p53 and PCNA expression in carcinogenesis of the oropharyngeal mucosa

Girod, Sabine; Pape, H.-D.; Krueger, G. R. F.

doi:10.1016/0964-1955(94)90023-x

Cited by 40 publications

(27 citation statements)

References 16 publications

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“…Girod SC et al, on quantitative analysis showed a gradual increase in PCNA expression from normal mucosa to moderately differentiated squamous cell carcinoma [12]. Our study also showed a similar pattern of increase in PCNA index [Table/ Fig-1,3-7].…”

Section: Discussionsupporting

confidence: 85%

Proliferating Cell Nuclear Antigen in Premalignancy and Oral Squamous Cell Carcinoma

Poosarla

Ramesh

Gudiseva

et al. 2015

JCDR

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Section: Discussionsupporting

confidence: 85%

Proliferating Cell Nuclear Antigen in Premalignancy and Oral Squamous Cell Carcinoma

Poosarla

Ramesh

Gudiseva

et al. 2015

JCDR

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“…Both of these are considered to be areas of active cell division. This might support the suggestion of a correlation between positive p53 staining and proliferative activity of these cells as reported by others [38,39].…”

Section: Discussionsupporting

confidence: 79%

Expression of biomarkers (p53, transforming growth factor alpha, epidermal growth factor receptor, c-erbB-2/neu and the proliferative cell nuclear antigen) in oropharyngeal squamous cell carcinomas

et al. 1999

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Using immunohistochemistry, expression of p53, transforming growth factor-alpha (TGF-a), epidermal growth factor receptor (EGFR), c-erbB-2/neu and proliferating cell nuclear antigen (PCNA) was examined in 26 fresh frozen tissue specimens of oropharyngeal squamous cell carcinomas (SCCs). p53 gene mutations were examined by polymerase chain reaction (PCR)/DNA sequencing methods in 22 carcinomas. The ®ndings were examined for correlations with patients' clinicopathological parameters. Expressions of p53 and PCNA were also examined in 21 formalin-®xed corresponding tissues. Of the fresh frozen tissue specimens, 77% (20/26) showed expression and 68% (15/22) showed mutations (substitutions) of the p53, with signi®cant clustering of the mutations in exons 5 (8/22; 36%), 7 (4/22; 18%) and 8 (5/22; 23%). No mutations were found in exon 6. There was a discordance between expression of p53 protein and mutations of the gene. Parallel to expression and mutations of the p53 found in most of the specimens, expression of TGF-a, EGFR, c-erbB-2/neu and PCNA was found in 88% (22/25), 92% (23/25), 58% (14/24) and 91% (21/23) of the specimens, respectively. For the formalin-®xed tissue specimens, 62% (13/21) and 90% (19/21) expressed p53 and PCNA, respectively. Examining for correlations with patients' clinicopathological parameters, expression of p53, TGF-a, EGFR and c-erbB-2/neu seemed to negatively correlate with the increase of the tumour grade. The present work suggests that: (1) lack of negative growth regulation due to inactivation of the p53 gene together with activation of other proto-oncogenes are necessary genetic events in the carcinogenesis of oropharyngeal SCCs; (2) in oropharyngeal SCCs, p53 gene mutations were clustered in exons 5 (codons 130±186), 7 (codons 230±248) and 8 (codons 271±282) which perhaps suggests that tobacco carcinogens probably aect the mutational hot spots of the p53 gene at codons 157, 175, 186, 248, 273 and 282; and (3) fresh frozen and formalin-®xed tissue specimens give similar results when an immunohistochemical method is applied. The importance of p53, TGF-a, EGFR, c-erbB-2/ neu and PCNA as biomarkers in oropharyngeal SCCs deserves particular attention because it might oer further understanding of the development of these carcinomas. #

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“…To uncover some of the molecular genetic aberrations associated with OLP, investigators have used molecular and genetic methods such as loss of heterozygosity (LOH) (Zhang et al, 2000), chromosome in situ hybridization (Kim et al, 2001), p53 and c-erbB2 expression (Girod et al, 1994(Girod et al, , 1995Kilpi et al, 1996;Ogmundsdottir et al, 2002), and telomerase activity (O'Flatharta et al, 2002). However, none of these methods appears to provide definitive predictive information with regard to the malignant potential of a lesion diagnosed as OLP.…”

Section: Chromosomal Numerical Aberrations In Oral Lichen Planusmentioning

confidence: 97%

Chromosomal Numerical Aberrations in Oral Lichen Planus

et al. 2009

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The malignant potential of oral lichen planus (OLP) has been a matter of serious controversy. We aimed to detect chromosomal numerical aberrations in cells of brush samples collected from affected mucosa. The samples were simultaneously analyzed for morphology and fluorescent in situ hybridization (FISH) with chromosomes 2 and 8 centromeric probes. We analyzed 57 persons with OLP and 33 control individuals. A cut-off value of aneuploid cells was determined as 1.1%. Aneuploid cells were found in 16 persons with OLP (28.1%); in 10 individuals (17.5%), over 5% of the cells were aneuploid. Aneuploid cells were also detected in normal-looking mucosa of seven persons with OLP. One person with OLP developed squamous cell carcinoma; 10% of the cells examined were aneuploid. OLP carries an increased risk for chromosomal instability. Identifying aneuploid cells in a brush sample and the combined morphological and FISH analysis can increase the specificity in predicting the malignant potential of OLP.

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p53 and PCNA expression in carcinogenesis of the oropharyngeal mucosa

Cited by 40 publications

References 16 publications

Proliferating Cell Nuclear Antigen in Premalignancy and Oral Squamous Cell Carcinoma

Proliferating Cell Nuclear Antigen in Premalignancy and Oral Squamous Cell Carcinoma

Expression of biomarkers (p53, transforming growth factor alpha, epidermal growth factor receptor, c-erbB-2/neu and the proliferative cell nuclear antigen) in oropharyngeal squamous cell carcinomas

Chromosomal Numerical Aberrations in Oral Lichen Planus

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