK4b), p16(INK4a) and p14(ARF) are overexpressed in both dysplasia and carcinoma. P53 immunostain is negative in all normal cervical tissue, and positive in dysplasia and carcinoma. Although the expression of bcl-2 is increased in dysplasia, this marker is negative in approximately half of SCC cases. These results suggest that some senescence pathways are activated and are still maintained in cervical dysplasia and carcinoma. However proliferation is increased and carcinogenesis is not thwarted, leading to eventual development of cervical cancer. Other mechanisms, such as those that account for the apparent overexpression of p53 and paradoxical loss of bcl-2 expression in some SCC cases, as well as additional senescence and apoptotic pathways, may play key roles carcinogenesis of cervical SCC.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
cervix uteri carcinoma in situ  IEP 2289695protein:increased expression:uterine cervixRGD 
cervix uteri carcinoma in situ  ISOCDKN2B (Homo sapiens)2289695; 2289695protein:increased expression:uterine cervixRGD 
Uterine Cervical Neoplasms  IEP 2289695protein:increased expression:uterine cervixRGD 
Uterine Cervical Neoplasms  ISOCDKN2B (Homo sapiens)2289695; 2289695protein:increased expression:uterine cervixRGD 

Objects Annotated

Genes (Rattus norvegicus)
Cdkn2b  (cyclin-dependent kinase inhibitor 2B)

Genes (Mus musculus)
Cdkn2b  (cyclin dependent kinase inhibitor 2B)

Genes (Homo sapiens)
CDKN2B  (cyclin dependent kinase inhibitor 2B)


Additional Information