Detection of p16 gene alteration in cervical cancer using tissue microdissection and LOH study

The p16 gene was identified as cyclin-dependent kinase inhibitor (CDKI) and this may negatively regulate the cell cycle by acting as a tumor suppressor. Using tissue microdissection, the molecular changes at p16 and Rb genes were analysed in the spectrum of disease from dysplasia to invasive cancer...

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Bibliographic Details
Published in:Cancer letters 1999-02, Vol.136 (1), p.101-108
Main Authors: Park, Jong Sup, Dong, Seung Myung, Kim, Hy Sook, Lee, Jung Young, Um, Soo Jong, Park, In Seo, Kim, Seung Jo, Namkoong, Sung Eun
Format: Article
Language:English
Subjects:
Biological and medical sciences
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - pathology
Carcinoma, Squamous Cell - virology
Cervical cancer
DNA Primers
DNA, Neoplasm - chemistry
DNA, Neoplasm - isolation & purification
DNA, Viral - chemistry
Female
Female genital diseases
Genes, p16 - genetics
Genes, Retinoblastoma - genetics
Gynecology. Andrology. Obstetrics
HPV
Humans
LOH
Loss of Heterozygosity
Medical sciences
Microdissection
Neoplasm Invasiveness
p16
Papillomaviridae - genetics
Polymorphism, Single-Stranded Conformational
Sequence Analysis, DNA
Tumors
Uterine Cervical Dysplasia - genetics
Uterine Cervical Dysplasia - virology
Uterine Cervical Neoplasms - genetics
Uterine Cervical Neoplasms - pathology
Uterine Cervical Neoplasms - virology
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Summary:The p16 gene was identified as cyclin-dependent kinase inhibitor (CDKI) and this may negatively regulate the cell cycle by acting as a tumor suppressor. Using tissue microdissection, the molecular changes at p16 and Rb genes were analysed in the spectrum of disease from dysplasia to invasive cancer of the uterine cervix. Six of 27 (22%) cases informative for D9S171 and IFNA of 9p21-22 marker ( p16INK4a) showed loss of one or both alleles in at least one of these loci. LOH of pRb was detected in 29% (5/17). Gene alterations at p16 and pRb loci were only detectable in some cases of HPV-16/18 DNA positive cervical cancer. Three cases demonstrated mutational changes of p16INK4a, and the alterations were determined to be G to T shift, suggesting transitional missense mutation. In summary, the inactivation of the p16/cdk-cyclin/Rb cascade may play an additional role during the malignant progression in HPV-16/18 positive cervical cancers.
ISSN:0304-3835
1872-7980
DOI:10.1016/S0304-3835(98)00366-8